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RELA (Transcription factor p65) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Gastric & gastro-oesophageal junction cancer.
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. The heterodimeric RELA-NFKB1 complex appears to be most abundant one.
IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Stomach Adenocarcinoma.
In plain words · RELA (Transcription factor p65) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Gastric & gastro-oesophageal junction cancer.
RELA (Transcription factor p65) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Gastric & gastro-oesophageal junction cancer.
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.
No product in this corpus aims at RELA yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
First described 1991. Earliest sequence paper UniProt cites for the protein: Ruben S.M. et al, Science, 1991, "Isolation of a rel-related human cDNA that potentially encodes the 65-kD subunit of NF-kappa B". Source.
Sources: HGNC HGNC:9955 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q04206 (protein name, function text, keywords and locations (REST API)); IntOGen RELA (driver in 1 cohort (Act 0, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
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. The heterodimeric RELA-NFKB1 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. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. Location: Nucleus; Cytoplasm (UniProt). Locus 11q13.1 (HGNC).
Query for this target: (TITLE:"RELA" OR ABSTRACT:"RELA" OR TITLE:"RELA proto-oncogene, NF-kB subunit" OR ABSTRACT:"RELA proto-oncogene, NF-kB subunit" OR TITLE:"Transcription factor p65" OR ABSTRACT:"Transcription factor p65" OR TITLE:"p65" OR ABSTRACT:"p65" OR TITLE:"NFKB3" OR ABSTRACT:"NFKB3") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about RELA, not a curated reading list.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen, Gastric & gastro-oesophageal junction cancer.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen, Gastric & gastro-oesophageal junction cancer.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), IntOGen.