NFkB p65 (phospho Thr254) Antibody | 79-107

NFkB p65 (phospho Thr254) Antibody | 79-107 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: NFkB-p65 (Phospho-Thr254) antibody was raised against a peptide sequence around phosphorylation site of threonine 254 (F-R-T (p) -P-P) derived from Human NFκB-p65.

Research Area: Phospho-Specific, Apoptosis, Cancer

Tested Application: WB, IHC, IF

Application: Western Blot: 1:500~1:1000, Immunohistochemistry: 1:50~1:100, Immunofluorescence: 1:100~1:200

Specificiy: This antibody detects endogenous level of NFκB p65 only when phosphorylated at threonine 254.

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 65 kDa

Validation: N/A

Isoform: N/A

Purification: Antibodies were purified by affinity-chromatography using epitope-specific phosphopeptide. Non-phospho specific antibodies were removed by chromatogramphy using non-phosphopeptide.

Clonality: Polyclonal

Clone: N/A

Isotype: N/A

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Antibody supplied in phosphate buffered saline (without Mg2+ and Ca2+) , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Concentration: 1 mg/mL

Storage Condition: Store antibody at -20˚C for up to one year.

Alternate Name: p65, NFKB3, CTNNB, OK/SW-cl.35, PRO2286, RELA, TF65, Transcription factor p65, p65

User Note: N/A

BACKGROUND: 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 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-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-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-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-kappa-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.