PTPRC
PTPRC (Receptor-type tyrosine-protein phosphatase C) is an enzyme. The public catalogues list it as an oncogene driver and a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Anal cancer, Hepatocellular carcinoma, Skin cancer and 5 more.
Overview
Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4. The first PTPase domain has enzymatic activity, while the second one seems to affect the substrate specificity of the first one.
Open Targets scores its association with cancer at 0.67 (direct and indirect evidence; datatypes literature 0.99, animal model 0.46, genetic association 0.18, somatic mutation 0.85). IntOGen calls it a driver in 4 cohorts (1 activating, 3 loss-of-function), covering Anal Squamous Cell Carcinoma, Diffuse Large B-Cell Lymphoma, NOS, Hepatocellular Carcinoma, Melanoma.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · PTPRC (Receptor-type tyrosine-protein phosphatase C) is an enzyme. The public catalogues list it as an oncogene driver and a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Anal cancer, Hepatocellular carcinoma, Skin cancer and 5 more.
- 1 · What it is
PTPRC (Receptor-type tyrosine-protein phosphatase C) is an enzyme. The public catalogues list it as an oncogene driver and a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Anal cancer, Hepatocellular carcinoma, Skin cancer and 5 more.
- 2 · What goes wrong in cancer
Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4.
- 3 · How drugs use it
No product in this corpus aims at PTPRC yet. Inhibitors are shaped to fit the enzyme's active site so the reaction the cancer relies on stops.
External identifiers
Sources: HGNC HGNC:9666 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P08575 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000081237 (association with cancer (MONDO_0004992) 0.67; per-cancer scores at or above 0.5: colorectal cancer 0.55, gastric cancer 0.52, melanoma 0.55, skin cancer 0.56, breast cancer 0.54, lung cancer 0.55 (GraphQL API, CC0)); IntOGen PTPRC (driver in 4 cohorts (Act 1, LoF 3); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Biology
Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4. The first PTPase domain has enzymatic activity, while the second one seems to affect the substrate specificity of the first one. Upon T-cell activation, recruits and dephosphorylates SKAP1 and FYN. Dephosphorylates LYN, and thereby modulates LYN activity. Interacts with CLEC10A at antigen presenting cell-T cell contact; CLEC10A on immature dendritic cells recognises Tn antigen-carrying PTPRC/CD45 receptor on effector T cells and modulates T cell activation threshold to limit autoreactivity. Location: Cell membrane; Membrane raft; Synapse (UniProt). Locus 1q31.3-q32.1 (HGNC).
- Anal cancer: IntOGen driver in 1 cohort (ANSC)
- Hepatocellular carcinoma: IntOGen driver in 1 cohort (HCC)
- Skin cancer: Open Targets association 0.56 with skin cancer (MONDO_0002898)
- Colorectal cancer: Open Targets association 0.55 with colorectal cancer (MONDO_0005575)
- Lung cancer: Open Targets association 0.55 with lung cancer (MONDO_0008903)
- Breast cancer: Open Targets association 0.54 with breast cancer (MONDO_0007254)
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: IntOGen calls it an activating (Act) driver in 1 cohort; IntOGen calls it a loss-of-function (LoF) driver in 3 cohorts. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery for this target: (TITLE:"PTPRC" OR ABSTRACT:"PTPRC" OR TITLE:"protein tyrosine phosphatase receptor type C" OR ABSTRACT:"protein tyrosine phosphatase receptor type C" OR TITLE:"Receptor-type tyrosine-protein phosphatase C" OR ABSTRACT:"Receptor-type tyrosine-protein phosphatase C" OR TITLE:"T200" OR ABSTRACT:"T200" OR TITLE:"GP180" OR ABSTRACT:"GP180" OR TITLE:"LY5" OR ABSTRACT:"LY5") 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 PTPRC, not a curated reading list.
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