Product Search for novus: Novus Biologicals

NB600-501

beta-Actin Antibody (AC-15)

(27 Reviews)

(565 Publications)

0.1 ml

NB600-501

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - Cell line lysates were separated on SDS-PAGE and probed with 1:5000 Monoclonal Anti-beta-Actin Clone: AC-15 . The antibody was developed using Goat Anti-Mouse IgG-Peroxidase and a chemiluminescent substrate.Lanes: 1. HeLa, 2. JURKAT, 3. COS7, 4. NIH-3T3, 5. PC-12, 6. RAT2, 7.CHO, 8. MDBK, 9. MDCK

Immunocytochemistry/Immunofluorescence: beta-Actin Antibody (AC-15) [NB600-501] - Analysis of beta-Actin antibody on mouse fibroblasts. Image from verified customer review.

Immunohistochemistry: beta-Actin Antibody (AC-15) [NB600-501] - Staining of formalin-fixed, paraffin-embedded human heart sections with 1:1000 Monoclonal Anti-beta-Actin Clone: AC-15.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - Analysis of beta-Actin in bovine whole skeletal muscle lysate. Image from verified customer review.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - Whole cell extract of human fibroblasts was separated on SDS-PAGE and blotted with Monoclonal Anti-beta-Actin. The antibody was developed with Goat Anti-Mouse IgG, Peroxidase conjugate and AEC substrate. Lanes A: Antibody dilution 1:5,000 B: Negative control (only secondary antibody).

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - beta-Actin expression in human glioma cells using anti-beta-Actin antibody. Image from verified customer review.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - HEK293T cells transfected with Niaph virus Matrix Protein, expression 24h later. This image was submitted via customer review.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - MMP-11 expression in oral cancer cell lines and the MMP-11 knockdown in SCC9 cells reduce cell migration. Western blot analysis showing the expression of MMP-11 protein in five oral cancer cell lines. Beta-Actin is included as a loading control. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0113129), licensed under a CC-BY license.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - HSP90 and HSP70 interact with PABPN1. Interaction of PABPN1 with HSP90. Lysates from HEK293 cells transfected with Flag-HSP90 and GFP-tagged A17-PABPN1 were immunoprecipitated with an anti-Flag antibody. Immunoprecipitates (IP) were analyzed by Western blot (IB).Beta-Actin is included as a loading control. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0138936), licensed under a CC-BY license.

Western Blot: beta-Actin Antibody (AC-15) [NB600-501] - GFAP and IL-6 are elevated in cultures of spinal cord compared to cortical astrocytes. ((G, H) Analysis of protein homogenates from brain or spinal cord astrocyte cultures also demonstrated higher levels of GFAP expression, but no differences in ALDH1L1. Beta-Actin is included as a loading control. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0180697), licensed under a CC-BY license.

Immunocytochemistry/Immunofluorescence: beta-Actin Antibody (AC-15) [NB600-501] - Cultured FS-11 human fibroblast cell line stained using Monoclonal Anti-Beta-Actin, Clone No. AC-15 (NB600-501).

Immunocytochemistry/Immunofluorescence: beta-Actin Antibody (AC-15) [NB600-501] - HS-68 cells.

Simple Western: beta-Actin Antibody (AC-15) [NB600-501] - Analysis using the HRP conjugate of NB600-501. Electropherogram image(s) of corresponding Simple Western lane view. Beta-Actin antibody was used at 1:500 dilution on Hela, MCF-7, SH-SY5Y, & Jurkat lysate(s).

Simple Western: beta-Actin Antibody (AC-15) [NB600-501] - Analysis using the HRP conjugate of NB600-501. Image shows a specific band for Beta-Actin in 0.2 mg/mL of Hela, MCF-7, SH-SY5Y, & Jurkat lysate(s). This experiment was performed under reducing conditions using the 12-230 kDa separation system. * Non-specific interaction with the 230 kDa Simple Western standard may be seen with this antibody.

Activation of the mTOR signaling pathway during spheroid formation on chitosan film. (b and c) Whole-cell lysates were analyzed by western blotting with specific antibodies against indicated molecules. beta-tubulin and actin were used as the loading control. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-017-10708-0), licensed under a CC-BY licence.

$alphav regulates TLR signalling by engagement of autophagy machinery. (g,h) Western blot analysis of phosphorylated IKKalpha in cytoplasmic fractions (g), and NF-kappaB and IRF7 in nuclear fractions (h) from sorted MZ B cells isolated from alphav-CD19 and control mice, stimulated with CpG DNA for the indicated time (mins). Also shown are staining of actin (g) or LSD1 (h) to confirm equivalent protein loading. In both cases, representative blots from at least three independent experiments are shown. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/ncomms10917), licensed under a CC-BY licence.$

Wnt effect on AChR clustering requires interaction with MuSK. D) Wnt9a and Wnt11 induce MuSK tyrosine phosphorylation. C2C12 myotubes were treated by agrin or Wnts for 1 h. MuSK was purified by immunoprecipitation and probed with the 4G10 antibody. E, Wnt9a and Wnt11 induce MuSK dimerization. Flag-MuSK and MuSK-Myc were transfected into C2C12 myoblasts and resulting myotubes were treated by Wnts, agrin or control media for 1 h. Flag-MuSK was precipitated by Flag antibody and associated MuSK-Myc was determined by anti-Myc antibody. Band intensity of immunoblot was analyzed by ImageJ software. *, p 1.5 cutoff. Red and blue indicate high and low expression of genes, respectively. b Heatmaps of signal intensity illustrating H3K27me3 ChIP-seq genomic mapping in a window of ±2.5 kb identified in Ezh2+/+ and Ezh2−/− Tet-ON PyVmt tumours. c Overlap between differentially upregulated genes in Ezh2−/− endpoint Tet-ON PyVmT tumours and genes identified by ChIP-seq to be targeted by H3K27me3. d Differential H3K27me3 levels in the upstream promoter region of Foxc1 in Ezh2+/+ vs. Ezh2−/− endpoint Tet-On PyVmT tumours. Image from the IGV browser. e Left- Significant upregulation of Foxc1 mRNA in Ezh2−/− Tet-ON PyVmT endpoint tumours compared to wild-type tumours. Right- Immunoblot of Ezh2+/+ or Ezh2−/− Tet-ON PyVmT endpoint tumours for Foxc1 and Ezh2 levels. Vinculin loading control. *p 10 larvae/sample). Lc3 c and e, or p62 and Optineurin d protein levels were detected in absence or presence of BafA1, c and d, or in the presence or absence of Mm e. Actin was used as a loading control. Western Blots were repeated three, c and d, or two e times with protein extracts derived from independent experiments. The Lc3II/Actin or p62/Actin and Optineurin/Actin ratio, normalized to the control sample, is indicated below the blots. f–g Representative confocal micrographs and quantification of GFP-Lc3 co-localization with Mm clusters in infected dram1∆19n/∆19n and dram1+/+ larvae. The top images f show the entire region of imaging, while the bottom images f′ and f″ show details of GFP-Lc3 colocalization of Mm clusters in dram1∆19n/∆19n and dram1+/+ larvae. The arrowheads indicate GFP-Lc3-positive Mm clusters. The data is accumulated from two independent experiments (≥15 larvae/group) and represented by scatter and boxplots as detailed in the “Methods” section. Scale bars, 10 μm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/32332700), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Effects of in vitro hypoxia on the expression of mouse HIF-1 alpha in HIF-1 alpha +/- and HIF-1 alpha +/+ astrocytes. Confluent astrocyte monolayers of both cell types were exposed to a 6 h in vitro hypoxia. HIF-1 alpha mRNA expression was determined by RT-PCR as described in Materials and Methods. Each bar represents the mean ± SD of relative density/volumes of the bands on film negatives from at least three experiments. Asterisks and number sign indicate significant difference (p 5 53BP1 nuclear bodies in cells treated as in a. Similar analyses were conducted using stable cells lines expressing either WT or CI human MUS81. Error bars represent s.d. (n=3). *P0.05. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/24124516), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Tamoxifen administration-induced PHD2 deletion in skeletal muscle in Phd2f/f/Rosa26CreERT2 mice. a. PHD1, 2, and 3 deletion efficiency in the gastrocnemius muscles of tamoxifen-treated Phd2f/f/Rosa26CreERT2 mice was determined using qRT-PCR. Relative gene expression was determined using gastrocnemius muscle tissue cDNA (n = 3–4 mice per group). b. Anti-PHD2 and PHD3 Western blotting of gastrocnemius and soleus muscles at 6 weeks after tamoxifen administration. c. The expression of HIF-1 alpha in gastrocnemius and soleus at 5 weeks after tamoxifen administration. d. The level of hif-1 alpha mRNA in gastrocnemius at 5 weeks after tamoxifen administration. *p < 0.05; **p < 0.01 compared to control. Values are means ± SEM Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/26949511), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Effect of silencing Cx43 on the expression of HIF-1 alpha in astrocytes.Astrocytes were transfected with NT-siRNA or with Cx43-siRNA. At the indicated times the expression of HIF-1 alpha and Cx43 was analysed by Western blot. A) Representative Western blot of HIF-1 alpha , Cx43 and GAPDH showing that the decrease in Cx43 expression was concomitant with HIF-1 alpha up-regulation. B) HIF-1 alpha quantification. C) Cx43 quantification. The results are expressed as percentages of the level found in the NT-siRNA condition at time 0. ***p<0.001 versus the corresponding NT-siRNA values. Image collected and cropped by CiteAb from the following open publication (//dx.plos.org/10.1371/journal.pone.0032448), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Analysis of NS5B protein expression after transfecting NS5B and La autoantigen siRNAs: HCV-infected Huh-7.5 cells were treated with siRNAs against La autoantigen and NS5B as mentioned above. After 48 h total cellular protein was isolated and subjected to western blot analysis. (a) indicates downregulation of La autoantigen (upper gel) and NS5B (middle gel) and beta -actin (lower gel). (b) represents densitometric analysis of La autoantigen and HCV NS5B expressed in percentage. Immunofluorescence of NS5B from single and combination of siRNAs transfected cells as represented in (c) where row (A) indicates cells in bright field and row (B) is the merging of DAPI and FITC stained cells. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/27446609), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

SLD-LPS-mediated Keap1 accumulation is correlated with a pro-inflammatory monocyte phenotype. BMDMs were treated with either PBS or SLD-LPS (100 pg/mL) for 5 days. (A) Representative Co-IP result with no lysate IP (just antibody and beads) (Con.) and the whole cell lysate input (WCL) controls. Keap1 antibody was used to pull-down Nrf2 (upper blot), and Nrf2 was used to pull down Keap1 (lower blot). See Supplemental Figures S3, S4 for un-altered blots. (B–D) The levels of Ly6C (B), Keap-1 (C), and CD200R (D) were analyzed and quantified using geometric mean fluorescence intensity (MFI) by flow cytometry. (E–G) Representative western blots of IKK beta (E), p-p65 (S536) (F), and total NF-kappa B p65 (G) in monocytes with quantification on the left. (H) p-p65/total p65 ratio. All data are representative of at least 3 separate experiments (n = 3, except for IKK-beta where n = 5). Unpaired student t-test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/32765513), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Effect of alcohol on TERT expression in vitro.Acute alcohol treatment of RAW 264.7 cells can be achieved with 25 mM EtOH for 24 h. (a) TERT mRNA and protein expression in EtOH-stimulated RAW 264.7 cells were analyzed by real-time PCR and western blot. The results are shown as relative expression against control expression without treatment. The values represent means ± SD. *P < 0.05, **P < 0.01 vs control. #P<0.05, ##P<0.01 vs EtOH-treated group. (b) Effect of alcohol on M1 macrophage markers (TNF-alpha , IL-1 beta , CCL2 and NOS2) in RAW 264.7 cells without or with LPS stimulation. (c) Effect of alcohol on M2 macrophage markers (Arg-1, IL-10, Mrc2 and CD163) in RAW 264.7 cells without or with LPS stimulation. (d) Effect of alcohol on the production of cytokines including TNF-alpha , IL-1 beta , IL-6, IL-12 and IL-10 in RAW 264.7 cells without or with LPS stimulation. The results are shown as line chart. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/26725521), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Widespread dysregulation of shelterin protein expression in bortezomib-treated HEL and BGC-823 cellsA. and B. mRNA levels of shelterin factors TRF1, TRF2, TPP1, POT1, RAP1 and TIN2 in bortezomib-treated cells. Cells were treated with bortezomib for 24 hours and qPCR was used for quantitative assays. The levels of each target mRNA in bortezomib-treated cells were expressed as percentages of those in untreated cells. (A) HEL cells and (B) BGC-823 cells. C. and D. Immunoblotting assessment of TRF1, TRF2 and POT1 protein expression in bortezomib-treated cells. Same sets of cells above were analyzed for TRF1, TRF2 and POT1 protein levels and shown was representative of three independent experiments. (C) HEL cells and (D) BGC-823 cells. * and **: P < 0.05 and 0.01, respectively. BTZ, bortezomib. Image collected and cropped by CiteAb from the following open publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.5752), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

AMPK‐activating AICAR treatment activates FANCD2, a pivotal molecule of Fanconi anemia DNA damage signaling pathway. (A) AICAR treatment induces FANCD2 monoubiquitination in transformed normal fibroblasts (GM00637I). GM00637I cells were treated with 1 mm 2‐deoxyglucose, 0.25 mM AICAR, or 1 mm phenformin for 24 h. Lysates were subjected to western blotting with anti‐FANCD2, phospho‐AMPK alpha 1 (T172), and AMPK alpha and beta ‐actin. In FANCD2 blots, the position of monoubiquitinated FANCD2 (Ub‐FANCD2) is indicated by an arrow. (B) AICAR treatment induces formation of FANCD2 nuclear foci in GM00637I fibroblasts. Cells grown on coverslips in 12‐well plates were treated with 0.25 mm AICAR for 24 h. Cells were immunostained with FANCD2 antibody and Alexa 488‐conjugated anti‐rabbit secondary antibody. FANCD2 foci were visualized by confocal microscopy. Representative images are shown at the top. The number of foci per cell was counted and plotted for ≥ 20 cells (bottom panel). The values represent the mean ± SEM (Student's t‐test, ***P < 0.001). (C) AICAR treatment induces FANCD2 monoubiquitination in Caki‐1 cells. Caki‐1 cells were treated with 0.25 mm AICAR for 24 h and monoubiquitination of FANCD2 was monitored as in (A). Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28174693), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

RNA:DNA hybrid formation is central to ATM-53BP1 repair pathway.(a) Immunofluorescence using the anti-flag to quantify nuclear hybrid-binding (HB) domain foci signal in pre-permeabilized RPE cells and quantification of HB domain signal in cells treated with siATM, (b) Western blot showing ATM depletion. (c) Immunofluorescence and HB-domain foci quantification in cells treated with ATM inhibitor. (d) Quantitation of gamma H2AX foci in cells expressing HB domain or active RNAseH1, in presence or absence of H2O2 dependent oxidative stress. siC, non-targeted control siLuciferease RNA. Column bars represent the mean of n number of cells (described on each column) from three independent experiments. Error bars represent SEM. *P ≤ 0.05; **P < 0.01, ***P < 0.001 using Mann-Whitney test (a,c) and Kruskal-Wallis test followed by Dunn’s post hoc test (d). Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/30345028), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po, Bv, Ca, Ch, Fe, Fi, Gp, Ha, Le, Ma, Pm, Rb, Sh, Sq, Tr, Ze, Dr(-)

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Bv, Ca, Ch, Fe, Fi, Gp, Ha, Le, Ma, Pm, Rb, Sh, Sq, Tr, Ze, Dr(-)

Applications:

, , , , , , , , ,

Applications: , , , , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB110-67828AF350
Alexa Fluor 405	NB110-67828AF405
Alexa Fluor 488	NB110-67828AF488
Alexa Fluor 532	NB110-67828AF532
Alexa Fluor 594	NB110-67828AF594
Alexa Fluor 647	NB110-67828AF647
Alexa Fluor 700	NB110-67828AF700
Alexa Fluor 750	NB110-67828AF750
Biotin	NB110-67828B
DyLight 350	NB110-67828UV
DyLight 405	NB110-67828V
DyLight 488	NB110-67828G
DyLight 550	NB110-67828R
DyLight 594	NB110-67828DL594
DyLight 650	NB110-67828C
DyLight 680	NB110-67828FR
DyLight 755	NB110-67828IR
FITC	NB110-67828F
HRP	NB110-67828H
Janelia Fluor 549	NB110-67828JF549
Janelia Fluor 646	NB110-67828JF646
PerCP	NB110-67828PCP
mFluor Violet 450 SE	NB110-67828MFV450
mFluor Violet 500 SE	NB110-67828MFV500
mFluor Violet 610 SE	NB110-67828MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NB110-67828

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MAB1835

TGF beta 1/2/3 Antibody (1D11) [Unconjugated]

(1 Review)

(222 Publications)

100 μg

MAB1835

Recombinant Human TGF‑ beta 1 (Catalog # 240‑B) inhibits Recombinant Mouse IL‑4 (Catalog # 404-ML) induced proliferation in the HT‑2 mouse T cell line in a dose-dependent manner (orange line). Inhibition of Recombinant Mouse IL‑4 (7.5 ng/mL) activity elicited by Recombinant Human TGF‑ beta 1 (1 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-TGF‑ beta 1, 2, 3 Monoclonal Antibody (Catalog # MAB1835). The ND50 is typically0.25‑1.25 µg/mL.

Apoptotic cell-induced immunomodulation in mice with collagen-induced arthritis (CIA) is dependent on transforming growth factor (TGF)-beta . CIA mice that received or did not receive apoptotic cells, with or without anti-TGF-beta blocking antibody were scored daily (a). Data are shown as mean ± SEM of five mice per group from one of two representative experiments; *p < 0.05, **p < 0.01 (Friedman test analysis of variance (ANOVA) with Dunn's multiple comparisons test). Anti-collagen IgG2a antibodies (Ab) were quantified in plasma (b). Data from 5 to 16 mice from two to three independent experiments (no difference, Kruskal-Wallis test ANOVA with Dunn’s multiple comparisons test). Lymph node cells were collected, cultured, and T cell proliferation in response to collagen protein or CD3-specific Ab stimulations was evaluated (c). Data are shown as mean ± SEM from one of two representative experiments; *p < 0.05, **p < 0.01 (nonparametric unpaired t test). Percent and absolute number of Foxp3+ T regulatory cells (Treg) were evaluated in the spleen (d) and suppressive assays were performed by isolating and adding Treg at a different ratio into collagen-specific cultures and responder T cell proliferation was assessed (e). Data are shown as mean ± SEM from one experiment (d Kruskal-Wallis test ANOVA with Dunn’s multiple comparisons test; e Friedman test ANOVA with Dunn’s multiple comparisons test). Plasmacytoid dendritic cells (pDC), conventional dendritic cells (cDC) and macrophages (macro) were isolated and cultured with naïve allogenic T cells to determine Treg polarization (f), and their response to TLR ligand was assessed through evaluation of CD40 costimulatory molecule expression (g). Data from individual mouse plus mean (black bar) from one experiment representative of four are shown; *p < 0.05, ***p < 0.001 (f ordinary one-way ANOVA with Tukey’s multiple comparisons test; g Kruskal-Wallis test ANOVA with Dunn’s multiple comparisons test). BrDU 5-Bromo-2’-deoxyuridine Image collected and cropped by CiteAb from the following publication (//arthritis-research.biomedcentral.com/articles/10.1186/s13075-016-1084-0), licensed under a CC-BY license. Not internally tested by R&D Systems.

TGF beta 1 stimulates the expression of ECM components in human and rabbit primary cells. (A) Selected ECM mRNA transcripts were measured using qRT-PCR in human RPTEC or human IPF134 following 48 hr stimulation with TGF beta 1 (10 ng/mL). Data show transcript abundance relative to the unstimulated control (indicated by the dashed line) and are shown as mean ± SD of four (RPTEC) or seven (IPF134) independent experiments. ****P < 0.0001; ****P < 0.001; **P < 0.01; Student’s t-test. (B) The accumulation of ECM in human RPTEC (i) or human IPF (ii) cells stimulated with 10ng/mL TGF beta 1 was evaluated via measurement of the incorporation of 14C-labelled amino acids into the deposited ECM. Data presented are the mean ± SD of three independent experiments. **P < 0.01; Student’s t-test. (C) Increased mature ECM accumulation following treatment of cells with a pro-fibrotic stimulus can be visualised following in-situ fluorescent staining using the Flamingo dye. Cells from three different systems (primary human RPTEC; primary human IPF134; co-culture of primary rabbit RPTEC with primary rabbit renal fibroblasts) were cultured in the absence (top) or presence (bottom) of 10 ng/ml TGF beta 1 before decellularised matrix was fixed and stained in situ with Flamingo fluorescent dye. Images show a single field. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28855577), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reactivity:

All-Multi

Species Glossary

Reactivity: All-Multi

Applications:

, ,

Applications: , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	FAB1835U
Alexa Fluor 405	FAB1835V
Alexa Fluor 488	FAB1835G
Alexa Fluor 532	FAB1835X
Alexa Fluor 594	FAB1835T
Alexa Fluor 647	FAB1835R
Alexa Fluor 700	FAB1835N
Alexa Fluor 750	FAB1835S
Allophycocyanin	FAB1835A
Biotin	FAB1835B
DyLight 350	FAB1835D
DyLight 405	FAB1835E
DyLight 488	FAB1835K
DyLight 550	FAB1835L
DyLight 594	FAB1835M
DyLight 650	FAB1835W
DyLight 680	FAB1835Y
DyLight 755	FAB1835Z
FITC	FAB1835F
HRP	FAB1835H
Janelia Fluor 549	FAB1835I
Janelia Fluor 646	FAB1835J
PerCP	FAB1835C
mFluor Violet 450 SE	FAB1835MFV450
mFluor Violet 500 SE	FAB1835MFV500
mFluor Violet 610 SE	FAB1835MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	MAB1835-SP
Carrier Free	MAB1835-500

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NB100-132

HIF-2 alpha/EPAS1 Antibody (ep190b)

(9 Reviews)

(184 Publications)

0.1 ml

NB100-132

Immunohistochemistry-Paraffin: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Analysis of HIF-2 in human cardiac myocytes using HIF-2 alpha/EPAS1 Antibody (ep190b).

Flow Cytometry: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - HIF-2 alpha antibody was tested at 1:400 in HepG2 cells using an Alexa Fluor 488 secondary (shown in purple). M1 is defined by unstained cells.

Western Blot: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Mouse aortic endothelial cells treated (1%) or not treated (20.9%) in hypoxia for 3 hrs. Cells where also transfected with a specific siRNA against (siHIF-2) or a control siRNA (-). Western blot image submitted by a verified customer review.

Immunohistochemistry-Paraffin: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Renal tubule specific models of Vhl deletion. Histological images of representative renal sections from 12 month old control, Pax8-CreERT2/Vhldelta/delta and Slc22a6-CreERT2/Vhldelta/delta mice (stains and antibodies as indicated, arrowheads indicate abnormal vascularization). Scale bars, 100 um. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0148055), licensed under a CC-BY license.

<b>Biological Strategies Validation. </b>Western Blot: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Analysis of HepG2 without Cobalt (II) Chloride (1), HepG2 with Cobalt (II) Chloride (2), HepG2 normoxic (3), HepG2 hypoxic (4), HepG2 without Cobalt (II) Chloride (5), HepG2 with Cobalt (II) Chloride (6), HepG2 normoxic (7), and HepG2 hypoxic (8) using this antibody (NB100-132) at 1 - 2 ug/mL.

<b>Biological Strategies Validation. </b>Western Blot: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - [HRP] [NB100-132H] - Analysis of HIF-2 alpha stabilization over time in HOS cells following exposure to hypoxia. Image using the HRP form of this antibody (NB100-132H). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/23785417/) licensed under a CC-BY license.

<b>Biological Strategies Validation. </b>Western Blot: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Western blot analysis and quantification of HIF-2 alpha expression in the cortex 4.5 hours after lipopolysaccharide (LPS) administration for all LPS groups and the control group (SHAM, white bar). With the exception of the vagotomy group (VGX LPS, gray bar), no significant differences to the SHAM group were found in the LPS-treated and sham-operated (SHAM+LPS, light gray bar) or vagus nerve-stimulated groups (VGX LPS+STIM, black bar). The significant increase in the VGX LPS (gray bar) group is an indicator of a hypoxic condition; * P<0.05 compared to SHAM; n=6 rats each. Data are given as the mean+/-SEM. Image collected and cropped by CiteAb from the following publication (//jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-9-183), licensed under a CC-BY license.

<b>Biological Strategies Validation. </b>Western Blot: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - 4-OOHCPA exposure induced HIF-2 alpha/EPAS1. A: Western blot analysis of HIF-2 alpha/EPAS1 protein (118KD) and actin (43KD) in limbs at 10 min, 1, 3, 6, and 24 h after treatment with 4-OOHCPA at 0.3 ug/mL (L) 1.0 ug/mL (M) or 3.0 ug/mL (H). P represents the positive control. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0051937), licensed under a CC-BY license.

Immunohistochemistry: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Analysis of HIF-2 alpha in human endometrium using. Donkey anti-mouse Alexa Fluor 488 secondary antibody was used. IHC image submitted by a verified customer review.

<b>Biological Strategies Validation and Genetic Strategies Validation.</b>Knockdown Validated: HIF-2 alpha/EPAS1 Antibody (ep190b) [NB100-132] - Functional role of HIF2A in the transcriptional regulation of amphiregulin (AREG) in human cardiac myocytes. Immunoblot for HIF1A or HIF2A from shRNA-transfected normoxic or hypoxic HCM. Beta-Actin (ACTb) served as a loading control. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/29483579/) licensed under a CC-BY license.

In vitro effects of diclofenac on proliferation and MYC expression in the human melanoma cell line MelIm. (E-G) MYC, STAT3, HIF1a and HIF2a protein expression were determined in cell lysates of MelIm incubated for 2 or 24 h with or without diclofenac (E,F) or ASA (G). The effect of diclofenac on MYC promoter activity was determined by transient transfection of a 2632-bp MYC promoter fragment (H). MelIm were transfected in 6-well-plates and diclofenac was added after 5 h. Luciferase activity was determined 24 h after transfection. Results represent the mean +/- standard deviation of 3 independent experiments. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0066987), licensed under a CC-BY licence.

BAY 87-2243 inhibits hypoxia-inducible factor (HIF-1alpha) and HIF-2alpha protein accumulation in hypoxic H460 cells H460 under hypoxia but has no effect on HIF-1alpha protein levels induced by hypoxia mimetics and has no effect on prolyl hydroxylase 2 (PHD2) activity. (A, B) H460 cells were cultured for 16 h under normoxia or hypoxia (1% pO2) in the absence or presence of various concentrations of BAY 87-2243. HIF-1alpha (A) and HIF-2alpha (B) protein levels were assessed by Western Blot in whole cell extracts. beta-actin was used as a loading control. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/24403227), licensed under a CC-BY licence.

HIF2alpha inhibitor 76 suppressed CoCl2-induced immature phenotypic characteristics of BCSCs. (A) The inhibitory effect of small molecule HIF2alpha inhibitor 76 for 24h (10 uM for 4T1 cells; 25 uM for Hs578T cells) on CoCl2-induced expression of HIF2alpha was assessed in both 4T1 and Hs578T cells by western blot analysis. Image collected and cropped by CiteAb from the following publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.9846), licensed under a CC-BY licence.

Hypoxic repression of ER-alpha is dependent on HIF-1alpha. a Representative western blots of HIF-1alpha, HIF-2alpha and beta-actin protein in ten ER-positive cell lines grown at normoxia or hypoxia (1% O2, 24 h). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28320353), licensed under a CC-BY licence.

Western blot analysis and quantification of HIF-2alpha expression in the cortex 4.5 hours after lipopolysaccharide (LPS) administration for all LPS groups and the control group (SHAM, white bar). With the exception of the vagotomy group (VGX LPS, gray bar), no significant differences to the SHAM group were found in the LPS-treated and sham-operated (SHAM + LPS, light gray bar) or vagus nerve-stimulated groups (VGX LPS + STIM, black bar). The significant increase in the VGX LPS (gray bar) group is an indicator of a hypoxic condition; * P < 0.05 compared to SHAM; n = 6 rats each. Data are given as the mean +/- SEM. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/22830560), licensed under a CC-BY licence.

Cytosol-restricted Acss2 is enzymatically active.(A) Acetylation of ectopic HA-tagged HIF-2alpha detected by immunoblotting (IB) with anti-HA or anti- acetylated lysine antibodies following immunoprecipitation (IP) with anti-HA antibody in stably transformed HT1080 cells with knockdown of endogenous Acss2 and rescue with ectopic wild-type (WT) or cytosol-restricted mutant (CYT) Acss2 without or with an SV40 nuclear localization signal fused to the amino terminus. Studies were performed under hypoxia, low glucose, or acetate exposure for the indicated periods. Image collected and cropped by CiteAb from the following publication (//dx.plos.org/10.1371/journal.pone.0190241), licensed under a CC-BY licence.

$Localisation of CDS1 immunoreactivity and CDS activity to mitochondria.[A, B] Differentiated H9c2 cells fractionated and analysed for [A] CDS1 immunoreactivity by Western blot; [B] CDS activity. [C-E] Rat heart fractionated and analysed for [C] CDS1 immunoreactivity and markers, [D] CDS1 immunoreactivity (entire Western blot shown) and [E] CDS activity. [F–H] Rat heart fractionated in the presence of the protease, subtilisin and analysed for [F] CDS1 immunoreactivity by western blot, [G] CDS activity and [H] PI synthase (PIS) activity. CDS and PIS activity was monitored in triplicate and error bars denote ± S.E.M. COXIV, GRP75 and cyto c are markers for mitochondria, PITPNC1 and PITP alpha are cytosolic markers and calnexin is a marker for the ER. WCL, whole cell lysate; Micro, microsomes; C.Mito, crude mitochondria; Cyto, cytosol; P.Mito, pure mitochondria, MAMs, mitochondrial associated membranes; PIS, PI synthase; CDS, CDP-diacylglycerol synthase. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29253589), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

Effect of overexpression or knockdown of PAL31 in C6 on H2O2-induced toxicity. (A) Representative micrographs showing C6 overexpressing GFP or GFP-tagged PAL31 after being treated with H2O2 (0 ~ 1 mM) for 4 hours. (B) MTT assay in GFP- or GFP-PAL31-overexpressed C6 after H2O2 treatment showing significant difference (cytoprotective effect of PAL31) at 0.5 mM and 1 mM H2O2 treatment between C6/GFP and C6/PAL31 groups. The data in each dosage were analyzed by two-way ANOVA and Bonferroni post hoc test. *P < 0.05, GFP (+H2O2) compared to PAL31 (+H2O2), n = 4, at 0.5 mM and 1 mM. (C) Western blot analysis of pal31 siRNA-treated C6 showing knockdown of PAL31 expression by PAL31 silencer using 41.5 (lane1), 83 (lane2), and 166 (lane 3) picomole of pal31 siRNA or 332 picomole negative control. Actin works as a loading control. (D) MTT assay in Negative- or PAL31 silencer transfected C6 after H2O2 treatment showing significant difference at 1 mM H2O2 treatment between C6/Negative and C6/PAL31 siRNA groups. *P < 0.05, Negative (+H2O2) compared to PAL31 siRNA (+H2O2), n = 4. Magnification 100X (A). Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/25034417), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Expression of PRDX2 or PRDX4 does not affect HIF-1 alpha or HIF-2 alpha protein levelsA. and B. HeLa cells were transfected with EV or vector encoding PRDX2-V5 (A, P2) or PRDX4-V5 (B, P4), and exposed to 20% or 1% O2 for 24 h. WCL was subject to immunoblot assays with antibody against HIF-1 alpha , HIF-2 alpha , V5, or acin. C. HeLa-shSC (sc) and HeLa-shPRDX(2+4) (2+4) cells were exposed to 20% or 1% O2 for 24 h in the presence of doxycycline. WCL was subject to immunoblot assays with antibodies against HIF-1 alpha , HIF-2 alpha , PRDX2, PRDX4, and actin. Image collected and cropped by CiteAb from the following open publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.7142), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

SAN1 functions independently of the FA pathway and does not affect FA pathway activation. a, b CSAs of HeLa WT and SAN1−/− cells treated with scrambled ctrl siRNA or FANCD2 siRNA, in response to Cisplatin and MMC (N = 3). Statistical significance determined by two-way ANOVA. Error bars denote s.e.m. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. c Immunoblot showing siRNA knockdown of FANCD2 in HeLa WT and SAN1−/− cells. d IF staining of FANCD2 foci in HeLa WT cells and SAN1−/− cells treated with 0.045 μM MMC. e Immunoblot of FANCD2 showing mono-ubiquitylation in HeLa WT and SAN1−/− cells treated with vehicle or 0.045 μM MMC. f, g CSAs of HeLa WT and SAN1−/− cells treated with ctrl or SNM1A siRNA and exposed to Cisplatin or MMC. Statistical significance was determined by two-way ANOVA test. h Immunoblot of SNM1A in HeLa WT and SAN1−/− cells treated with ctrl or SNM1A siRNA Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29968717), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

GAS6 triggers p-Axl, p-DAPK and CIP2A to form a protein complex in RSC96 cells(A-B) Co-immunoprecipitation between p-Axl, p-DAPK and CIP2A with GAS6 stimulation for 30 min in RSC96 cells. Total lysate indicates 1/10 input in each experiment. The relative quantification of protein expression was normalized with respect to beta -actin expression. (C) Immunofluorescence image demonstrating co-localized CIP2A and p-Axl and co-localized p-Axl and p-DAPK (D) after GAS6 stimulation for 30 min in RSC96 cells. Image collected and cropped by CiteAb from the following open publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.23978), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

FKBP51 increases expression of melanoma CSC markers. (a) FKBP51 silencing decreases ABCB5 levels. (Left) Normalized expression rates (arbitrary units (AU)) (mean±S.D.) of FKBP51 (black) and ABCB5 mRNA (grey) (n=3). FKBP51-treated sample expression=1. (Right) Western blot assay of ABCB5 and FKBP51 levels. (b) FKBP51 overexpression enhances ABCB5 levels. (Left) Normalized expression of FKBP51 mRNA (black) and ABCB5 mRNA (grey) measured in WT, EV-, or FKBP51-stably transfected melanoma cells. WT sample expression=1; n=3. (Left) Western blot assay of ABCB5 and FKBP51 levels in the same cells. Anti-Flag-labelled exogenous FKBP51. (c) ABCG2+ melanoma cells increase in FKBP51-overexpressing cells. (Upper) Normalized expression of FKBP51 mRNA (black) and ABCG2 mRNA (grey) measured in WT, EV-, or FKBP51-stably transfected melanoma cells. WT sample expression=1; n=5. (Lower) Flow cytometric histograms of ABCG2 expression (green population); mean±S.D. of counts are shown. (d) Enhanced FKBP51 mRNA levels in sorted ABCG2+ melanoma cells (SAN, upper; A375, lower). Whole cell expression=1; (n=3). (e) Enhanced EMT gene transcripts in sorted ABCG2+ melanoma cells. ABCG2− sample expression=1; n=3. (f) Expression of ABCG2 transcript in 9 deparaffinized tumours, 4 primary melanoma (M) samples, and 5 metastases (MM). A naevus sample was arbitrarily chosen with expression=1 Image collected and cropped by CiteAb from the following open publication (//www.nature.com/articles/cddis2013109), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Spy1 stable protein accelerates tumorigenesis in vivo.(A) Percentage of mice presenting with palpable tumors from 0-19 days post-transplant. Each data point represents 4 mice per indicated construct. The entire experiment was repeated three times using three independently derived overexpressing cell lines for each construct. Mann-Whitney Test was performed (p < 0.05). (A; lower blot) Western blots were conducted to measure the stability of Myc-Spy1-WT (left) and Myc-Spy1-TST (right) from representative time points. Empty vector control (Cntl) cell expression levels of Spy1 are seen in lane 1 of each blot. (B) Total tumor volume was calculated for both Spy1-HC11 (Spy1-WT) and Spy1-TST-HC11 (Spy1-TST) transplanted glands. Results were taken from 45 transplants using cells from 3 separate transfections. Error bars reflect SE between transplants from different transfections. Left hand panel reflects overall volume, right hand panel reflects volumes of tissues taken over a month post-transplant. Image collected and cropped by CiteAb from the following open publication (//bmccancer.biomedcentral.com/articles/10.1186/1471-2407-12-45), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Livin staining in normal adrenal glandLivin staining in normal adrenal gland (A). It is possible to recognize the three different zone of the adrenal gland: the zona glomerulosa (ZG), the zona fasciculata (ZF) and the zona reticularis (ZR). The Figures (B) and (C) are 20× enlarged and detailed images of the 10× ZG, ZF and ZR, respectively. Scale bar: 100 μm. Image collected and cropped by CiteAb from the following open publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.14067), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Curcumin Analogs Induce Apoptosis in Cancerous Cells by Several Pathways. (a) E6-1 (Jurkat), dominant negative FADD (dnFADD) Jurkat, and overexpressing BCL-2 Jurkat were treated for 48 hours then stained for Annexin V and PI (b) E6-1 cells were plated and treated with or without the broad spectrum caspase inhibitor ZVAD(oMe)-FMK for 48 hours. Cells were stained for Annexin V and PI. Results were obtained using image-based cytometry with the Y-axis representative of percent of cells positive for Annexin V (green), PI (red), Annexin V and PI (yellow), or negative for both Annexin V and PI (blue). Values are expressed as a mean ± SD from three independent experiments. (c) E6-1 cells were treated for 24 hours with or without the broad spectrum caspase inhibitor ZVAD(oMe)-FMK and the studied compounds, lysed and subjected to Western blot analysis. (d) NHF and NCM460 cells were treated for 48 hours and 72 hours respectively, lysed and subjected to Western blot analysis. Bands were visualized with a chemiluminescence reagent. Images are representative of three independent experiments. Statistical calculations were performed using Two-Way ANOVA multiple comparison. *p < 0.05 vs % viable of Control (DMSO); #p < 0.05 vs % viable cells for groups without Z-VAD(oMe)FMK. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28439094), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Effect of TSA treatment on the subcellular localization of Crm1.Control ES or Nup98-HoxA9 expressing ES cells were cultured in the presence or absence of 50 nM TSA for 24 hr. Then, the cells were fixed and stained with antibodies against FLAG (M2) and Crm1. Merged images of FLAG (green) and Crm1 (red) are shown. Nuclei were stained with DAPI. Bar, 10 μm. DAPI, 4',6-diamidino-2-phenylindole; ES, embryonic stem; TSA, trichostatin A.DOI://dx.doi.org/10.7554/eLife.09540.020 Image collected and cropped by CiteAb from the following open publication (//elifesciences.org/articles/09540), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Bv, Ha

Species Glossary

Reactivity: Hu, Mu, Rt, Bv, Ha

Applications:

, , , , , , , , , , ,

Applications: , , , , , , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NB100-132AF350
Alexa Fluor 405	NB100-132AF405
Alexa Fluor 488	NB100-132AF488
Alexa Fluor 532	NB100-132AF532
Alexa Fluor 594	NB100-132AF594
Alexa Fluor 647	NB100-132AF647
Alexa Fluor 700	NB100-132AF700
Alexa Fluor 750	NB100-132AF750
Allophycocyanin	NB100-132APC
Biotin	NB100-132B
DyLight 350	NB100-132UV
DyLight 405	NB100-132V
DyLight 488	NB100-132G
DyLight 550	NB100-132R
DyLight 594	NB100-132DL594
DyLight 650	NB100-132C
DyLight 680	NB100-132FR
DyLight 755	NB100-132IR
FITC	NB100-132F
HRP	NB100-132H
PE	NB100-132PE
PerCP	NB100-132PCP
mFluor Violet 450 SE	NB100-132MFV450
mFluor Violet 500 SE	NB100-132MFV500
mFluor Violet 610 SE	NB100-132MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Azide and BSA Free	NBP2-80766

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MAB208

CXCL8/IL-8 Antibody (6217) [Unconjugated]

(1 Review)

(180 Publications)

100 μg

MAB208

Western blot shows lysates of THP‑1 human acute monocytic leukemia cell line untreated (-) or treated (+) with 200 nM PMA and 10 ug/mL LPS for 24 hours and 3 hours. PVDF membrane was probed with 3 µg/mL of Mouse Anti-Human IL-8/CXCL8 Monoclonal Antibody (Catalog # MAB208) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (HAF018). A specific band was detected for IL-8/CXCL8 at approximately 10 kDa (as indicated). This experiment was conducted under reducing conditions and using Western Blot Buffer Group 1.

IL-8/CXCL8 was detected in immersion fixed human peripheral blood mononuclear cells (PBMCs) using Mouse Anti-Human IL-8/CXCL8 Monoclonal Antibody (Catalog # MAB208) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). View our protocol for Fluorescent ICC Staining of Non-adherent Cells.

Simple Western lane view shows human PBMC conditioned media untreated (-) or treated (+) with 1 μg/mL LPS for 24 hrs, loaded at 0.2 mg/mL. A specific band was detected for IL-8/CXCL8 at approximately 8 kDa (as indicated) using 50 µg/mL of Mouse Anti-Human IL-8/CXCL8 Monoclonal Antibody (Catalog # MAB208) . This experiment was conducted under reducing conditions and using the 2-40 kDa separation system.

Recombinant Human IL-8/CXCL8 (Catalog # 208-IL) chemoattracts the BaF3 mouse pro‑B cell line transfected with human CXCR2 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (Catalog # AR002). Chemotaxis elicited by Recombinant Human IL-8/CXCL8 (20 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Human IL-8/CXCL8 Monoclonal Antibody (Catalog # MAB208). The ND50 is typically0.08-0.4 µg/mL.

Reactivity:

Hu

Species Glossary

Reactivity: Hu

Applications:

, , , , , ,

Applications: , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	IC208U-100UG
Alexa Fluor 350	FAB208U
Alexa Fluor 405	IC208V-100UG
Alexa Fluor 405	FAB208V
Alexa Fluor 488	IC208G-100UG
Alexa Fluor 488	FAB208G
Alexa Fluor 532	FAB208X
Alexa Fluor 594	IC208T-100UG
Alexa Fluor 594	FAB208T
Alexa Fluor 647	IC208R-100UG
Alexa Fluor 647	FAB208R
Alexa Fluor 700	IC208N-100UG
Alexa Fluor 700	FAB208N
Alexa Fluor 750	IC208S-100UG
Alexa Fluor 750	FAB208S
Allophycocyanin	FAB208A
Biotin	FAB208B
DyLight 350	FAB208D
DyLight 405	FAB208E
DyLight 488	FAB208K
DyLight 550	FAB208L
DyLight 594	FAB208M
DyLight 650	FAB208W
DyLight 680	FAB208Y
DyLight 755	FAB208Z
Fluorescein	IC208F
HRP	FAB208H
Janelia Fluor 549	FAB208I
Janelia Fluor 646	FAB208J
PerCP	FAB208C
Phycoerythrin	IC208P
mFluor Violet 450 SE	FAB208MFV450
mFluor Violet 500 SE	FAB208MFV500
mFluor Violet 610 SE	FAB208MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	IC208F
Carrier Free	IC208P
Carrier Free	MAB208-SP
Carrier Free	MAB208-500
Carrier Free	IC208V-100UG
Carrier Free	IC208U-100UG
Carrier Free	IC208T-100UG
Carrier Free	IC208S-100UG
Carrier Free	IC208R-100UG
Carrier Free	IC208N-100UG
Carrier Free	IC208G-100UG

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MAB1259

Nestin Antibody (196908) [Unconjugated]

(3 Reviews)

(154 Publications)

100 μg

MAB1259

$Cardiolipin is externalized to the mitochondrial surface in alpha -syn mutant hNs and transgenic mice in response to alpha -syn accumulation. a Western analysis of lysates from corrected and A53T cells at DIV 14 and DIV 60 labeled for total alpha -syn, PS129, TH (DA neuronal marker), nestin (NPC marker) or GAPDH show that levels of PS129-modified alpha -syn are elevated in A53T hNs at DIV 14 and remain elevated at DIV 60 relative to corrected cells. b, c Mitochondria were purified from A53T cells and genetically corrected cells at both DIV 14 and DIV 60. Lysates were then separated based on TX-100 solubility (soluble) or urea solubility (insoluble). Western analysis of A53T cells shows elevated soluble alpha -syn at the mitochondria relative to corrected cells at DIV 14 and DIV 60 (denoted by ** and * respectively). Quantification of soluble and insoluble alpha -syn levels in mitochondrial fractions normalized to Coomassie (c). Data represent mean ± s.e.m. *P < 0.05, **P < 0.01 by ANOVA followed by Tukey’s post hoc test, n = 4. d, e Micrographs of corrected and A53T-mutant NPCs expressing the negative charge probe RPRE-RFP and CL-GFP show RPRE-RFP translocation from a primarily plasma membrane localization in isogenic-corrected hNs to a punctate intracellular localization in A53T hNs in tight cellular localization with CL-GFP (d). Quantification of percent total cell number with colocalized RPRE-RFP and CL-GFP (e). Data represent mean ± s.e.m. **P < 0.0001 by t-test, n = 3 coverslips over 2 independent differentiations, DIV: 14; scale bar: 10 μm. f, g Fluorescence resonance energy transfer (FRET) from CL-GFP to RPRE-RFP in hiPSC-derived A53T and corrected hNs or hESC-derived WT, A53T and E46K hNs was assessed (f) and mean FRET intensity was quantified (g). Data represent mean ± s.e.m. **P < 0.01 by ANOVA followed by Tukey’s post hoc test, for hiPSCs, n = 6, for hESCs, n = 8 coverslips over two independent differentiations, DIV: 14. Scale bar: 10 µm. h Mitochondria were isolated from the SNpc of 6-month-old WT and A53T transgenic animals and labeled with Annexin V to measure the abundance of cardiolipin on the mitochondrial surface. Controls were rotenone-exposed WT samples. Animals were not randomized, nor was the analysis blinded. Data represent mean ± s.e.m. **P < 0.01 by ANOVA followed by Dunnett post hoc test, n = 4. Clipart was obtained at clker.com Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41467-018-03241-9), licensed under a CC-BY license. Not internally tested by R&D Systems.$

MET and TMZ effects in in vivo glioma models(A) Variation of U251 tumor volume measured at contrast-enhanced T1 MRI after treatment expressed as percentage of volume change. Error bars indicate SEM. (B) U251 derived orthotopic brain tumors from vehicle (CTRL), TMZ or TMZ/metformin (Combo) treated mice were analyzed for Ki67, Nestin and CD133 markers by immunohistochemistry. No difference between the tumor edge and bulk areas in IHC staining intensities or percentages of positive cells was observed for any of the investigated markers. H&E was performed for morphological evaluation of the tumors. Representative images are shown with original magnification x200. (C) Variation of T98G tumor volume measured using caliper after treatment expressed as percentage of volume variation. In T98G xenograft model already at 7 days, the combined treatment significantly slowed down tumor growth compared to control (p value = 0.005), moreover a transient reduction was observed with MET (p value = 0.03). After 3 weeks, only Combo-treated mice displayed tumor smaller than vehicle (p value = 0.04). Error bars indicate SEM. (D) T98G tumors from vehicle (CTRL), TMZ, MET or TMZ/metformin (Combo) treated mice, were analyzed for Ki67, Nestin and CD133 markers expression by immunohistochemistry. No difference between the tumor edge and bulk areas in IHC staining intensities or percentages of positive cells was observed for any of the investigated markers. Hematoxylin and eosin staining (H&E) was performed for morphological evaluation of the tumors. Representative images are shown with Original magnification x200. Image collected and cropped by CiteAb from the following publication (//www.oncotarget.com/lookup/doi/10.18632/oncotarget.23028), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neural stem cells could proliferate and differentiate into neurons and astrocytes.(A) Representative photomicrograph of neurospheres in culture. (B) Immunocytochemical staining of purified NSCs with Nestin. (C) Immunocytochemical staining of purified protoplasmic astrocytes with GFAP. (D) Immunocytochemical staining of purified neurons with beta -tubulin-III. (E) Nucleus staining of differentiated cells from NSCs with DAPI. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/26431046), licensed under a CC-BY license. Not internally tested by R&D Systems.

miR–381 promoted neural stem cells proliferation.(A) The expression of miR–381 was measured by qRT-PCR. (B) CCK–8 was performed to detect the neural stem cells proliferation. (C) The mRNA expression of nestin was detected by qRT-PCR. (D) The protein expression of nestin was measured by Western blot. **p<0.01 and ***p<0.001. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/26431046), licensed under a CC-BY license. Not internally tested by R&D Systems.

Dissimilar tumorigenesis in the in vivo animal model.(a) Kaplan-Meier survival plots; 3 mice were used for cells of each clone. (b) Representative brain tumors of NOD-SCID mice harboring xenografts of the clones #2 (upper left), #3 (lower left), #4 (upper right) and #5 (lower right); H.E. staining, arrows: tumor, scale bar = 5 mm. (c) A representative xenograft of the clone #4; nestin-positive cells infiltrated the contralateral hemisphere (arrows). Scale bars = 5 mm (left), 1 mm (middle), 50 μm (right). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/25623281), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reactivity:

Hu

Species Glossary

Reactivity: Hu

Applications:

, ,

Applications: , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	IC1259U-100UG
Alexa Fluor 405	IC1259V-100UG
Alexa Fluor 488	IC1259G-100UG
Alexa Fluor 532	FAB1259X
Alexa Fluor 594	IC1259T-100UG
Alexa Fluor 647	IC1259R-100UG
Alexa Fluor 700	IC1259N-100UG
Alexa Fluor 750	IC1259S-100UG
Allophycocyanin	IC1259A
Biotin	FAB1259B
DyLight 350	FAB1259D
DyLight 405	FAB1259E
DyLight 488	FAB1259K
DyLight 550	FAB1259L
DyLight 594	FAB1259M
DyLight 650	FAB1259W
DyLight 680	FAB1259Y
DyLight 755	FAB1259Z
Fluorescein	IC1259F
HRP	FAB1259H
Janelia Fluor 549	FAB1259I
Janelia Fluor 646	FAB1259J
PerCP	FAB1259C
Phycoerythrin	IC1259P
mFluor Violet 450 SE	FAB1259MFV450
mFluor Violet 500 SE	FAB1259MFV500
mFluor Violet 610 SE	FAB1259MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	IC1259A
Carrier Free	IC1259P
Carrier Free	IC1259F
Carrier Free	MAB1259-SP
Carrier Free	IC1259V-100UG
Carrier Free	IC1259U-100UG
Carrier Free	IC1259T-100UG
Carrier Free	IC1259S-100UG
Carrier Free	IC1259R-100UG
Carrier Free	IC1259N-100UG
Carrier Free	IC1259G-100UG

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NBP2-22203

ERK1 Antibody (1E5) - BSA Free

(1 Publication)

0.1 ml

NBP2-22203

Immunohistochemistry-Paraffin: ERK1 Antibody (1E5) [NBP2-22203] - Immunohistochemical analysis of paraffin-embedded breast cancer tissues using ERK1 mouse mAb with DAB staining.

Flow Cytometry: ERK1 Antibody (1E5) [NBP2-22203] - Flow cytometric analysis of Hela cells using ERK1 mouse mAb (blue) and negative control (red).

Western Blot: ERK1 Antibody (1E5) [NBP2-22203] - Analysis using MAPK3 mAb against human ERK1 (AA: 9-143) recombinant protein. (Expected MW is 40.8 kDa)

Western Blot: ERK1 Antibody (1E5) [NBP2-22203] - Western blot analysis using ERK1 mouse mAb against Hela (1), Jurkat (2), RAW264.7 (3), HEK293 (4), K562 (5), NIH/3T3 (6), Cos7 (7) and PC-12 (8) cell lysate.

Immunohistochemistry-Paraffin: ERK1 Antibody (1E5) [NBP2-22203] - Analysis of paraffin-embedded bladder cancer tissues using ERK1 mouse mAb with DAB staining.

ELISA: ERK1 Antibody (1E5) [NBP2-22203] - Red: Control Antigen (100ng); Purple: Antigen (10ng); Green: Antigen (50ng); Blue: Antigen (100ng)

Reactivity:

Hu, Mu, Rt, Pm

Species Glossary

Reactivity: Hu, Mu, Rt, Pm

Applications:

, , , ,

Applications: , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NBP2-22203-0.025ml

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MAB350

CXCL12/SDF-1 Antibody (79018) [Unconjugated]

(1 Review)

(144 Publications)

100 μg

MAB350

CXCL12/SDF‑1 was detected in immersion fixed human peripheral blood mononuclear cells (PBMCs; positive staining) and K562 human chronic myelogenous leukemia cell line (negative staining) using Mouse Anti-Human/Mouse CXCL12/SDF‑1 Monoclonal Antibody (Catalog # MAB350) at 8 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to cell membranes. View our protocol for Fluorescent ICC Staining of Non-adherent Cells.

CXCL12/SDF‑1 was detected in immersion fixed paraffin-embedded sections of human tonsil using 15 µg/mL Human/Mouse CXCL12/SDF‑1 Monoclonal Antibody (Catalog # MAB350) overnight at 4 °C. Tissue was stained with the Anti-Mouse HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS002) and counterstained with hematoxylin (blue). Specific labeling was localized to epithelial cells in cripts. View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections.

CXCL12/SDF‑1 was detected in immersion fixed paraffin-embedded sections of human tonsil using Human/Mouse CXCL12/SDF‑1 Monoclonal Antibody (Catalog # MAB350) at 25 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Mouse HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS002) and counterstained with hematoxylin (blue). View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections.

HT1080 human fibrosarcoma cell line was stained with Mouse Anti-Human/Mouse CXCL12/SDF‑1 Monoclonal Antibody (Catalog # MAB350, filled histogram) or isotype control antibody (Catalog # MAB002, open histogram), followed by Phycoerythrin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0102B). To facilitate intracellular staining, cells were fixed and permeabilized with FlowX FoxP3 Fixation & Permeabilization Buffer Kit (Catalog # FC012). View our protocol for Staining Intracellular Molecules.

<b>Orthogonal Strategies Validation. </b>CXCL12/SDF-1a mRNA was detected in formalin-fixed paraffin-embedded tissue sections of human tonsil probed with ACD RNAScope®Probe (Catalog # 422991) and stained using ACD RNAscope®2.5 HD Detection Reagents-Red (top image, Catalog # 32260). Adjacent tissue section was processed for immunohistochemistry using R&D Systems Mouse Anti-Human CXCL12/SDF-1a Monoclonal Antibody (Catalog # MAB350) at 5 ug/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte HRP Polymer Antibody (R&D Systems, Catalog # VC001) and DAB chromogen (lower image, yellow-brown). Tissues were counterstained with hematoxylin (blue).

CXCR4 and CXCL12 expression and BM infiltration. (a) Expression analysis of CXCR4 and CXCL12 in uninfiltrated and infiltrated bone marrow specimens at the time of diagnosis by RQ-PCR. (b) Expression analysis of CXCR4 and CXCL12 in infiltrated bone marrow biopsies and the respective paired sample in patients under remission by RQ-PCR. (c) Representative immunohistochemical stains of CXCR4 (I–II) and CXCL12 (III–IV) on selected bone marrow specimens of DLBCL patients (magnification 20×). (I) and (III) represent the CXCR4 and CXCL12 staining of uninfiltrated bone marrow specimens, and (II) and (IV) represent those of the infiltrated bone marrow specimens. mRNA expression levels were calculated as a relative expression in comparison to uninfiltrated bone marrow specimens. Each bar represents the mean values of expression levels ± standard error of the mean (SEM). The comparison of the expression levels was performed by using the Mann–Whitney U-test or the Student’s t-test. All images were captured using an Olympus BX51 microscope and an Olympus E-330 camera. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31554271), licensed under a CC-BY license. Not internally tested by R&D Systems.

RhoA modulates the CXCR4-CXCL12 axis in breast tumors. (a) Representative immunohistochemical (IHC) staining images of breast primary tumor sections of mice orthotopically injected with 4T1 GFP-LUC cells carrying indicated lentiviral modifications, stained with antibodies for CD31 (top, left), F4/80 (middle, left) and alpha -SMA (bottom, left). CD31+ area (top, right), F4/80+ cells (middle, right) and alpha -SMA+ area (bottom, right) per tumor field of view (FOV) (mean ± SE) quantifications of IHC images. N = 4. (b) Representative IHC staining images of breast primary tumor sections of above mice stained with CXCL12 antibody (left). CXCL12+ area per tumor FOV (mean ± SE) quantification of IHC images. N = 4. (c) Representative immunofluorescent images of breast primary tumor sections of above mice co-stained with alpha -SMA, CXCL12 and DRAQ5 nuclear stain, showing the co-localization of alpha -SMA and CXCL12 signals. Scale bar: 50 µm. (d) Representative IHC staining images of breast primary tumor sections of above mice stained with CXCR4 antibody (left). CXCR4+ area per tumor FOV (mean ± SE) quantification of IHC images. N = 4. (e) Relative mCXCR4 mRNA levels normalized with mActin (mean ± SE), as quantified by qRT-PCR in primary breast tumors of above mice (top) and in 4T1 GFP-LUC cells carrying indicated lentiviral modifications (bottom). N = 4, ns- not significant *P < 0.05, unpaired Student’s t-test (two-tailed). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31705019), licensed under a CC-BY license. Not internally tested by R&D Systems.

CXCR4 and CXCL12 expression in DLBCL. (a) Expression analysis of CXCR4 and CXCL12 in non-neoplastic control germinal center B cells (GC-B) and diffuse large B cell lymphoma cells (DLBCL) consisting of DLBCL-NGCB and DLCBL-GCB, by RQ-PCR. GCB-DLBCL were further subdivided into primary (DLBCL-pGCB) and transformed DLBCL (DLBCL-pGCB) originating from follicular lymphoma. (b) Expression analysis of CXCR4 and CXCL12 in DLBCL samples with early (stage 1) and advanced stage (stage 2–4) (left graphs) and DLBCL samples with and without bone marrow infiltration (right graphs) by RQ-PCR. (c) Probability of 5-year-survival in DLBCL patients (our cohort left panel and the cohort of Lenz et al. right [20]) stratified by the third quartile of CXCR4 expression, respectively. (d) Representative immunohistochemical stains of CXCR4 (I–III) and CXCL12 (IV–VI) on DLBCL samples (magnification 20×). mRNA expression levels were calculated as a relative expression in comparison to the GC-B cells. All images were captured using an Olympus BX51 microscope and an Olympus E-330 camera. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31554271), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reactivity:

Hu, Mu

Species Glossary

Reactivity: Hu, Mu

Applications:

, , , , ,

Applications: , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	FAB350U-100UG
Alexa Fluor 405	FAB350V-100UG
Alexa Fluor 488	IC350G-100
Alexa Fluor 488	FAB350G-100UG
Alexa Fluor 532	FAB350X
Alexa Fluor 594	FAB350T-100UG
Alexa Fluor 647	FAB350R-100UG
Alexa Fluor 700	FAB350N-100UG
Alexa Fluor 750	FAB350S-100UG
Allophycocyanin	FAB350A
Allophycocyanin	IC350A
Biotin	FAB350B
DyLight 350	FAB350D
DyLight 405	FAB350E
DyLight 488	FAB350K
DyLight 550	FAB350L
DyLight 594	FAB350M
DyLight 650	FAB350W
DyLight 680	FAB350Y
DyLight 755	FAB350Z
Fluorescein	IC350F
HRP	FAB350H
Janelia Fluor 549	FAB350I
Janelia Fluor 646	FAB350J
PE	FAB350P
PerCP (Peridinin-chlorophyll Protein Complex)	IC350C
Phycoerythrin	IC350P
mFluor Violet 450 SE	FAB350MFV450
mFluor Violet 500 SE	FAB350MFV500
mFluor Violet 610 SE	FAB350MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	IC350C
Carrier Free	IC350F
Carrier Free	IC350P
Carrier Free	IC350A
Carrier Free	MAB350-SP
Carrier Free	MAB350-500
Carrier Free	IC350G-100
Carrier Free	FAB350V-100UG
Carrier Free	FAB350U-100UG
Carrier Free	FAB350T-100UG
Carrier Free	FAB350S-100UG
Carrier Free	FAB350R-100UG
Carrier Free	FAB350N-100UG
Carrier Free	FAB350G-100UG

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NB100-309

ATM Antibody (2C1)

(3 Reviews)

(130 Publications)

100 ul

NB100-309

Western Blot: ATM Antibody (2C1) [NB100-309] - Detection of human ATM protein using ATM antibody (2C1) [NB100-309] by western blot or immunoprecipitation. Theoretical molecular weight 351 kDa.

Immunohistochemistry-Paraffin: ATM Antibody (2C1) [NB100-309] - Human breast carcinoma. ATM stained by ATM antibody [2C1] diluted at 1:100.Antigen Retrieval: Citrate buffer, pH 6.0, 15 min.

Western Blot: ATM Antibody (2C1) [NB100-309] - Analysis of ATM in U2OS sarcoma cells using ATM antibody (2C1) [NB100-309]. Theoretical molecular weight 351 kDa. Western blot image submitted by a verifeid customer review.

Western Blot: ATM Antibody (2C1) [NB100-309] - Whole cell extract (30 ug) was separated by 5% SDS-PAGE, and the membrane was blotted with ATM antibody (2C1) [NB100-309] diluted at 1:1000. Theoretical molecular weight 351 kDa.

Immunohistochemistry-Paraffin: ATM Antibody (2C1) [NB100-309] - Human Kidney (formalin-fixed, paraffin-embedded) stained with ATM antibody (2C1) [NB100-309] at 5 ug/ml followed by biotinylated anti-mouse IgG secondary antibody, alkaline phosphatase-streptavidin and chromogen.

Knockdown Validated: ATM Antibody (2C1) [NB100-309] - Non-transfected (-) and transfected (+) HeLa whole cell extracts (60 ug) were separated by 5% SDS-PAGE, and the membrane was blotted with ATM antibody (2C1) [NB100-309] diluted at 1:500.

<b>Genetic Strategies Validation. </b>Knockdown Validated: ATM Antibody (2C1) [NB100-309] - Methylated EDSBs may be repaired by an ATM-dependent pathway. Immunoblots of ATM and DNA-PKcs in ATM shRNA-transfected HeLa cells, using ATM antibody (2C1) [NB100-309]. GAPDH is included as a loading control. Image collected and cropped by CiteAb from the following publication (//molecular-cancer.biomedcentral.com/articles/10.1186/1476-4598-9-70), licensed under a CC-BY license.

Immunoprecipitation: ATM Antibody (2C1) [NB100-309] - MDA-MB-231 whole cell lysates were immunoprecipitated with 2 ug ATM Antibody (NB100-309), followed by Western blot (primary antibody: NB100-309 at 1:1000, 4C overnight. Western blot image submitted by a verified customer review.

<b>Biological Strategies Validation. </b>Western Blot: ATM Antibody (2C1) [NB100-309] - MCELNs decreased the DNA damage of H9C2 cells after radiation. Western blot images of p-ATM (NB100-306) and ATM (NB100-309) in H9C2 cells after 48 h of culture with indicated treatment. IR (-/+): 0/16 Gy X-ray; MCELNs (-/+): 0/10 ug/mL. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35509278/) licensed under a CC-BY license.

Western blot analysis of the extent of knockdown MRE11 and ATM, and the lack of effect of Mirin activation of ATM. The extent of shRNA-mediated knockdown of MRE11 and ATM are shown for (A) clones GFP-7F1 and GFP-6D1 and (B) clones EDS-7F2 and EDS-6J8. The extent of knockdown was determined by analyzing the intensity of the ATM and MRE11 bands relative to the intensity of the loading control GAPDH bands (see Table 1). (C) The effect of Mirin on activation of ATM was determined by analysis of phosphorylation of ATM in response to ionizing radiation. Cultures treated with DMSO alone, 20 uM Mirin, or knockdown of ATM were analyzed by western blot 30 min after exposure to 10 Gy of ionizing radiation. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/26209132), licensed under a CC-BY licence.

Methylated EDSBs may be repaired by an ATM-dependent pathway. (A) Immunoblots of ATM and DNA-PKcs in ATM shRNA-transfected HeLa cells. GAPDH is included as a loading control. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/20356374), licensed under a CC-BY licence.

$Role of HIF-1 alpha , FOXO3 in hypoxia-induced BNIP3 expression. (A) UCB-hMSCs were incubated with various durations of hypoxia (0–48 h). The protein expressions of HIF-1 alpha and beta -actin were detected by western blot. n = 4. (B) UCB-hMSCs were pretreated with NAC (5 mM) for 30 min prior to hypoxia incubation for 24 h. The protein expressions of HIF-1 alpha , lamin A/C and beta -tubulin in non-nuclear and nuclear fractionized cell samples were assessed by using western blot. n = 3. (C) UCB-hMSCs were immuno-stained with HIF-1 alpha and PI (magnification ×600). Scale bars, 37.5 µm. (D) HIF1A siRNA or NT siRNA was transfected to cells prior to hypoxia treatment for 24 h. The mRNA expression of BNIP3 was analyzed by qPCR. n = 6. (E) The protein expressions of BNIP3 and HIF-1 alpha were detected by western blot. n = 4. (F) NAC (5 mM) was pretreated to UCB-hMSCs prior to hypoxia treatment for 24 h. FOXO3, lamin A/C and beta -tubulin proteins expressions were assessed by western blot. n = 3. (G) FOXO3 siRNA transfected to UCB-hMSCs prior to hypoxia treatment for 24 h. The FOXO3 mRNA expression was measured by qPCR. n = 6. (H) BNIP3, FOXO3 and beta -actin expressions were detected by western blot. n = 3. Western blot data were normalized by beta -actin, and qPCR data were normalized by ACTB mRNA expression level. Lamin A/C and beta -tubulin were used as nuclear and non-nuclear protein controls, respectively. Quantitative data are presented as a mean ± S.E.M. All blots and confocal images are representative. *p < 0.05 versus control, #p < 0.05 versus hypoxia. Image collected and cropped by CiteAb from the following open publication (//linkinghub.elsevier.com/retrieve/pii/S2213231717303804), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

Reactivity:

Hu, Mu, Rt, Pm

Species Glossary

Reactivity: Hu, Mu, Rt, Pm

Applications:

, , , , , , , , ,

Applications: , , , , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Conjugate:

Unconjugated

Validated by:

Validated by:

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MAB206

IL-6 Antibody (6708) [Unconjugated]

(2 Reviews)

(111 Publications)

100 μg

MAB206

Western blot shows 25 ng of Recombinant Human IL‑6 (Catalog # 206-IL), Recombinant Mouse IL‑6 (Catalog # 406-ML) and Recombinant Rat IL‑6 (Catalog # 506-RL). PVDF Membrane was probed with 1 µg/mL of Mouse Anti-Human/Primate IL‑6 Monoclonal Antibody (Catalog # MAB206) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF007). A specific band was detected for IL‑6 at approximately 18 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 3.

IL‑6 was detected in immersion fixed frozen sections of hyperplastic human skin using Mouse Anti-Human/Primate IL‑6 Monoclonal Antibody (Catalog # MAB206) at 8 µg/mL overnight at 4 °C. Tissue was stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to cytoplasm. View our protocol for Fluorescent IHC Staining of Frozen Tissue Sections.

Recombinant Human IL‑6 (Catalog # 206-IL) stimulates proliferation in the T1165.85.2.1 mouse plasmacytoma cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Human IL‑6 (2.5 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Human/PrimateIL‑6 Monoclonal Antibody (Catalog # MAB206). The ND50 is typically 0.05-0.15 µg/mL.

The role of IL‐6 signaling in the upregulation of PD‐L1 and downregulation of NKG2D ligands in CRPC cells. (A) PD‐L1 level in C4‐2siIL‐6/sc and CWRsiIL‐6/sc cell lines (left panel, mRNA level; right panel, protein level). (B) PD‐L1 IHC staining of tumor tissues. Error bars and significance values were obtained by counting positively stained cells in one randomly chosen phase of slides of three different stains. Magnification, 20× (inlet, 100×). (C) Blocking of IL‐6 Ab by neutralizing Ab of IL‐6 and the effect on PD‐L1 level in C4‐2sc and CWRsc cells. Cells were treated with either IL‐6 Ab or control IgG, total RNA extracted, cDNA converted, and the expression of PD‐L1 was compared in qPCR analyses. (D) PD‐L1 level in parental C4‐2 and CWR22Rv1 cells upon the addition of rhIL‐6. Parental cells (C4‐2P and CWR22Rv1P) were treated with rhIL‐6 (20 ng·mL−1) and PD‐L1 mRNA level was analyzed. (E) IHC staining of CRPC patient tumor samples. Two sets of adjacent tumor tissues (both samples, CRPC stage, Gleason score 8, patient age 70, Ningbo hospital in China) were stained with IL‐6 and PD‐L1. Arrows indicate the area showing positive staining of two molecules. (F) NKG2D ligand levels in IL‐6‐expressing cells and in IL‐6‐knockdown cells. Levels of five NKG2D ligands in C4‐2siIL‐6/sc and CWRsiIL‐6/sc cells were analyzed in qPCR analyses. (G) NKG2D ligand levels in parental C4‐2 and CWR22Rv1 cells upon the addition of rhIL‐6. Parental cells (C4‐2P and CWR22Rv1P) were treated with rhIL‐6 (20 ng·mL−1) and the NKG2D ligand levels (mRNA) were analyzed. (H) Flow cytometric analyses of NKG2D and PD‐1 on NK cells. Left two panels, primary NK cells were stained with PE‐NKG2D or APC‐PD‐1 and positive staining was analyzed. Right two panels, flow cytometric analyses of PD‐1 on NK cells, after coculture with tumor cells (6 h of incubation). Primary NK cells were added into tumor cells (1 : 1 ratio, tumor cells/NK cells) and collected after 6 h of incubation. PD‐1 levels in the collected NK cells were analyzed in flow cytometric analysis (using APC‐PD‐1 Ab). *P < 0.05, **P < 0.01, ***P < 0.001. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28865178), licensed under a CC-BY license. Not internally tested by R&D Systems.

Autocrine IL-6 activates STAT3 signalling in lung cancer cell-induced epidural ADSCs. a Epidural ADSCs were pre-treated with CM from lung cancer cells for 48 h, and pSTAT3 and STAT3 expression levels were detected by western blotting. Epidural ADSCs cultured in untreated medium served as a control. b The effects of lung cancer cell CM on epidural ADSC proliferation were evaluated using the CCK-8 assay. Epidural ADSCs were treated with CM from one of four lung cancer cell lines, and the optical density of both groups at 450 nm was analysed. Data from three separate experiments are shown. c Western blot analysis of pSTAT3 and STAT3 in epidural ADSCs treated with either 10 ng/mL recombinant IL-6, 10 ng/mL recombinant IL-11 or 50 ng/mL recombinant LIF in the presence or absence of either neutralizing antibodies or isotype controls. Loading control, actin. d Western blot analysis of pSTAT3 and alpha -SMA expression in epidural ADSCs treated with lung cancer cell CM in the presence or absence of neutralizing antibodies against IL-6, IL-11 or LIF. Loading control, actin. *P < 0.05; **P < 0.01; ***P < 0.001 Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31196220), licensed under a CC-BY license. Not internally tested by R&D Systems.

Activated ADSCs trigger the proliferation and invasion of lung cancer cells by regulating MMP2/9 expression and EMT. a The effects of activated ADSCs on lung cancer cell proliferation were evaluated using the CCK-8 assay. Four lung cancer cell lines were cultured in the presence of ADSC-CM or aADSC-CM, and the optical density at 450 nm was analysed. The cancer cells cultured alone in normal growth medium were used as negative controls. Data from three separate experiments are shown. b The number of lung cancer cells that migrated through 8-μm Transwell membrane pores was counted to determine the changes in the invasive capabilities in response to CM from epidural ADSCs or aADSCs. c MMP2/9, E-cadherin and vimentin expression levels in four lung cancer cell lines treated with ADSC-CM or aADSC-CM were examined by western blotting. Lung cancer cells cultured in an untreated medium served as controls. d Lung cancer cells were treated with neutralizing antibodies against IL-6, isotype controls and aADSC-CM. Lung cancer cell invasion was analysed using a Transwell assay. Lung cancer cells cultured with untreated medium served as negative controls. e Lung cancer cells were treated with neutralizing antibodies against IL-6, isotype controls and aADSC-CM. MMP2/9, E-cadherin and vimentin expression levels in four lung cancer cell lines were analysed using western blotting. Lung cancer cells cultured with untreated medium served as negative controls. ***P < 0.001 Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31196220), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reactivity:

Hu, Pm

Species Glossary

Reactivity: Hu, Pm

Applications:

, , ,

Applications: , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	MAB206-SP
Carrier Free	MAB206-500

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NBP2-25241

STAT6 Antibody (177C322.1) - BSA Free

(4 Publications)

0.1 mg

NBP2-25241

Reactivity:

Hu, Mu

Species Glossary

Reactivity: Hu, Mu

Applications:

, ,

Applications: , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Alt Catalog#

IMG-6901A

Alt Catalog# IMG-6901A

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NBP2-25241AF350
Alexa Fluor 405	NBP2-25241AF405
Alexa Fluor 488	NBP2-25241AF488
Alexa Fluor 532	NBP2-25241AF532
Alexa Fluor 594	NBP2-25241AF594
Alexa Fluor 647	NBP2-25241AF647
Alexa Fluor 700	NBP2-25241AF700
Alexa Fluor 750	NBP2-25241AF750
Biotin	NBP2-25241B
DyLight 350	NBP2-25241UV
DyLight 405	NBP2-25241V
DyLight 488	NBP2-25241G
DyLight 550	NBP2-25241R
DyLight 594	NBP2-25241DL594
DyLight 650	NBP2-25241C
DyLight 680	NBP2-25241FR
DyLight 755	NBP2-25241IR
FITC	NBP2-25241F
HRP	NBP2-25241H
Janelia Fluor 549	NBP2-25241JF549
Janelia Fluor 646	NBP2-25241JF646
mFluor Violet 450 SE	NBP2-25241MFV450
mFluor Violet 500 SE	NBP2-25241MFV500
mFluor Violet 610 SE	NBP2-25241MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
BSA Free	NBP2-25241SS
Azide and BSA Free	NBP2-80965

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MAB8929

beta-Actin Antibody (937215) [Unconjugated]

(3 Reviews)

(103 Publications)

100 μg

MAB8929

Western blot shows lysates of A431 human epithelial carcinoma cell line, C2C12 mouse myoblast cell line, and Rat‑2 rat embryonic fibroblast cell line. PVDF membrane was probed with 0.01 µg/mL of Mouse Anti-Human/Mouse/Rat beta ‑Actin Monoclonal Antibody (Catalog # MAB8929) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF018). A specific band was detected for beta ‑Actin at approximately 45 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

beta ‑Actin was detected in immersion fixed NIH‑3T3 mouse embryonic fibroblast cell line using Mouse Anti-Human/Mouse/Rat beta ‑Actin Monoclonal Antibody (Catalog # MAB8929) at 0.1 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Cells were fixated in methanol. Specific staining was localized to cytoskeleton.

Simple Western lane view shows lysate of A431 human epithelial carcinoma cell line, loaded at 0.2 mg/mL. A specific band was detected for beta ‑Actin at approximately 49 kDa (as indicated) using 1 µg/mL of Mouse Anti-Human/Mouse/Rat beta ‑Actin Monoclonal Antibody (Catalog # MAB8929). This experiment was conducted under reducing conditions and using the 12-230 kDa separation system.

Simple Western lane view shows lysates of Jurkat human acute T cell leukemia cell line, HeLa human cervical epithelial carcinoma cell line, C2C12 mouse myoblast cell line, and C6 rat glioma cell line, loaded at 0.2 mg/mL. A specific band was detected for beta ‑Actin at approximately 48 kDa (as indicated) using 1 µg/mL of Mouse Anti-Human/Mouse/Rat beta ‑Actin Monoclonal Antibody (Catalog # MAB8929) . This experiment was conducted under reducing conditions and using the 12-230 kDa separation system.

The treatment of n-BP rescued the progression of QA-induced excitotoxicity in SCA3 PPs. The control and/or SCA3 PPs were treated with or without QA (1 μM) in the presence of n-BP (0, 10, 20, and 40 μg/mL) for 12 h. (A) Images of QA-treated SCA3 PPs in the presence of BP (40 μg/mL). (B) Confocal images of poly Q localization in BP (40 μg/mL)-treated SCA3 PPs in the presence of QA (1 um). When compared with Figure 2C, 40 μg/mL of n-BP prevented the amounts of colocalized polyQ in the cell nucleus of PPs. The distribution of polyQ in the nucleus is indicated by white arrowheads. Scale bar = 100 μm; (C) protein analysis of wild-type, mutant ATXN3 and its proteolytic fragment in cell lysates of control and SCA3 PPs, as assessed by immunoblots. Soluble, soluble protein; Insoluble, insoluble protein; (D,E) representative immunoblot of control and cleaved PARP1 in cell lysates of control and SCA3 PPs, as assessed by immunoblots. The HDAC2 were used as loading controls. The quantification from three independent images is presented as the means ± standard deviation. t(4) = 2.824, p < 0.05, for lane 1 vs. lane 2; t(4) = 5.613, p < 0.01, for lane 1 vs. lane 3; t(4) = 3.522, p < 0.05, for lane 1 vs. lane 4; (F) the quantification result of calcium concentration in SCA3 PPs, as assessed by Fura-2 indicator. Cells were treated with QA (1 μM) in the presence of n-BP (0, 10, 20, and 40 μg/mL). Data are presented as the means ± standard deviation. t(4) = 2.95, p < 0.05; (G) the calpain activity in control and SCA3 PPs cell lysates, as assessed by ELISA assay. The quantification results from three independent replicates are presented as the means ± standard deviation. t(4) = 3.27, p < 0.05, for lane 3 vs. lane 4; t(4) = 17.55, p < 0.01, for lane 3 vs. lane 5; t(4) = 9.019, p < 0.01, for lane 3 vs. lane 6. (H) Protein analysis of calpain 1, calpain 2 and calpastatin in cell lysates of SCA3 PPs, as assessed by immunoblots. Cells were treated with or without QA (1 μM) in the presence of n-BP (0, 10, 20, and 40 μg/mL). *, p < 0.05; **, p < 0.01. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35163312), licensed under a CC-BY license. Not internally tested by R&D Systems.

Identification of menin-associated proteins (MAPs) in breast cancer cells. (A) and (B) WES of BirA-Menin fusion proteins (A) and biotin-labeled proteins (B) in total lysates of BirA-MEN1 BioID engineered T47D or MCF-7 cells after incubating with or without doxycycline and biotin. (C) Schematic purification and proteomic identification of MAPs using LC–MS/MS. (D) Heatmap of the quantification of 35 MAPs commonly shared in T47D and MCF-7 cells. MAPs further verified by WES immunoassays were indicated by arrows. (E) Network analysis of 35 MAPs in MCF-7 cells. The distance between menin and MAPs represented the quantitative ratio of each MAP and menin. MAPs marked in blue were further assayed by WES. (F) Nuclear or cytoplasmic lysates of BirA-MEN1 BioID engineered T47D or MCF-7 cells after streptavidin beads pull-down were detected by WES with antibodies against menin, KMT2A, MED12, WAPL, GATA3, LaminA/C, or GAPDH. FL, full length; SP, spliced form. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32971831), licensed under a CC-BY license. Not internally tested by R&D Systems.

Identification of MEN1-modulated genes in breast cancer cells. (A) RT-qPCR of MEN1 in T47D or MCF-7 cells treated with vehicle or MEN1 shRNA lentivirus (n = 3). (B) Quantitative Western immunoassays (WES) of menin expression in T47D or MCF-7 cells treated with vehicle or MEN1 shRNA lentivirus (n = 3). (C) Venn diagrams of differentially expressed genes (fold change ≥1.5 or ≤0.66) in T47D or MCF-7 cells after shMEN1 knockdown compared with vehicle controls (n = 2). (D) Pathway annotation analysis of MEN1-upregulated and MEN1-downregulated genes in T47D or MCF-7 cells using DAVID including cancer hallmark pathways. (E) Schematic illustration of five major metabolic pathways. (F) Expression heat maps of oxidative phosphorylation (OXPHOS) and glycolytic genes in both MEN1 knockdown T47D and MCF-7 cells (fold changes relative to vehicle controls). (G) Bar charts of the expression levels of representative OXPHOS and glycolytic genes affected by MEN1 knockdown in T47D or MCF-7 cells using RT-qPCR. Data are presented as mean ± S.D. Unpaired two-tailed Student’s t-test was used for statistics. * p < 0.05, ** p < 0.01, and *** p < 0.001. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32971831), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reactivity:

Hu, Mu, Rt

Species Glossary

Reactivity: Hu, Mu, Rt

Applications:

, ,

Applications: , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Formulations

Formulation	Catalog #	Availability	Price
Carrier Free	MAB8929-SP

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NB200-112

TSG101 Antibody (4A10)

(2 Reviews)

(97 Publications)

0.1 ml

NB200-112

Flow Cytometry: TSG101 Antibody (4A10) [NB200-112] - TSG101 antibody [4A10] (NB200-112) detects TSG101 protein by flow cytometry analysis.Sample: THP-1 cell.Black: Unlabelled sample was used as a control.Red: TSG101 antibody [4A10] (NB200-112).Acquisition of 20,000 events were collected using a Dylight 488-conjugated secondary antibody for FACS analysis.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - A. 30 ug NIH-3T3 whole cell lysate/extract. B. 30 ug JC whole cell lysate/extract. C. 30 ug BCL-1 whole cell lysate/extract.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - Various whole cell extracts (30 ug) were separated by 10% SDS-PAGE, and the membrane was blotted with TSG101 antibody [4A10] diluted at 1:500. The HRP-conjugated anti-mouse IgG antibody (NBP2-19382) was used to detect the primary antibody.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - Lane 1: MWM, Lane 2: TSG101 in RAW 264.7 Whole Cell Lysate, Lane 3: Exosome Lysate. Used primary antibody at 1:500 and Donkey Anti-Mouse at 0.5 ug/mL (this could be titrated down to reduce background). Used picogram sensitivity ECL reagents. Image from verified customer review.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - K562 whole cell extracts (30 ug) was separated by 10% SDS-PAGE, and the membrane was blotted with TSG101 antibody [4A10] diluted at 1:500. The HRP-conjugated anti-mouse IgG antibody (NBP2-19382) was used to detect the primary antibody.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - Various tissue extracts (50 ug) were separated by 10% SDS-PAGE, and the membrane was blotted with TSG101 antibody [4A10] diluted at 1:500. The HRP-conjugated anti-mouse IgG antibody (NBP2-19382) was used to detect the primary antibody.

Western Blot: TSG101 Antibody (4A10) [NB200-112] - Characterization of exosomes. Western blot analysis of exosomes revealed differential expression of TSG101 between HCT116-R exosomes and HCT116-P exosomes. Image collected and cropped by CiteAb from the following publication (//www.nature.com/articles/s41598-019-53063-y), licensed under a CC-BY license.

Immunohistochemistry-Paraffin: TSG101 Antibody (4A10) [NB200-112] - Human breast carcinoma. TSG101 stained by TSG101 antibody [4A10] (NB200-112).Antigen Retrieval: Citrate buffer, pH 6.0, 15 min

Immunohistochemistry-Paraffin: TSG101 Antibody (4A10) [NB200-112] - Human lung cancer. TSG101 stained by TSG101 antibody [4A10] (NB200-112).Antigen Retrieval: Citrate buffer, pH 6.0, 15 min

Flow Cytometry: TSG101 Antibody (4A10) [NB200-112] - An intracellular stain was performed on HeLa cells with TSG101 Antibody (4A10) NB200-112F (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 5 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to FITC.

Flow Cytometry: TSG101 Antibody (4A10) [NB200-112] - An intracellular stain was performed on Hek293 cells with TSG101 Antibody [4A10] NB200-112PE (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeablized with 0.1% saponin. Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to Phycoerythrin.

ELISA: TSG101 Antibody (4A10) [NB200-112] - ELISA detection of TSG101 for capture at a concentration of 5 ug/mL and TSG101 for detection at a concentration of 1.5 ug/mL.

Knockdown Validated: TSG101 Antibody (4A10) [NB200-112] - Non-transfected (-) and transfected (+) 293T whole cell extracts (30 ug) were separated by 10% SDS-PAGE, and the membrane was blotted with TSG101 antibody [4A10] diluted at 1:500.

Characterization of exosomes. (A) Representative TEM images of exosomes at 22000x magnification (Left) HCT116-R exosomes and (Right) HCT116-P exosomes. (B) Enlarged planar view of a cup-shaped structure for single exosome in our samples at 87000x magnification. (C) Western blot analysis of exosomes revealed differential expression of TSG101, CD9, and CD63 between HCT116-R exosomes and HCT116-P exosomes. (D) Average size distribution and zeta potential of exosomes measured in Zetasizer.

Characterization of pECs-EVs from different women in secretory and proliferative phase of cycle. Western blot showing the presence of different canonical EV markers (CD63, CD9, Alix and TSG101) in secretory and proliferative phase pECs-EVs (n = 4) (G). Negative EV markers used were Calnexin (ER), beta-tubulin and the cytosolic form of DCXR (H). The same markers were evaluated in pECs protein extract as controls for EV enrichment of these markers. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/32483153), licensed under a CC-BY licence.

Reactivity:

Hu, Mu, Rt, Po, Ca, Ha, Pm, Pm

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Ca, Ha, Pm, Pm

Applications:

, , , , , , , ,

Applications: , , , , , , , ,

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Conjugate:

Unconjugated

Available Conjugates:

Conjugate	Catalog #	Availability	Size	Price
FITC	NB200-112F

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At	=	A. thaliana	SyHa	=	Golden Syrian Hamster
All	=	All Species	Ha	=	Hamster
An	=	Animal	Hu	=	Human
ArHa	=	Armenian Hamster	I	=	Insect
Av	=	Avian	Ll	=	Llama
Bb	=	Baboon	Ma	=	Mammal
Ba	=	Bacteria	Mk	=	Monkey
Bv	=	Bovine	Mu	=	Mouse
Ca	=	Canine	Multi	=	Multi-species
Ce	=	C. Elegans	NA	=	Non-species specific
Ch	=	Chicken	Or	=	Orangutan
ChHa	=	Chinese Hamster	Pl	=	Plant
Cm	=	Cynomolgus Monkey	Pm	=	Primate
Do	=	Donkey	Po	=	Porcine
Dr	=	Drosophilia	Rb	=	Rabbit
Ec	=	E. Coli	Rt	=	Rat
Eq	=	Equine	RM	=	Rhesus Macaque
Fe	=	Feline	Sh	=	Sheep
Ft	=	Ferret	Vb	=	Vertebrate
Fi	=	Fish	Vi	=	Virus
Fu	=	Fungi	Xp	=	Xenopus
Ge	=	Gerbil	Ye	=	Yeast
GP	=	Guinea Pig	Ze	=	Zebrafish
Gt	=	Goat

Category

Protein/Target

Applications

Reactivity

Citation

Antibody Validation

Reviews

Host

Available Conjugates

Format

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Modification

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Species Glossary

beta-Actin Antibody (AC-15)

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Nestin Antibody (196908) [Unconjugated]

ERK1 Antibody (1E5) - BSA Free

CXCL12/SDF-1 Antibody (79018) [Unconjugated]

ATM Antibody (2C1)

IL-6 Antibody (6708) [Unconjugated]

STAT6 Antibody (177C322.1) - BSA Free

beta-Actin Antibody (937215) [Unconjugated]

TSG101 Antibody (4A10)