RelB Recombinant Rabbit mAb (一抗) - WB,IHC-P,IHC-F,IF,IP | Bioss

bsm-62968R

重组兔单抗

RelB Recombinant Rabbit mAb

转录因子RelB蛋白重组兔单抗

I-REL; IMD53; IREL; REL-B; shep; RELB_HUMAN; RELB; RELB_MOUSE; RELB proto-oncogene, NF-kB subunit; v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3)

Rabbit

A synthesized peptide derived from human RelB: 515-579/579

IgG

Liquid

affinity purified by Protein A

Recombinant

14D9

62 kDa

62 kDa

10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.

Store at 4℃ for short term. Store at -20℃ for long term. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

RELB

Transcription factor RelB

Component of the NF-kappa-B RelB-p50 complex. Component of the NF-kappa-B RelB-p52 complex. Self-associates; the interaction seems to be transient and may prevent degradation allowing for heterodimer formation with p50 or p52. Interacts with NFKB1/p50, NFKB2/p52 and NFKB2/p100. Interacts with NFKBID.

Nucleus. Cytoplasm, cytoskeleton, centrosome. Note=Co-localizes with NEK6 in the centrosome.

Phosphorylation at 'Thr-103' and 'Ser-573' is followed by proteasomal degradation.

Contains 1 RHD (Rel-like) domain.

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. 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 RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49. As a member of the NUPR1/RELB/IER3 survival pathway, may provide pancreatic ductal adenocarcinoma with remarkable resistance to cell stress, such as starvation or gemcitabine treatment.