anti-NF-κB p65, pAb

CHF 315.00
In stock
YIF-LF-PA0062100 µlCHF 315.00
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Product Details
Synonyms RELA; NFKB3; Transcription Factor p65; Nuclear Factor NF-κ-B p65 Subunit; Nuclear Factor of κ Light Polypeptide Gene Enhancer in B-Cells 3
Product Type Polyclonal Antibody
Immunogen/Antigen Synthetic peptide.

Western Blot (1:2,000)

Crossreactivity Human
Purity Detail Protein A purified.
Formulation Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Other Product Data

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Our product description may differ slightly from the original manufacturers product datasheet.

Declaration Manufactured by AbFrontier
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
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Product Specification Sheet
Datasheet Download PDF

NF-κB (Nuclear Factor κ B) is a nuclear transcription factor found in all cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Consistent with this role, incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection and improper immune development. There are five members in the NF-κB family: NF-κB1, NF-κB2, RelA (also named p65), RelB, and c-Rel. RelA(p65) subunit of NF-κB is a crucial regulator of apoptosis. RelA subunit mediates resistance to programmed cell death induced by many stimuli, including TNF, chemotherapy agents and ionizing radiation, through inducing the expression of a wide variety of anti-apoptotic genes. NF-κ-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κ-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 κ-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different κ-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-κ-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-κ-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-κ-B inhibitor (I-κ-B) family. In a conventional activation pathway, I-κ-B is phosphorylated by I-κ-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-κ-B complex which translocates to the nucleus. NF-κ-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-κ-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-κ-B upon NF-κ-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-κ-B complex.

Product References

1) Campbell KJ, Perkins ND. Cell Cycle. 2004; vol.3(7): p.869-72. (General)
2) Perkins ND. Trends Cell Biol. 2004; vol.14(2): p.64-9. (General)
3) Zanetti M, et al, Ann N Y Acad Sci. 2003; vol.987: p.249-57. (General)

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