Recombinant NF-kB p65 Antibody

抗体

细胞核因子/k基因结合核因子抗体 | 细胞核因子/k基因结合核因子单克隆抗体 | 细胞核因子/k基因结合核因子重组单克隆抗体 | NF-kB p65抗体 | NF-kB p65单克隆抗体 | NF-kB p65重组单克隆抗体 | RELA抗体 | RELA单克隆抗体 | RELA重组单克隆抗体

NFKB3 | RELA | TF65 | Transcription factor p65 | p65 | NFkB | NF-KB p65 Rabbit mAb | Avian reticuloendotheliosis viral (v rel) oncogene homolog A antibody | MGC131774 antibody | NF kappa B p65delta3 antibody | nfkappabp65 antibody | NFkB p65 antibody | NF

Liquid

Ab117947-10μl

10μl

重组

见COA

-20°C储存,避免反复冻融

超低温冰袋运输

短期储存2-8℃（1-2周）；长期储存-20℃（24个月）；收货后建议分装，避免反复冻融。

10mM PBS, 150mM NaCl, 50% Glycerol, 0.05% BSA, 0.02% Sodium azide, pH 7.4

0.02% Sodium azide

NF-kappa-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-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 directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Post-translational: Ubiquitinated, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response. Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity (By similarity). Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity. Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of 'Lys-310'.

A synthetic peptide derived from human NF-kB p65 (AA 500-551).

兔(Rabbit)

人(Human), 大鼠(Rat), 小鼠(Mouse) | 人(Human),大鼠(Rat),小鼠(Mouse)

NF-kB p65

WB: HT-1080, K562, HEK293, Jurkat, HeLa and NIH/3T3 cell lysates. IHC: Human bladder cancer tissue. IF/ICC: HeLa cells. IP: HeLa cells.

150 kDa

Unconjugated

Rabbit IgG

重组抗体

kappa

Protein A purified

Whole IgG