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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 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 Genome-wide deletion of Rela in mice is embryonic lethal.3 Silencing of NF-κB p65 induces tumor cell apoptosis in a murine Lewis lung carcinoma model and decreases secreted levels of IL-1β and TNF-α induced by LPS in THP-1 monocytes.4,5 NF-κB p65 is overexpressed in 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-κB p65 (human, recombinant) protein can be used for Western blot and ELISA applications. Cayman’s NF-κB (p65) Polyclonal Antibody can be used for ELISA and Western blot applications. The antibody recognizes NF-κB at 65 kDa from human samples.
WARNING This product is not for human or veterinary use.
1. NF-
2. Mechanisms of NF-
3. An essential role for NF-
4. Knockdown of NF-
5. siRNA directed against NF‑κB inhibits mononuclear macrophage cells releasing proinflammatory cytokines in vitro. Mol. Med. Rep. 16(6), 9060-9066 (2017).
6. NF-
7. Genetic variants associated with autoimmunity drive NFκB signaling and responses to inflammatory stimuli. Sci. Transl. Med. 7(291), 291ra293 (2015).