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Rel B

Domain

Both N- and C-terminal domains are required for transcriptional activation.

Function

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. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-BMAL1 heterodimer in a CRY1/CRY2 independent manner. Increased repression of the heterodimer is seen in the presence of NFKB2/p52. Is required for both T and B lymphocyte maturation and function (PubMed:26385063).

Involvement in disease

Immunodeficiency 53

IMD53

An autosomal recessive primary immunodeficiency apparent from early infancy and resulting in recurrent infections, severe autoimmune skin disease rheumatoid arthritis, and failure to thrive. Immunologic workup shows increased CD4+/CD8+ ratio, impaired T-cell proliferative response to multiple antigen, T-cell developmental and functional defects, and impaired ability to produce specific immunoglobulins.

None

The disease is caused by variants affecting the gene represented in this entry.

Post-translational modifications

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

Cellular localization

  • Nucleus
  • Cytoplasm
  • Cytoskeleton
  • Microtubule organizing center
  • Centrosome
  • Colocalizes with NEK6 in the centrosome.

Alternative names

  • Transcription factor RelB
  • I-Rel
  • RELB

Target type

Proteins

Primary research area

Immunology & Infectious Disease

Molecular weight

62134Da

We found 15 products in 3 categories

Primary Antibodies

Target

Reactive species

Assay Kits

Target

Reactive species

Detection method

Proteins & Peptides

Target

Species of origin

Nature

Search our catalogue for 'Rel B' (15)

Products

ab33907

Anti-Rel B antibody [EP614Y]

Recombinant
RabMAb
KO Validated

ab33917

Anti-Rel B antibody [EP613Y]

Recombinant
RabMAb

ab283878

Human Rel B ELISA Kit

Recombinant
SimpleStep

ab247279

Anti-Rel B antibody [EP614Y] - BSA and Azide free

Recombinant
RabMAb
KO Validated

ab212214

PE Anti-Rel B antibody [EP614Y]

Recombinant
RabMAb