NF-κB (p65) Polyclonal Antibody (aa 2-17)

NF-κB p65 is a ubiquitously expressed transcription factor that is a subunit of the NF-κB complex and is encoded by the RELA gene in humans.¹ It is composed of an N-terminal Rel homology domain, which contains the nuclear localization signal (NLS), and mediates dimerization, nuclear localization, and DNA and protein interactions, and two C-terminal transactivation domains that are subject to a variety of post-translational modifications and regulate the transcriptional activity of p65.^1,2 NF-κB p65 regulates the expression of a large number of genes in response to inflammatory and environmental cues that play critical roles in innate and adaptive immunity and cellular differentiation.² Silencing of Rela induces tumor cell apoptosis in a murine Lewis lung carcinoma model, and RELA silencing in THP-1 monocytes decreases secreted levels of IL-1β and TNF-α induced by LPS.^3,4 Genome-wide deletion of Rela in mice is embryonic lethal.⁵ NF-κB p65 is overexpressed in the inflamed joints of patients with rheumatoid arthritis, and naïve CD4 T cells isolated from the whole blood of patients with multiple sclerosis have increased phosphorylation of NF-κB p65.^6,7 Cayman's NF-ĸB (p65) Polyclonal Antibody (aa 2-17) can be used for Western blot (WB) applications. The antibody recognizes amino acids 2-17 of NF-κB (p65) at 60 kDa from human, chimpanzee, and monkey samples.

WARNING This product is not for human or veterinary use.

1. Peterson, J.M., Bakkar, N., and Guttridge, D.C. NF-κB signaling in skeletal muscle health and disease. Current Topics in Developmental Biology 96, 85-119 (2011).

2. Giridharan, S., and Srinivasan, M. Mechanisms of NF-κB p65 and strategies for therapeutic manipulation. J. Inflamm. Res. 11, 407-419 (2018).

3. Qu, Y., Zhang, X., and Wu, R. Knockdown of NF-κB p65 subunit expression suppresses growth of nude mouse lung tumor cell xenografts by activation of Bax apoptotic pathway. Neoplasma 62(1), 34-40 (2015).

4. Wu, C., Zhao, J., Zhu, G., et al. siRNA directed against NF‑κB inhibits mononuclear macrophage cells releasing proinflammatory cytokines in vitro. Mol. Med. Rep. 16(6), 9060-9066 (2017).

5. Beg, A.A., and Baltimore, D. An essential role for NF-κB in preventing TNF-α-induced cell death. Science 274(5288), 782-784 (1996).

6. Makarov, S.S. NF-κB in rheumatoid arthritis: A pivotal regulator of inflammation, hyperplasia, and tissue destruction. Arthritis Res. 3(4), 200-206 (2001).

7. Housley, W.J., Fernandez, S.D., Vera, K., et al. Genetic variants associated with autoimmunity drive NFκB signaling and responses to inflammatory stimuli. Sci. Transl. Med. 7(291), 291ra293 (2015).