Aliases for RELA Gene
- V-Rel Avian Reticuloendotheliosis Viral Oncogene Homolog A 2 3
- Nuclear Factor Of Kappa Light Polypeptide Gene Enhancer In B-Cells 3 2 3 4
- NFKB3 3 4 6
- Nuclear Factor NF-Kappa-B P65 Subunit 3 4
- V-Rel Reticuloendotheliosis Viral Oncogene Homolog A 3
- Transcription Factor P65 3
- NF-Kappa-B P65delta3 3
- P65 3
External Ids for RELA Gene
Previous Symbols for RELA Gene
NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor, NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene, RELA. Four transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2011]
GeneCards Summary for RELA Gene
RELA (V-Rel Avian Reticuloendotheliosis Viral Oncogene Homolog A) is a Protein Coding gene. Diseases associated with RELA include ependymoma and hypersplenism. Among its related pathways are PI3K-Akt signaling pathway and PI-3K cascade. GO annotations related to this gene include sequence-specific DNA binding transcription factor activity and identical protein binding. An important paralog of this gene is NFKB1.
UniProtKB/Swiss-Prot for RELA Gene
NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes 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 and the heterodimeric p65-p50 complex appears to be most abundant one. 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 p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells (PubMed:15790681).