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SMARCA2 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Salivary gland cancers.
ATPase involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically.
CIViC holds 2 clinical evidence items and 0 assertions across 2 variants. IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Salivary Carcinoma.
In plain words · SMARCA2 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Salivary gland cancers.
SMARCA2 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Salivary gland cancers.
ATPase involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology).
No product in this corpus aims at SMARCA2 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); 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 SMARCA2: RNA low tissue specificity; high antibody staining in 15 normal tissues; highest cancer staining head and neck cancer (2 of 4 high). Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Salivary gland cancers); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P51531; CIViC gene SMARCA2; IntOGen SMARCA2; Human Protein Atlas SMARCA2 tissue; Open Targets ENSG00000080503 associations
First described 1993. Earliest sequence paper UniProt cites for the protein: Muchardt et al, EMBO J, 1993, "A human homologue of Saccharomyces cerevisiae SNF2/SWI2 and Drosophila brm genes potentiates transcriptional activation by the glucocorticoid receptor". Source.
Sources: HGNC HGNC:11098 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P51531 (protein name, function text, keywords and locations (REST API)); CIViC gene SMARCA2 (2 evidence items, 0 assertions, 2 variants; diseases: (GraphQL API, CC0)); IntOGen SMARCA2 (driver in 1 cohort (Act 1, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
ATPase involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. Location: Nucleus (UniProt). Locus 9p24.3 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
Medium: Adipose tissue, Appendix, Bronchus, Cervix, Colon, Duodenum, Endometrium, Esophagus.
Medium only: carcinoid, colorectal cancer, endometrial cancer, liver 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:"SMARCA2" OR ABSTRACT:"SMARCA2" OR TITLE:"SWI/SNF related BAF chromatin remodeling complex subunit ATPase 2" OR ABSTRACT:"SWI/SNF related BAF chromatin remodeling complex subunit ATPase 2" OR TITLE:"SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2" OR ABSTRACT:"SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2" OR TITLE:"BAF190" OR ABSTRACT:"BAF190" OR TITLE:"hSNF2a" OR ABSTRACT:"hSNF2a" OR TITLE:"hBRM" OR ABSTRACT:"hBRM") 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 SMARCA2, not a curated reading list.
Shares Salivary gland cancers, IntOGen.
Shares Salivary gland cancers, IntOGen.
Shares Salivary gland cancers, CIViC, IntOGen.
Shares Salivary gland cancers, CIViC, IntOGen.
Shares Salivary gland cancers, CIViC, IntOGen.
Shares Salivary gland cancers, IntOGen.
Shares SWI/SNF chromatin remodelling, CIViC, IntOGen.
Shares Salivary gland cancers, IntOGen.