Anti phospho nf κb p65 93h1

Manufactured by Cell Signaling Technology

The Anti-phospho NF-κB p65 (93H1) is a rabbit monoclonal antibody that detects phosphorylation of the NF-κB p65 subunit at serine 536. It is designed for use in Western blotting applications.

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Lab products found in correlation

Image studio lite 4, by LI COR (1 mentions) Azure c600 western blot imaging system, by Azure Biosystems (1 mentions) Anti βtubulin 66240 1 ig, by Proteintech (1 mentions) Anti nf κb p65 8242, by Cell Signaling Technology (1 mentions)

Close spelling variants of this product

Anti-phospho-NF-κB p65 (S536) and anti-NF-κB p65 (93H1 and D14E12, Anti-phospho-NF-κB p65 (Ser536) (93H1) Anti-phospho-NF-κB p65 Phospho-NF-κB p65 Anti-NF-κB p65 Anti-phospho-NF-κB NF-κB p65 Phospho-NF-κB Anti-NF-κB Anti-phospho-p65

2 protocols using anti phospho nf κb p65 93h1

NF-κB Activation in SHIV-infected RM-PBMCs

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Cytoplasmic and nuclear protein extracts obtained from RM-PBMCs infected with NF-κB promoter-variant SHIVs and control cells were subjected to western blot analysis and probed with a polyclonal anti-phospho NF-κB p65 (93H1; Cell Signaling Technology, Danvers MA) or monoclonal GAPDH (1D4, ThermoFisher). Appropriate Goat anti mouse or rabbit secondary antibodies were utilized. Enhanced Chemiluminescence (Azure, Dublin CA) was utilized to detect secondary antibody. Azure c600 western blot imaging system was utilized to capture the chemiluminescent signal. Image Studio™ Lite 4.0 Software (LI-COR, Lincoln NE) was utilized to measure band intensities.

Dave R.S., Ali H., Sil S., Knight L.A., Pandey K., Madduri L.S., Qiu F., Ranga U., Buch S, & Byrareddy S.N. (2020). NF-κB Duplications in the Promoter-Variant HIV-1C LTR Impact Inflammation Without Altering Viral Replication in the Context of Simian Human Immunodeficiency Viruses and Opioid-Exposure. Frontiers in Immunology, 11, 95.

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Immunoblotting and Immunohistochemistry Protocols

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The following antibodies were used for immunohistochemistry (IHC) and Western blot analysis: rabbit anti‐CD8⁺ (ZA‐0508; ZSGB‐Bio, Beijing, China), rabbit anti‐CCL5 (ab9679), and anti‐PDE5 (ab14672) (both from Abcam, Cambridge, UK), mouse anti‐glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) (60004‐1‐Ig) and anti‐β‐tubulin (66240‐1‐Ig) (both from Proteintech Group Inc, Chicago, IL), rabbit anti‐CCND1 (92G2), anti‐STAT5 (9363), anti‐phospho‐STAT5 (9314), anti‐NF‐κB p65 (8242), and anti‐phospho‐NF‐κB p65 (93H1) (all from Cell Signaling Technology, Denver, MA). Recombinant human (rh)CCL5 (278‐RN) and anti‐CCL5 neutralizing antibody (MAB678) were purchased from R&D systems (Minneapolis, MN), tadalafil (S1512) and a PKG inhibitor KT5823 (S4684) were obtained from Selleckchem (Houston, TX), and a PDE5‐insensitive PKG agonist Sp‐8‐Br‐PET‐cGMP was purchased from Biolog (Hayward, CA). All reagents were used in low androgen medium to reproduce the conditions of finasteride treatment.

Jin S., Xiang P., Liu J., Yang Y., Hu S., Sheng J., He Q., Yu W., Han W., Jin J, & Peng J. (2019). Activation of cGMP/PKG/p65 signaling associated with PDE5‐Is downregulates CCL5 secretion by CD8 + T cells in benign prostatic hyperplasia. The Prostate, 79(8), 909-919.

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