NF-kB p65 (RELA) Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	IHC, WB
Recommend Dilution	ELISA: 1:1,000 - 1:6,000, WB: 1:200 - 1:2,000, IHC: 5 ug/ml
Reactivity	Human
Host	Rabbit
Clonality	Polyclonal
Immunogen	This affinity purified antibody was prepared from whole rabbit serum produced by repeated immunizations with a synthetic peptide corresponding to residues surrounding S536 of human p65 (RelA) protein.
Formulation	0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
Concentration	lot specific
Conjugation	Unconjugated
Storage Condition	Store at -20°C as received.
Gene Name	RELA proto-oncogene, NF-kB subunit
Database Link	NP_001138610 Entrez Gene 5970 Human UniProt ID Q04206
Synonyms	NFKB3; p65
Note	This antibody is suitable for Cancer, Immunology and Nuclear Signaling research. NFkB was originally identified as a factor that binds to the immunoglobulin kappa light chain enhancer in B cells. It was subsequently found in non-B cells in an inactive cytoplasmic form consisting of NFkB bound to IkB. NFkB was originally identified as a heterodimeric DNA binding protein complex consisting of p65 (RelA) and p50 (NFKB1) subunits. Other identified subunits include p52 (NFKB2), cRel, and RelB. The p65, cRel, and RelB subunits are responsible for transactivation. The p50 and p52 subunits possess DNA binding activity but limited ability to transactivate. p52 has been reported to form transcriptionally active heterodimers with the NFkB subunit p65, similar to p50/p65 heterodimers. Lowlevels of p52 and p50 homodimers can also exist in cells. The heterodimers of p52/p65 and p50/p65 are regulated by physical inactivation in the cytoplasm by IkB-a. IkB-a binds to the p65 subunit, preventing nuclear localization, and DNA binding. Activators mediate a rapid phosphorylation of IkB by IkB kinase (IKK), which results in subsequent ubiquitination and proteolytic degradation. NFkB is then transported to the nucleus, where it activates transcription of target genes through binding to NFkB target sequences within the promoter. The HTLV-I protein Tax can induce constitutive NFkB activation through phosphorylation of both I?B-a and I?B-β. The transforming protein Tax inhibits p53 transcriptional activity through the NFkB signaling pathway, specifically via the p65 (RelA) subunit. The inhibition of p53 activity is dependent upon phosphorylation of p65 (RelA) at S536 by the upstream kinase IKKβ.
Reference Data
Protein Families	Druggable Genome, Transcription Factors
Protein Pathways	Acute myeloid leukemia, Adipocytokine signaling pathway, Apoptosis, B cell receptor signaling pathway, Chemokine signaling pathway, Chronic myeloid leukemia, Cytosolic DNA-sensing pathway, Epithelial cell signaling in Helicobacter pylori infection, MAPK signaling pathway, Neurotrophin signaling pathway, NOD-like receptor signaling pathway, Pancreatic cancer, Pathways in cancer, Prostate cancer, RIG-I-like receptor signaling pathway, Small cell lung cancer, T cell receptor signaling pathway, Toll-like receptor signaling pathway

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