Anti-RelB Antibody [SD07-39]

HUABIO

Anti-RelB Antibody [SD07-39]

7

ImmunoFluorescence, ImmunoPrecipitation, Western Blot, ImmunoHistoChemistry, ImmunoHistoChemistry Paraffin

WB,IF-Cell,IF-Tissue,IHC-P,IP

Research Use Only

Monoclonal

SD07-39

1 mg/ml

Unconjugated

RELB

RELB proto-oncogene, NF-kB subunit

I-REL, IMD53, IREL, REL-B, transcription factor RelB, v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3), v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3

Rabbit

IgG

Transcription factor RelB

In resting cells, RelB is sequestered by the NF-kappaB precursor protein p100 in the cytoplasm. A select set of TNF-R superfamily members, including lymphotoxin beta-receptor (LTbetaR), BAFF-R, CD40 and RANK, activate the non-canonical NF-kappaB pathway. In this pathway, NIK stimulates the processing of p100 into p52, which in association with RelB appears in the nucleus as RelB:p52 NF-kappaB heterodimers. RelB:p52 activates the expression homeostatic lymphokines,which instruct lymphoid organogenesis and determine the trafficking of naive lymphocytes in the secondary lymphoid organs. Recent studies has suggested that the functional non-canonical NF-kappaB pathway is modulated by canonical NF-kappaB signalling. For example, syntheses of the constituents of the non-canonical pathway, viz RelB and p52, are controlled by canonical IKK2-IkappaB-RelA:p50 signalling.Moreover, generation of canonical and non-canonical dimers, viz RelA:p50 and RelB:p52, within the cellular milieu are mechanistically interlinked. These analyses suggest that an integrated NF-kappaB system network underlies activation of both RelA and RelB containing dimer and that a malfunctioning canonical pathway will lead to an aberrant cellular response also through the non-canonical pathway. Most intriguingly, a recent study identified that TNF-induced canonical signalling subverts non-canonical RelB:p52 activity in the inflamed lymphoid tissues limiting lymphocyte ingress.Mechanistically, TNF inactivated NIK in LTbetaR-stimulated cells and induced the synthesis of Nfkb2 mRNA encoding p100; these together potently accumulated unprocessed p100, which attenuated the RelB activity. A role of p100/Nfkb2 in dictating lymphocyte ingress in the inflamed lymphoid tissue may have broad physiological implications.

Human

Human

-20°C,2°C to 8°C

41116161