JUN
JUN (Transcription factor Jun) is a protein that switches other genes on and off. The public catalogues list it as a drug target and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Skin cancer and Melanoma.
Overview
Transcription factor that recognises and binds to the AP-1 consensus motif 5'-TGA[GC]TCA-3'. Heterodimerises with proteins of the FOS family to form an AP-1 transcription complex, thereby enhancing its DNA binding activity to the AP-1 consensus sequence 5'-TGA[GC]TCA-3' and enhancing its transcriptional activity. Together with FOSB, plays a role in activation-induced cell death of T cells by binding to the AP-1 promoter site of FASLG/CD95L, and inducing its transcription in response to activation of the TCR/CD3 signalling pathway.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant, naming Irbesartan. Open Targets scores its association with cancer at 0.75 (direct and indirect evidence; datatypes literature 1.00, affected pathway 0.71, animal model 0.33, somatic mutation 0.96).
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · JUN (Transcription factor Jun) is a protein that switches other genes on and off. The public catalogues list it as a drug target and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Skin cancer and Melanoma.
- 1 · What it is
JUN (Transcription factor Jun) is a protein that switches other genes on and off. The public catalogues list it as a drug target and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Skin cancer and Melanoma.
- 2 · What goes wrong in cancer
Transcription factor that recognises and binds to the AP-1 consensus motif 5'-TGA[GC]TCA-3'.
- 3 · How drugs use it
No product in this corpus aims at JUN yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
External identifiers
Sources: HGNC HGNC:6204 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P05412 (protein name, function text, keywords and locations (REST API)); CIViC gene JUN (1 evidence items, 0 assertions, 1 variants; diseases: Colorectal Adenocarcinoma (GraphQL API, CC0)); Open Targets ENSG00000177606 (association with cancer (MONDO_0004992) 0.75; per-cancer scores at or above 0.5: colorectal cancer 0.54, melanoma 0.56, skin cancer 0.56 (GraphQL API, CC0))
Biology
Transcription factor that recognises and binds to the AP-1 consensus motif 5'-TGA[GC]TCA-3'. Heterodimerises with proteins of the FOS family to form an AP-1 transcription complex, thereby enhancing its DNA binding activity to the AP-1 consensus sequence 5'-TGA[GC]TCA-3' and enhancing its transcriptional activity. Together with FOSB, plays a role in activation-induced cell death of T cells by binding to the AP-1 promoter site of FASLG/CD95L, and inducing its transcription in response to activation of the TCR/CD3 signalling pathway. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signalling pathway stimulation. Involved in activated KRAS-mediated transcriptional activation of USP28 in colorectal cancer (CRC) cells. Binds to the USP28 promoter in colorectal cancer (CRC) cells. Location: Nucleus (UniProt). Locus 1p32.1 (HGNC).
- Colorectal cancer: Open Targets association 0.54 with colorectal cancer (MONDO_0005575); CIViC evidence names this disease
- Skin cancer: Open Targets association 0.56 with skin cancer (MONDO_0002898)
- Melanoma: Open Targets association 0.56 with melanoma (MONDO_0005105)
Notes
top- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 1 therapies; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery for this target: (TITLE:"JUN" OR ABSTRACT:"JUN" OR TITLE:"Jun proto-oncogene, AP-1 transcription factor subunit" OR ABSTRACT:"Jun proto-oncogene, AP-1 transcription factor subunit" OR TITLE:"Transcription factor Jun" OR ABSTRACT:"Transcription factor Jun" OR TITLE:"c-Jun" OR ABSTRACT:"c-Jun" OR TITLE:"AP-1" OR ABSTRACT:"AP-1") 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 JUN, not a curated reading list.