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NB100-56566

TLR4 Antibody (76B357.1) - BSA Free

(5 Reviews)

(138 Publications)

0.1 mg

NB100-56566

Dual RNAscope ISH-IHC: TLR4 Antibody (76B357.1) [NB100-56566] - FFPE tissue sections of human tonsil were probed for TLR4 mRNA (ACD RNAScope Probe, ACD catalog # 311281; Fast Red chromogen, ACD catalog # 322750). Adjacent tissue section was processed for immunohistochemistry using Mouse Monoclonal (Novus Biologicals catalog # NB100-56566) at 5ug/mL with 1 hour incubation at room temperature followed by incubation with anti-mouse IgG VisUCyte HRP Polymer Antibody (Catalog # VC001) and DAB chromogen (yellow-brown). Tissue was counterstained with hematoxylin (blue). Specific staining was localized to lymphocytes.

<b>Orthogonal Strategies Validation. </b>Flow Cytometry: TLR4 Antibody (76B357.1) [NB100-56566] - Analysis using the Alexa Fluor (R) 647 conjugate of NBP2-27149. TLR4 expression on monocytes from human peripheral blood. PBMC were stained in a 2 color flow test, with CD14 PE version of this antibody and 1 ug of either isotype control (left) or TLR4-Alexa Fluor 647 (right). PPI negative, CD14+ cells were gated for analysis.

Immunohistochemistry: TLR4 Antibody (76B357.1) [NB100-56566] - Pericryptal Myofibroblasts are Responsible for Increased TLR4 Expression in a Subset of CRCs. Double-stained immunofluorescence for TLR4 (green) and vimentin (red) in normal (I), adenoma (II), and colon adenocarcinoma (III) (10x). In the stromal compartment of CRCs, immunofluorescent staining for TLR4 localized to the pericryptal myofibroblasts in a subset of samples. Image collected and cropped by CiteAb from the following publication (//www.jeccr.com/content/33/1/45), licensed under a CC-BY license.

Western Blot: TLR4 Antibody (76B357.1) [NB100-56566] - Analysis using 2 ug/mL on (A) human intestine and 6 ug/mL on (B) mouse intestine and (C) rat intestine lysate.

Immunohistochemistry: TLR4 Antibody (76B357.1) [NB100-56566] - Pericryptal Myofibroblasts are Responsible for Increased TLR4 Expression in a Subset of CRCs. IHC staining of colon adenocarcinoma for TLR4, vimentin, and alpha-SMA (40x). Staining co-localizes to the pericryptal space, confirming the signal arises from pericryptal myofibroblasts. Image collected and cropped by CiteAb from the following publication (//www.jeccr.com/content/33/1/45), licensed under a CC-BY license.

Flow (Intracellular): TLR4 Antibody (76B357.1) [NB100-56566] - Analysis using PE conjugate of NBP2-27149. An intracellular stain was performed on Jurkat cells with TLR4 antibody (76B357.1) NBP2-27149PE (blue) and an isotype control MAB004 (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.

Immunocytochemistry/Immunofluorescence: TLR4 Antibody (76B357.1) [NB100-56566] - RH-30 cells were fixed in 4% paraformaldehyde for 10 minutes and permeabilized in 0.05% Triton X-100 in PBS for 5 minutes. The cells were incubated with anti-TLR4 Antibody (76B357.1) NB100-56566 at 1 ug/ml overnight at 4C and detected with an anti-mouse Dylight 488 (Green) at a 1:1000 dilution for 60 minutes. Nuclei were counterstained with DAPI (Blue). Cells were imaged using a 100X objective and digitally deconvolved.

Immunohistochemistry: TLR4 Antibody (76B357.1) [NB100-56566] - Immunofluorescent staining of TMAs. Representative tissue cores from normal (I), adenomatous polyps (II), and CRC (III and IV) are shown. Image collected and cropped by CiteAb from the following publication (//www.jeccr.com/content/33/1/45), licensed under a CC-BY license.

Immunohistochemistry-Paraffin: TLR4 Antibody (76B357.1) [NB100-56566] - Analysis of rat salivary gland tissue section at 1:100 dilution. The antibody generated a membrane-cytoplasmic staining in the tissue with stronger signal in ductal epithelial cells.

Immunohistochemistry-Paraffin: TLR4 Antibody (76B357.1) [NB100-56566] - Tissue section of normal human skin stained with antibody at 5 ug/mL. Membrane-cytoplasmic immunopositivity of TLR4 was primarily observed in the pigmented basel cells and the adjacent keratinocytes in the epidermal layer.

Flow Cytometry: TLR4 Antibody (76B357.1) [NB100-56566] - An intracellular stain was performed on RH30 cells with TLR4 Antibody (76B357.1) NB100-56566 (blue) and a matched mouse IgG2b Kappa isotype control (orange) MAB004. Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature, followed by Mouse IgG (H+L) Cross-Adsorbed Secondary Antibody, Dylight 550 (35503, Thermo Fisher).

Immunohistochemistry-Paraffin: TLR4 Antibody (76B357.1) [NB100-56566] - Human skin stained with at 5 ug/mL, peroxidase-conjugate and DAB chromogen. Staining of formalin-fixed tissues is enhanced by boiling tissue sections in 10 mM sodium citrate buffer, pH 6.0 for 10-20 min followed by cooling at RT for 20 min.

Immunohistochemistry-Paraffin: TLR4 Antibody (76B357.1) [NB100-56566] - Analysis of TLR4 in FFPE human colon tissue using an isotype control (top) and NB100-56566 (bottom) at 5 ug/mL.

Immunohistochemistry-Paraffin: TLR4 Antibody (76B357.1) [NB100-56566] - Human testis tissue stained with antibody at 5 ug/mL.

Immunohistochemistry-Frozen: TLR4 Antibody (76B357.1) [NB100-56566] - This image is TLR4(green) and nucleus(blue) at area postrema of the adult male mouse brain, x20 magnification. Primary antibody diluted 1:500. IHC-Fr image submitted by a verified customer review.

Flow Cytometry: TLR4 Antibody (76B357.1) [NB100-56566] - Analysis of formaldehyde fixed THP-1 cells (human monocytic leukemia cells) using 2 ug/10^6 cells TLR4 antibody (clone 76B357.1) with detection employing a donkey anti-mouse IgG (H+L) cross adsorbed secondary antibody, (DyLight 488 conjugated). Isotype control samples incubated with mouse IgG2b isotype control antibody were processed in parallal under the same assay conditions.

Flow Cytometry: TLR4 Antibody (76B357.1) [NB100-56566] - An intracellular stain was performed on Jurkat cells with TLR4 Antibody (76B357.1) NB100-56566 (blue) and a matched mouse IgG2b Kappa isotype control (orange) MAB004. Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature, followed by Mouse IgG (H+L) Cross-Adsorbed Secondary Antibody, Dylight 550 (35503, Thermo Fisher).

Flow Cytometry: TLR4 Antibody (76B357.1) [NB100-56566] - An intracellular stain was performed on Raw264.7 cells with TLR4 Antibody (76B357.1) NB100-56566 (blue) and a matched mouse IgG2b Kappa isotype control (orange) MAB004. Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 2.5 ug/mL for 30 minutes at room temperature, followed by Mouse IgG (H+L) Cross-Adsorbed Secondary Antibody, Dylight 550 (35503, Thermo Fisher).

Representative images of immunohistochemical staining of pancreatic adenocarcinoma upregulated factor (PAUF) and toll-like receptor 4 (TLR4) in human ovarian cancer specimens. The top row (A,B) represents normal ovarian tissue, middle row (C,D) shows immunoreactivity of ovarian carcinomas and the bottom row (E,F) indicates immunonegativity of ovarian caricinoma. The stromal cells of normal ovarian tissue show immunonegativity for PAUF and TLR4. The scale bar represents 100 μm.

ALWPs significantly reduced LPS-induced cell-surface levels of TLR4. (C) BV2 microglial cells were pretreated with ALWPs (500 ug/ml) or PBS for 30 min, followed by treatment with LPS (1 ug/ml) or PBS for 5.5 h. Cell-surface biotinylation was then conducted with a TLR4 antibody recognizing the N-terminal region of TLR4. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/30319390), licensed under a CC-BY licence.

Effect of Cucumis sativus L. extract (CSE) on LPS induced TLR4 expression. b) Representative Western Blot of TLR4 and relative housekeeping alpha-tubulin were reported. c Expression of TLR4 protein in pAECs treated with LPS (10 ug/ml) in the presence or absence of increasing doses CSE (0.02; 0.2; 2 mg/ml); data shown are representative of at least three independent experiments and represent the mean +/- SEM. Different letters above the bars indicate significant differences (p < 0.05 ANOVA post hoc Tukey's test) Image collected and cropped by CiteAb from the following publication (//bmccomplementalternmed.biomedcentral.com/articles/10.1186/s12906-018-2254-1), licensed under a CC-BY licence.

Dasatinib affects TLR4 signaling to regulate LPS-induced proinflammatory cytokine levels in BV2 microglial cells. d) BV2 microglial cells were treated with dasatinib (250 nM) or vehicle (1% DMSO) for 30 min followed by LPS (1 ug/ml) or PBS for 5.5 h, and cell surface biotinylation was conducted. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/31655606), licensed under a CC-BY licence.

Corroboration of human AKR2–protein interactions with highest confidence. (A) Representation of the components of the protein pull-down experiment using c-Myc magnetic beads with Myc-tagged human AKR2. (B) Western blot analysis of AKR2–protein interactions. Interacting proteins were incubated with AKR2 and immunopresipitated with c-Myc magnetic beads specific for the AKR2 protein tag (I) or with the c-Myc magnetic beads only as negative control (C-). Recombinant interacting proteins were included as positive control (C+). Mouse or rabbit antibodies specific for each protein were used as primary antibodies and then anti-mouse or anti-rabbit secondary antibodies were used to identify the presence of the interacting proteins (red arrow). The origin of the primary antibody is shown. (C) Corroboration of human AKR2–AKR2 interaction using protein pull-down with c-Myc magnetic beads with human Myc-tagged AKR2. The experiment was conducted as described in (B). The origin of the primary antibody and predicted size for AKR2 monomer, dimer, and trimer together with bands corresponding to fragments of the mouse anti-c-Myc antibody attached to magnetic beads are shown. (D) In order to identify unrelated proteins eluted from the c-Myc magnetic beads, a similar experiment was conducted with selected proteins but incubating only with the secondary antibody. A lane of SDS-PAGE stained with Bio-Safe Coomassie Stain corresponding to c-Myc magnetic beads alone eluted using Laemmli sample buffer was included (C--). The bands corresponding to fragments of the mouse anti-c-Myc antibody attached to magnetic beads are shown. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/32046307), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

$TDP1 depletion sensitizes glioblastoma-resistant cancer cells to temozolomide. (a) Cell lysates from RKO and DLD1 cancer cell lines were fractionated by SDS–PAGE and analyzed by immunoblotting using anti-TDP1 (Eurogentec), anti-Top1 (Santa Cruz), anti-Tubulin (Abcam) and anti-APE1 (Novus) antibodies (left). RKO and DLD1 cells were compared for their survival following exposure with the indicated doses of MMS for 15 min at 37°C (right). Data are the average of three independent experiments ± s.e.m. Where not visible, error bars are smaller than the symbol. (b) RKO cells were subjected to scrambled siRNA (Mock) or siRNA against TDP1 (TDP1KD) and cell lysates analyzed by immunoblotting (left). Control RKO (RKOSc siRNA) and RKO cells in which TDP1 levels were depleted (RKOTDP1 siRNA) were examined for their survival following exposure to the indicated doses of MMS, as described earlier in the text (right). (c) Glioblastoma multiforme T98G and U87 cancer cell lines were analyzed for methylguanine methyltransferase (MGMT) expression using anti-MGMT antibodies (Abcam) (left). High-MGMT expressing T98G cells were compared with low-MGMT expressing U87 cells for their survival following exposure to increasing concentrations of the alkylating agent temozolomide (right). (d) TG98 cells were subjected to scrambled siRNA (Mock) or siRNA against TDP1 (TDP1KD) and cell lysates analyzed by immunoblotting (left). Control T98G cells (T98GSc siRNA) and cells in which TDP1 levels were depleted (TG98TDP1 siRNA) were incubated with DMSO or 150 μM of the APE1 inhibitor CRT0044876 ‘APEi’ for 2 h followed by additional incubation with the indicated concentrations of MMS for 15 min at 37°C. Cell survival was blindly scored from three independent biological repeats, and data are the average ± s.e.m. (right). (e) Model for the repair of temozolomide-induced DNA breaks. Temozolomide delivers a methyl group to purine bases of DNA, resulting in O6-methyl guanine, N7-methyl guanine and N3-methyl adenine. The primary cytotoxic lesion is believed to be O6-methyl guanine, which can be removed by a direct repair mechanism mediated by methylguanine methyltransferase (MGMT). Inherent and acquired resistance to temozolomide via MGMT expression presents a major challenge in cancer therapy, particularly for glioblastoma multiforme. TDP1 promotes the repair of methylated purines induced by temozolomide via a distinct non-canonical BER pathway. Increasing the load of unrepaired methylated purines by exploiting the limited availability of TDP1 alone or in combination with canonical BER factors such as APE1 provides a new synthetic lethal setting to improve the clinical outcome of temozolomide-based cancer therapy. Asterisks denote statistical differences (P < 0.05; t-test) between control and TDP1-deficient cells. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/24335147), licensed under a CC-BY license. Not internally tested by Novus Biologicals.$

OTULIN overexpression reduced the number of Iba-1+ microglial cells in the cortical ischemic penumbra in focal cerebral ischemia/reperfusion rats. A Representative images of Iba-1+ microglial cells that were morphologically classified into three types; scale bar = 10 μm. B Iba-1+ microglial cells in the ischemic penumbra and contralateral cortex of each group were detected by confocal immunofluorescence at 24 h, 72 h, and 7 days; scale bar = 75 μm. C The histogram represents the quantitative analysis of mean Iba-1 immunofluorescence intensity in each group (n = 6). Data are presented as the means ± SEMs; ###P < 0.001 versus the tMCAO group; &&&P < 0.001 versus the tMCAO+LV-Scramble group Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29544517), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

FKBP51 modulates EMT hallmarks. (a and b) FKBP51 silencing of SAN melanoma cells decreases TGF-beta and T beta RIII expression. Normalized expression rates (mean±S.D.) of TGF-beta (a, left) and T beta RIII (b, left) mRNA levels; (a, n=3; b, n=5). FKBP51 siRNA-treated sample expression=1. Western blot assay of TGF-beta in SAN melanoma cells treated with nonsilencing (NS) RNA or FKBP51 siRNA (a, right). Flow cytometric analysis of T beta RIII (endoglin) expression (b, right): FKBP51 siRNA-treated cells moved to the left relative to NS RNA-treated cells because of reduced staining (MFI: 111±10 and 64±3 in NS RNA and FKBP51 siRNA-treated cells, respectively). (c, and d) FKBP51 overexpression enhances TGF-beta and T beta RIII expression. Normalized expression of TGF-beta (c, left) and T beta RIII (d, left) mRNA in WT, EV-, or FKBP51-stably transfected melanoma cells. WT sample expression=1. (c, n=3; d, n=5). Western blot assay of TGF-beta levels in the same cells (c, right). Anti-Flag-labelled exogenous FKBP51. Flow cytometric analysis of T beta RIII expression (d, right). FKBP51-overexpressing cells moved to the right relative to WT or EV cells, indicating increased expression. (e) Graphic representation of cell counts ( × 10−3) in WT, EV-, or FKBP51-stably transfected melanoma cell cultures. Results are means of six independent experiments each performed in triplicate. (f) FKBP51 upregulates colony number and size. Colonies were counted under low magnification ( × 10) at four points on each dish. The data represent the means of two independent experiments performed in triplicate. Magnification: upper, × 10; lower × 40. (g) Boyden chamber filters invaded by melanoma cells. Filter was stained with Crystal Violet. OD value was obtained by reading the eluted Crystal Violet with a spectrophotometer at a wavelength of 570 nm. The increased OD in FKBP51 samples indicated that FKBP51-overexpressing cells invaded matrigel more efficiently than control cells. The data represent the means of three independent experiments performed in triplicate 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.

Functional assessment of Fanconi anemia pathway. (a) The experimental scheme for MMC treatment. Twenty‐four hours after plating, cells were cultured with or without MMC 1 μM for an additional 24 hr, after which the cells were harvested for western blot or immunostaining. (b) Western blot with FANCD2 antibody of BJ, proband fibroblasts, FANCB mutant (null) fibroblasts and FANCD2 mutant (null) fibroblasts. (c) Western blot with FANCD2 antibody of non‐FA control lymphoblasts (LCL), proband LCL‐A‐2017, proband LCL‐B‐2017, FANCB mutant (null) LCL, and FANCD2 mutant (null) LCL. (d) Representative figures of FANCD2 foci formation in the indicated cells. (e) Quantification of FANCD2 foci formation following treatment with or without 1 μM MMC. Experiments were performed in triplicate. One hundred cells were counted for each experiment Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/29193904), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Pot1a prevents DDR in HSCs. a, b Telomeric DDR in 8 week-old LSK cells upon Pot1a knockdown. a Immunocytochemical staining of TRF1 (green) and 53BP1 (red). Foci co-stained with TRF1 and 53BP1 were identified as TIFs. Nuclei were stained with TOTO3 (blue). Scale bar, 2 μm. b Frequency of TIFs per cell after 1 week of culture. Data are expressed as the mean ± SD (n = 100, *p < 0.01 by t-test). Representative data from three independent experiments are shown. c–f Telomeric DDR in donor-derived control-GFP or Pot1a overexpressing 8 week-old LSK cells 4 months post BMT. c Immunocytochemical staining of TRF1 (green) and 53BP1 (red). Nuclei were stained with TOTO3 (blue). Scale bar, 2 μm. d Frequency of TIFs per cell. Data are expressed as the mean ± SD (n = 120, *p < 0.01 by t-test). Representative data from 3 independent experiments are shown. e Immunocytochemical staining of TRF1 (green) and RPA32 (red). f Immunocytochemical staining of TRF1 (green) and pChk1 (red). Scale bar, 2 μm. g Flow cytometric analysis of Chk1 and pChk1 in donor-derived GFP+ LSKCD48–CD150+ cells after 5 months of 2nd BMT. Mean fluorescence intensity of Chk1 and pChk1 (left panels). Data are expressed as the mean ± SD (n = 3, *p < 0.01 by t-test). Representative FACS profiles of Chk1 and pChk1 in donor-derived GFP+ LSKCD48–CD150+ cells (right panels) Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/28986560), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Lamin A/C-53BP1 interaction is regulated in a DNA damage-dependent manner. (A) Left; HDF were subjected to IR (10 Gy) and allowed to recover for 1 h. Association between A-type lamins and 53BP1 was assessed by immunoprecipitation of endogenous lamin A/C followed by immunoblotting with 53BP1 and lamin A/C antibodies. WCE, whole cell extract, IP: immunoprecipitates. WCE represents 5% input. Right; endogenous lamin A/C was immunoprecipitated and supernatants or pellets were analysed by immunoblotting for interaction with JMJD2A. (B) U2OS/GFP-lamin A cells were pretreated with caffeine (20 mm) for 1 h before exposure to IR (10 Gy, 1 h recovery). Cell extracts were then subjected to immunoprecipitation using GFP-Trap beads, and bound complexes were then analysed by immunoblotting using 53BP1 and GFP antibodies. WCE represents 1% input. (C) As in (C) except cells were pretreated with 10 μm ATMi for 1 h before IR. WCE represents 1% input. (D) U2OS/GFP-lamin A cells were subjected to laser micro-irradiation, fixed 1 h later and immunostained with gamma -H2AX antibody. Scale bar, 10 μm. (E) U2OS cells were transfected with siCTRL or siLMNA and subjected to laser micro-irradiation, fixed 15 min later and then processed for immunofluorescence with gamma -H2AX and 53BP1 antibodies. Scale bar, 10 μm. Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/25645366), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Reactivity:

Hu, Mu, Rt, Po, Bv, Ma, Pm, ChHa

Species Glossary

Reactivity: Hu, Mu, Rt, Po, Bv, Ma, Pm, ChHa

Applications:

, , , , , , , , , , , , , ,

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

Host:

Mouse Monoclonal

Host: Mouse Monoclonal

Alt Catalog#

IMG-5031A

Alt Catalog# IMG-5031A

Sizes:

Sample Size Available

Sizes: Sample Size Available

Conjugate:

Unconjugated

Available Conjugates:

Validated by:

Validated by:

Conjugate	Catalog #	Availability	Size	Price
Alexa Fluor 350	NBP2-27149AF350
Alexa Fluor 405	NBP2-27149AF405
Alexa Fluor 488	NBP2-27149AF488
Alexa Fluor 532	NBP2-27149AF532
Alexa Fluor 594	NBP2-27149AF594
Alexa Fluor 647	NBP2-27149AF647
Alexa Fluor 700	NBP2-27149AF700
Alexa Fluor 750	NBP2-27149AF750
Allophycocyanin	NBP2-27149APC
Allophycocyanin/Cy7	NB100-56566APCCY7
Biotin	NBP2-27149B
DyLight 350	NBP2-27149UV
DyLight 405	NBP2-27149V
DyLight 488	NBP2-27149G
DyLight 550	NBP2-27149R
DyLight 594	NB100-56566DL594
DyLight 650	NBP2-27149C
DyLight 680	NBP2-27149FR
DyLight 755	NBP2-27149IR
FITC	NBP2-27149F
HRP	NBP2-27149H
Janelia Fluor 549	NB100-56566JF549
Janelia Fluor 646	NB100-56566JF646
PE	NBP2-27149PE
PE/Atto594	NB100-56566PEATT594
PE/Cy5.5	NB100-56566PECY55
PE/Cy7	NB100-56566PECY7
PerCP	NBP2-27149PCP
mFluor Violet 450 SE	NBP2-27149MFV450
mFluor Violet 500 SE	NBP2-27149MFV500
mFluor Violet 610 SE	NBP2-27149MFV610

Available Formulations

Formulation	Catalog #	Availability	Price
Azide Free	NBP2-27149
BSA Free	NB100-56566SS
Azide Free	NBP2-27149SS

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