a core component of multiprotein chromatin-remodeling complexes that regulate transcriptional activation and repression of select genes by ATP-dependent chromatin remodeling (alteration of DNA-nucleosome topology). Is a component of remodeling complexes including Swi/Snf-A (BAF), Swi/Snf-B (PBAF), Brm, WINAC and Brg1. Each complex contains a catalytic subunit (either SMARCA4 or SMARCA2), and at least SMARCE1, BAF53A or BAF53B, SMARCC2 and SMARCB1. SWI/SNF complexes are required for mammalian development and are mutated in ~20% of all human primary tumors. Belongs to the neural progenitor-specific and the neuron-specific chromatin remodeling complexes (npBAF and nBAF, respectively). Transcriptional coactivator of nuclear hormone receptors. Colocalizes with ZEB1 in stroma of normal colon as well as in de-differentiated epithelial cells at the invasion front of colorectal carcinomas. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1. Can bind BRCA1, as well as regulate the expression of the tumorigenic protein CD44. SMARCA4, in consort with ZEB1, represses the transcription of E-cadherin and promotes the epithelial-to-mesenchymal transition (EMT). Required for stem cell maintenance in the mouse intestinal epithelium. Its loss inhibits aberrant Wnt-signaling and prevents tumorigenesis in the mouse small intestine. SMARCA4 mutations are the cause of a familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood. Belongs to the SNF2/RAD54 helicase family. The human protein includes 5 isoforms produced by alternative splicing. Note: This description may include information from UniProtKB.