Anti-NF-kB p65/RELA Antibody Picoband®

Transcription factor p65, also known as NFKB3 or NF-kB p65, is a protein that in humans is encoded by the RELA gene. It is mapped to 11q13.1. NFKB is an essential transcription factor complex involved in all types of cellular processes, including cellular metabolism, chemotaxis, etc, and it may play a role in inflammatory conditions of the peripheral nervous system. Phosphorylation and acetylation of NFKB3 are crucial post-translational modifications required for NFKB activation. It has also been shown to modulate immune responses, and activation of NFKB3 is positively associated with multiple types of cancer. In addition to that, NFKB3 antagonizes TNFR1-JNK proliferative signals in epidermis and plays a nonredundant role in restraining epidermal growth.

E.coli-derived human NF-kB p65 recombinant protein (Position: F99-S551) . Human NF-kB p65 shares 86% amino acid (aa) sequence identity with mouse NF-kB p65.

Isoform 1 is widely expressed, other isoforms are generally coexpressed with a more restricted distribution. Isoform 2 is expressed in skin, liver, skeletal muscle, cardiac muscle, placenta, umbilical vein endothelial cells, neuroblastoma cells, lymphoma cells, hepatoma cells and astrocytoma cells. Isoform 3 and isoform 4 are expressed in muscle, kidney, liver, placenta, cervical epithelium, umbilical vein endothelial cells, fibroblast cells, embryonal kidney cells, platelets and several blood cell lines. Isoform 4, rather than isoform 3, is selectively expressed in peripheral T-cells. Isoform 3 is expressed in non- proliferating and differentiated prostate gland epithelial cells and in platelets, on the surface of erythroleukemia cells and in various hematopoietic cell lines. Isoform 5 is expressed specifically in striated muscle (skeletal and cardiac muscle) . .

Apoptosis, Apoptotic Markers, Cancer, Cell Biology, Cell Death, Domain Families, Epigenetics and Nuclear Signaling, Intracellular, Metabolic Signaling Pathways, Metabolism, Mitochondrial Metabolism, NFKB Pathway, Nuclear Hormone Receptors, Nuclear Receptors, Nuclear Signaling, Nuclear Signaling Pathways, Nucleotide Metabolism, Pathways and Processes, Signal Transduction, Signaling Pathway, Transcription, Zinc Finger

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute ly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells (PubMed:15790681) . .

1. Nolan GP, Ghosh S, Liou HC, Tempst P, Baltimore D (April 1991) . DNA binding and I kappa B inhibition of the cloned p65 subunit of NF-kappa B, a rel-related polypeptide. Cell 64 (5) : 961–9. 2. Lim, C.-A., Yao, F., Wong, J. J.-Y., George, J., Xu, H., Chiu, K. P., Sung, W.-K., Lipovich, L., Vega, V. B., Chen, J., Shahab, A., Zhao, X. D., Hibberd, M., Wei, C.-L., Lim, B., Ng, H.-H., Ruan, Y., Chin, K.-C. Genome-wide mapping of RELA (p65) binding identifies E2F1 as a transcriptional activator recruited by NF-kappa-B upon TLR4 activation.Molec. Cell 27: 622-635, 2007. 3. Mazzeo, A., Aguennouz, M., Messina, C., Vita, G. Immunolocalization and activation of transcription factor nuclear factor kappa-B in dysimmune neuropathies and familial amyloidotic polyneuropathy. Arch. Neurol. 61: 1097-1102, 2004.

Store at -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freeze-thaw cycles.

Nucleus. Cytoplasm. Colocalized with DDX1 in the nucleus upon TNF-alpha induction (By similarity) . Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B) . Colocalizes with GFI1 in the nucleus after LPS stimulation. .