| Formulation | Catalog # | Availability | Price | |
|---|---|---|---|---|
| Carrier Free | AF-401-SP | |||
| Formulation | Catalog # | Availability | Price | |
|---|---|---|---|---|
| Carrier Free | MAB1835-SP | |||
| Carrier Free | MAB1835-500 | |||
| Formulation | Catalog # | Availability | Price | |
|---|---|---|---|---|
| Carrier Free | MAB421-SP | |||
| Carrier Free | MAB421-500 | |||
| Formulation | Catalog # | Availability | Price | |
|---|---|---|---|---|
| Carrier Free | MAB310-SP | |||
| Carrier Free | MAB310-500 | |||
| Formulation | Catalog # | Availability | Price | |
|---|---|---|---|---|
| Carrier Free | MAB415-SP | |||
| Carrier Free | MAB415-500 | |||
![P. gingivalis and its OMVs differentially induce inflammasome signaling and pyroptosis in murine macrophages. BMM were infected as before (2 h at MOI of 25:1, see Materials and Methods) with viable P. gingivalis (Pg), heat-killed-Pg (HK-Pg), OMVs, or heat-inactivated-OMVs (HI-OMVs) and (A) the activation of inflammasome components in the lysates [or supernatants (sup) where indicated] measured after 24 h by Western blot; beta -actin serves as a loading control throughout. Western blot data are representative of at least three independent experiments. (B) Production of IL-1 beta and IL-18 (by ELISA) from BMM was measured in the supernatant at 24 h. Data are mean ± SD from four independent experiments. Cell viability was determined by measuring extracellular LDH release and by 7-AAD exclusion (by flow-cytometry) at 24 h. 7-AAD is a membrane impermeant dye that is excluded from viable cells. The percent of 7-AAD positive (±SD) cells from three independent experiments was calculated relative to the untreated control. BMM treated with H2O2 (1 mM for 60 min) were included as positive control for 7-AAD. A representative histogram is shown. Cells were also treated where indicated with OMVs in the presence of KYT-1 and KYT-36 (10 μM of each). *p < 0.05. Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/28824884), licensed under a CC-BY license. Not internally tested by R&D Systems.](http://images.novusbio.com/fullsize/af-401-na_mouse-il-1-beta-il-1f2-affinity-purified-polyclonal-ab-4120241033831.jpg)
![In vivo assay: IKK gamma Inhibitor Peptide Set [NBP2-26504] - NBD peptide blocks constitutive NF-kB as shown by EMSA. U266 cells were treated with 100 uM of control or NBD peptide for different time periods. Nuclear extracts were isolated and checked for NF-kB-DNA binding activity.](http://images.novusbio.com/fullsize/IKK-gamma-Inhibitor-Peptide-Set-In-vivo-assay-NBP2-26504-img0010.jpg "In vivo assay: IKK gamma Inhibitor Peptide Set [NBP2-26504] - NBD peptide blocks constitutive NF-kB as shown by EMSA. U266 cells were treated with 100 uM of control or NBD peptide for different time periods. Nuclear extracts were isolated and checked for NF-kB-DNA binding activity.")
![In vivo assay: IKK gamma Inhibitor Peptide Set [NBP2-26504] - NBD peptide blocks constitutive NF-kB activation in human multiple myeloma cells. U266 cells were treated with 100 uM of control (A & B) or NBD peptide (C & D) for 12 hr, cytospun, plated on glass slides, air dried for 1 hr at room temperature and fixed with cold acetone. Slides were blocked with 5% normal goat serum for 1 hr and then incubated with rabbit polyclonal anti-human p65 antibody (A & C) followed by Ig-Alexa 594 second step. In control peptide treated cells, p65 translocates to nucleus (A), whereas NBD peptide prevents translocation of p65 into the nucleus (C). B & D: Nuclear staining with DNA binding dye.](http://images.novusbio.com/fullsize/IKK-gamma-Inhibitor-Peptide-Set-In-vivo-assay-NBP2-26504-img0012.jpg)
![IKK gamma Inhibitor Peptide Set [NBP2-26504] - The IKK complex consists of IKKalpha + IKKbeta+ NEMO. NEMO (IKKgamma/NF-kB Essential MOdulator) is a scaffold protein required for the kinase activity of IKKalpha + IKKbeta. NBD (NEMO Binding Domain) inhibits formation of the IKK complex (IKKalpha + IKKbeta+ NEMO) by binding to NEMO and blocking IKK complex formation. In this regard, NBD is considered to be an 'IKKalpha and IKKBeta decoy' Blocking IKK complex formation suppresses downstream events in the NF-kB signaling pathway that rely on the IKK complex including phosphorylation of IkBalpha, and subsequence IkBalpha ubiquination, degradation and release of NF-kB. Hence, NF-kB is retained in the cytoplasm in its inactive state.](http://images.novusbio.com/fullsize/IKK-gamma-Inhibitor-Peptide-Set-NBP2-26504-img0014.jpg)
![Functional (Inhibition): IKK gamma Inhibitor Peptide Set [NBP2-26504] - TLR5/NF-kB/SEAPorter HEK 293 (NBP2-26277) cells were plated in 96-well plates at 5 x 10^4 cells/well for 16 h. Cells were preincubated with different concentrations (0, 1, 5, 10, 25 and 50 uM) of Inhibitory Peptide (NBP2-26504) and Control Peptide (NBP2-29334) for 1 h. Cells were then stimulated with 1 ng/ml Flagellin (NBP2-25289) for 24 h. Secreted alkaline phosphatase (SEAP) was analyzed using SEAPorter Assay Kit (NBP2-25285). *p < 0.05 versus control peptide at the corresponding concentrations (Mann-Whitney U test).](http://images.novusbio.com/fullsize/IKK-gamma-Inhibitor-Peptide-Set-Functional-Inhibition-NBP2-26504-img0016.jpg)
![Immunocytochemistry/Immunofluorescence: Tat-Beclin 1 D11 Autophagy Inducing Peptide [NBP2-49888] - HeLa GFP-LC3B cells were treated with Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S for 1.5 hours. Thereafter, the cells were stained using NeuroTrace Red or DAPI and analyzed employing fluorescent microscopy. Note the higher number of autophagosomes/GFP-LC3B+ puncta in the images of Tat-D11 and Tat-L11 treated cells when compared to Tat-Beclin 1 and Tat-L11S treated cells.](http://images.novusbio.com/fullsize/Tat-Beclin-1-D11-Autophagy-Inducing-Peptide-Immunocytochemistry-Immunofluorescence-NBP2-49888-img0002.jpg "Immunocytochemistry/Immunofluorescence: Tat-Beclin 1 D11 Autophagy Inducing Peptide [NBP2-49888] - HeLa GFP-LC3B cells were treated with Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S for 1.5 hours. Thereafter, the cells were stained using NeuroTrace Red or DAPI and analyzed employing fluorescent microscopy. Note the higher number of autophagosomes/GFP-LC3B+ puncta in the images of Tat-D11 and Tat-L11 treated cells when compared to Tat-Beclin 1 and Tat-L11S treated cells.")
![In vitro assay: Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form [NBP2-49888] - Analysis of lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S. The lysates were analyzed for the expression of LC3-1/LC3-II and SQSTM1/p62 using 2 ug/mL each of anti-LC3B (NB100-2220) and anti-SQSTM1/p62 (MAB8028) respectively. Anti-Actin (AF4000) was used as a loading control. TatD11 exhibited superior induction of LC3-II and down-regulation of p62 protein when compared to other treatment and control groups.](http://images.novusbio.com/fullsize/Tat-Beclin-1-D11-Autophagy-Inducing-Peptide---Retroinverso-form-Western-Blot-NBP2-49888-img0001.jpg)
![In vivo assay: Tat-Beclin 1 D11 Autophagy Inducing Peptide - Retroinverso form [NBP2-49888] - In vivo dose study in 10wk old C57BL/6J mice. Either 1mg/kg or 10mg/kg IP once daily was administered for 2 days, mice were sacrificed, kidneys prepared for Western blot analysis. Lysosomal inhibitor bafilomycin A1 was used to provide a measurement of autophagic flux. *vehicle is scrambled tat-beclin (NBP2-49887-5mg). Image from verified customer review.](http://images.novusbio.com/fullsize/Tat-Beclin-1-D11-Autophagy-Inducing-Peptide---Retroinverso-form-In-vivo-assay-NBP2-49888-img0004.jpg)
![Western Blot: Tat-Beclin 1 L11S Autophagy Inducing Peptide - Inactive Form [NBP2-49887] - WB analysis of lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S. The lysates were analyzed for the expression of LC3-1/LC3-II and SQSTM1/p62 using 2ug/ml each of anti-LC3B (NB100-2220) and anti-SQSTM1/p62 (MAB8028) respectively. Anti-Actin (AF4000) was used as a loading control. TatD11 exhibited superior induction of LC3-II and down-regulation of p62 protein when compared to other treatment and control groups.](http://images.novusbio.com/fullsize/Tat-Beclin-1-L11S-Autophagy-Inducing-Peptide---Inactive-Form-Western-Blot-NBP2-49887-img0001.jpg "Western Blot: Tat-Beclin 1 L11S Autophagy Inducing Peptide - Inactive Form [NBP2-49887] - WB analysis of lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S. The lysates were analyzed for the expression of LC3-1/LC3-II and SQSTM1/p62 using 2ug/ml each of anti-LC3B (NB100-2220) and anti-SQSTM1/p62 (MAB8028) respectively. Anti-Actin (AF4000) was used as a loading control. TatD11 exhibited superior induction of LC3-II and down-regulation of p62 protein when compared to other treatment and control groups.")
![Immunocytochemistry/Immunofluorescence: Tat-Beclin 1 L11S Autophagy Inducing Peptide - Inactive Form [NBP2-49887] - HeLa GFP-LC3B cells were treated with Tat-D11, Tat-L11, Tat-Beclin 1 or Tat-L11S for 1.5 hours. Thereafter, the cells were stained using NeuroTrace Red or DAPI and analyzed employing fluorescent microscopy. Note the higher number of autophagosomes/GFP-LC3B+ puncta in the images of Tat-D11 and Tat-L11 treated cells when compared to Tat-Beclin 1 and Tat-L11S treated cells.](http://images.novusbio.com/fullsize/Tat-Beclin-1-L11S-Autophagy-Inducing-Peptide---Inactive-Form-Immunocytochemistry-Immunofluorescence-NBP2-49887-img0002.jpg)
![In vivo assay: Tat-Beclin 1 L11S Peptide - Scrambled Control [NBP2-49887] - In vivo dose study in mouse kidneys as control for tat-beclin D11 autophagy inducing peptide. Well tolerated by mice at dose of 1mg/kg for 2 days IP. Soluble in PBS. First two lanes (controls) are treated with 1mg/kg tat-beclin scrambled peptide; remaining lanes are treated with tat-beclin D11 autophagy inducing peptide. Image from verified customer review.](http://images.novusbio.com/fullsize/Tat-Beclin-1-L11S-Peptide---Scrambled-Control-In-vivo-assay-NBP2-49887-img0003.jpg)