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WAS (Actin nucleation-promoting factor WAS) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Skin cancer, Medulloblastoma and Melanoma.
Effector protein for Rho-type GTPases that regulates actin filament reorganisation via its interaction with the Arp2/3 complex. Important for efficient actin polymerisation. Possible regulator of lymphocyte and platelet function.
Open Targets scores its association with cancer at 0.61 (direct and indirect evidence; datatypes literature 0.79, animal model 0.63, genetic association 0.00, somatic mutation 0.96). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Medulloblastoma.
In plain words · WAS (Actin nucleation-promoting factor WAS) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Skin cancer, Medulloblastoma and Melanoma.
WAS (Actin nucleation-promoting factor WAS) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Skin cancer, Medulloblastoma and Melanoma.
Effector protein for Rho-type GTPases that regulates actin filament reorganisation via its interaction with the Arp2/3 complex. Important for efficient actin polymerisation.
No product in this corpus aims at WAS yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
First described 1994. Earliest sequence paper UniProt cites for the protein: Derry J.M.J. et al, Cell, 1994, "Isolation of a novel gene mutated in Wiskott-Aldrich syndrome". Source.
Sources: HGNC HGNC:12731 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P42768 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000015285 (association with cancer (MONDO_0004992) 0.61; per-cancer scores at or above 0.5: melanoma 0.52, skin cancer 0.55 (GraphQL API, CC0)); IntOGen WAS (driver in 1 cohort (Act 1, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Effector protein for Rho-type GTPases that regulates actin filament reorganisation via its interaction with the Arp2/3 complex. Important for efficient actin polymerisation. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganisation and the formation of actin pedestals upon infection by pathogenic bacteria. In addition to its role in the cytoplasmic cytoskeleton, also promotes actin polymerisation in the nucleus, thereby regulating gene transcription and repair of damaged DNA. Promotes homologous recombination (HR) repair in response to DNA damage by promoting nuclear actin polymerisation, leading to drive motility of double-strand breaks (DSBs). Location: Cytoplasm, cytoskeleton; Nucleus (UniProt). Locus Xp11.23 (HGNC).
Query for this target: (TITLE:"WAS" OR ABSTRACT:"WAS" OR TITLE:"WASP actin nucleation promoting factor" OR ABSTRACT:"WASP actin nucleation promoting factor" OR TITLE:"Actin nucleation-promoting factor WAS" OR ABSTRACT:"Actin nucleation-promoting factor WAS" OR TITLE:"WASPA" OR ABSTRACT:"WASPA" OR TITLE:"IMD2" OR ABSTRACT:"IMD2") 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 WAS, not a curated reading list.
Shares Medulloblastoma, Skin cancer (all types), IntOGen, Open Targets Platform.
Shares Medulloblastoma, Skin cancer (all types), IntOGen, Melanoma.
Shares Medulloblastoma, IntOGen, Open Targets Platform.
Shares Medulloblastoma, IntOGen.
Shares Medulloblastoma, IntOGen.
Shares Medulloblastoma, IntOGen.
Shares Medulloblastoma, Skin cancer (all types), IntOGen, Open Targets Platform.
Shares Medulloblastoma, Open Targets Platform.