RELA/NFκB p65 Antibody (4H212): sc-71677

NFκB p65 Antibody (4H212) is a mouse monoclonal IgG1 antibody raised against amino acids 526-539 of NFκB p65 of human origin, exhibiting strong species reactivity with mouse, rat, and human proteins in applications such as western blotting (WB) and immunoprecipitation (IP). NFκB p65, also known as RELA, is a critical subunit of the NFκB transcription factor complex, which plays a pivotal role in regulating genes involved in immune and inflammatory responses, cell proliferation, and survival. Structurally, NFκB p65 contains a Rel homology domain (RHD) at its N-terminus responsible for DNA binding and dimerization, and a transactivation domain (TAD) at its C-terminus. The TAD, located near the C-terminus, is essential for initiating transcription by interacting with other transcriptional co-activators and the basal transcription machinery. Anti-NFκB p65 antibody (4H212) targets the epitope within the TAD (amino acids 526-539), a region crucial for the transcriptional activity of NFκB p65. Understanding the structure of NFκB p65 is important because alterations or post-translational modifications in these domains can significantly affect its ability to regulate gene expression, impacting processes like inflammation, immune responses, and oncogenesis. In resting cells, NFκB p65 is sequestered in the cytoplasm by inhibitor proteins called IκBs. Upon activation by various stimuli such as cytokines or stress signals, IκBs are degraded, allowing NFκB p65 to translocate to the nucleus, where NFκB p65 binds to specific DNA sequences to modulate gene expression. NFκB p65 monoclonal antibody (4H212) is an invaluable tool for researchers studying the NFκB signaling pathway and its implications in health and disease.

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RELA/NFκB p65 Antibody (4H212) References:

1. NF-kappaB (p65/RelA) as a regulator of TNFalpha-mediated ML-1 cell differentiation.  |  Mudipalli, A., et al. 2001. Leukemia. 15: 808-13. PMID: 11368442
2. Inhibitor of growth 4 induces NFκB/p65 ubiquitin-dependent degradation.  |  Hou, Y., et al. 2014. Oncogene. 33: 1997-2003. PMID: 23624912
3. Disruption of the CREBBP gene and decreased expression of CREB, NFκB p65, c-JUN, c-FOS, BCL2 and c-MYC suggest immune dysregulation.  |  Torres, LC., et al. 2013. Hum Immunol. 74: 911-5. PMID: 23643710
4. Oxidative stress-mediated NFκB phosphorylation upregulates p62/SQSTM1 and promotes retinal pigmented epithelial cell survival through increased autophagy.  |  Song, C., et al. 2017. PLoS One. 12: e0171940. PMID: 28222108
5. Impaired p65 degradation by decreased chaperone-mediated autophagy activity facilitates epithelial-to-mesenchymal transition.  |  Tang, J., et al. 2017. Oncogenesis. 6: e387. PMID: 28991259
6. MiR-520b inhibits endothelial activation by targeting NF-κB p65-VCAM1 axis.  |  Yang, B., et al. 2021. Biochem Pharmacol. 188: 114540. PMID: 33819467
7. miR-181d/RBP2/NF-κB p65 Feedback Regulation Promotes Chronic Myeloid Leukemia Blast Crisis.  |  Zhou, M., et al. 2021. Front Oncol. 11: 654411. PMID: 33842368
8. Estrogen Receptor Beta Influences the Inflammatory p65 Cistrome in Colon Cancer Cells.  |  Indukuri, R., et al. 2021. Front Endocrinol (Lausanne). 12: 650625. PMID: 33859619
9. Lead exposure induces neuronal apoptosis via NFκB p65/RBBP4/Survivin signaling pathway.  |  Chen, H., et al. 2023. Toxicology. 499: 153654. PMID: 37866543
10. Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma.  |  Ahsan, H., et al. 2023. J Clin Med. 12: PMID: 37892820

The preferred RELA/NFκB p65 antibody is RELA/NFκB p65 Antibody (F-6): sc-8008.