| Gene Symbol |
RELB
|
| Entrez Gene |
5971
|
| Alt Symbol |
I-REL, IREL, REL-B
|
| Species |
Human
|
| Gene Type |
protein-coding
|
| Description |
v-rel avian reticuloendotheliosis viral oncogene homolog B
|
| Other Description |
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
|
| Swissprots |
Q6GTX7 Q9UEI7 Q01201
|
| Accessions |
AAC82346 ABC40746 EAW57316 Q01201 AK290594 BAF83283 AL583128 AW137991 BC028013 AAH28013 BI906507 BM684710 DA940587 M83221 AAA36127 XM_005259127 XP_005259184 XM_005259128 XP_005259185 NM_006509 NP_006500
|
| 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-
|
| Subcellular Location |
Nucleus {ECO:0000269|PubMed:20873783}. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome {ECO:0000269|PubMed:20873783}. Note=Colocalizes with NEK6 in the centrosome.
|
| Top Pathways |
MAPK signaling pathway, Osteoclast differentiation, HTLV-I infection, Epstein-Barr virus infection
|