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PREX2 is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Functions as a RAC1 guanine nucleotide exchange factor (GEF), activating Rac proteins by exchanging bound GDP for free GTP. Its activity is synergistically activated by phosphatidylinositol 3,4,5-trisphosphate and the beta gamma subunits of heterotrimeric G protein. Mediates the activation of RAC1 in a PI3K-dependent manner.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant, naming Vemurafenib. Open Targets scores its association with cancer at 0.73 (direct and indirect evidence; datatypes literature 0.91, animal model 0.42, genetic association 0.45, somatic mutation 0.82). IntOGen calls it a driver in 13 cohorts (10 activating, 3 loss-of-function), covering Bladder Urothelial Carcinoma, Invasive Breast Carcinoma, Colon Adenocarcinoma, Diffuse Large B-Cell Lymphoma, NOS, Oesophageal Adenocarcinoma, Oesophageal Squamous Cell Carcinoma and others.
In plain words · PREX2 is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
PREX2 is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response.
Functions as a RAC1 guanine nucleotide exchange factor (GEF), activating Rac proteins by exchanging bound GDP for free GTP.
No product in this corpus aims at PREX2 yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a tumour suppressor (IntOGen finds it knocked out more often than chance), so the direction differs between cohorts but the alteration is somatic either way; what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA PREX2: RNA low tissue specificity; high antibody staining in 6 normal tissues; highest cancer staining colorectal cancer (9 of 9 high). Distribution: 8 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Oesophageal cancer, Colorectal cancer, Gastric & gastro-oesophageal junction cancer, Breast cancer (all types), Bladder & urothelial cancer, Hepatocellular carcinoma, Ovarian cancer and more); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt Q70Z35; CIViC gene PREX2; IntOGen PREX2; Human Protein Atlas PREX2 tissue; Open Targets ENSG00000046889 associations
First described 2003. Earliest sequence paper UniProt cites for the protein: Joseph R.E. et al, 2003, "Cloning and characterization of P-Rex2: an inositol polyphosphate 4-phosphatase domain containing guanine nucleotide exchange factor". Source.
Sources: HGNC HGNC:22950 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q70Z35 (protein name, function text, keywords and locations (REST API)); CIViC gene PREX2 (1 evidence items, 0 assertions, 1 variants; diseases: Melanoma (GraphQL API, CC0)); Open Targets ENSG00000046889 (association with cancer (MONDO_0004992) 0.73; per-cancer scores at or above 0.5: colorectal cancer 0.55, gastric cancer 0.51, oesophageal cancer 0.52, melanoma 0.60, skin cancer 0.57, breast cancer 0.57 (GraphQL API, CC0)); IntOGen PREX2 (driver in 13 cohorts (Act 10, LoF 3); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Functions as a RAC1 guanine nucleotide exchange factor (GEF), activating Rac proteins by exchanging bound GDP for free GTP. Its activity is synergistically activated by phosphatidylinositol 3,4,5-trisphosphate and the beta gamma subunits of heterotrimeric G protein. Mediates the activation of RAC1 in a PI3K-dependent manner. May be an important mediator of Rac signalling, acting directly downstream of both G protein-coupled receptors and phosphoinositide 3-kinase. Locus 8q13.2 (HGNC).
RNA: low tissue specificity, detected in many normal tissues.
Medium: Adrenal gland, Bronchus, Endometrium, Fallopian tube, Gallbladder, Nasopharynx, Parathyroid gland, Placenta.
RNA cancer enhanced: Kidney Renal Clear Cell Carcinoma 7 pTPM.
Medium only: breast cancer, carcinoid, cervical cancer, endometrial cancer.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"PREX2" OR ABSTRACT:"PREX2" OR TITLE:"phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 2" OR ABSTRACT:"phosphatidylinositol-3,4,5-trisphosphate dependent Rac exchange factor 2" OR TITLE:"Phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 2 protein" OR ABSTRACT:"Phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 2 protein" OR TITLE:"DEP.2" OR ABSTRACT:"DEP.2" OR TITLE:"FLJ12987" OR ABSTRACT:"FLJ12987" OR TITLE:"P-REX2" OR ABSTRACT:"P-REX2") 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 PREX2, not a curated reading list.