| Gene Symbol |
Relb
|
| Entrez Gene |
19698
|
| Alt Symbol |
shep
|
| Species |
Mouse
|
| Gene Type |
protein-coding
|
| Description |
avian reticuloendotheliosis viral (v-rel) oncogene related B
|
| Other Description |
transcription factor RelB
|
| Swissprots |
Q04863 Q8VE46
|
| Accessions |
AAB33259 EDL23169 Q04863 AK146932 BAE27543 AK156767 BAE33846 BC019765 AAH19765 BC034523 AAH34523 BC117792 BC117793 AAI17794 DQ020178 AAY44746 DQ020179 AAY44747 DQ020180 AAY44748 DQ020181 AAY44749 M83380 AAA40041 S56076 AAB25493 XM_006539675 XP_006539738 XM_011250459 XP_011248761 XM_011250460 XP_011248762 XM_011250461 XP_011248763 XM_011250462 XP_011248764 NM_001290457 NP_001277386 NM_009046 NP_033072
|
| 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. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome {ECO:0000250}. Note=Colocalizes with NEK6 in the centrosome. {ECO:0000250}.
|
| Tissue Specificity |
Expressed in intestine, thymus and spleen. Undetectable in liver, bome marrow, kidney and testis.
|
| Top Pathways |
MAPK signaling pathway, Osteoclast differentiation, HTLV-I infection, Epstein-Barr virus infection
|