SMARCC2

SMARCC2 (also known as BAF170) is an invariant core subunit of the mammalian SWI/SNF (BAF) ATP-dependent chromatin-remodeling complex, where it regulates chromatin accessibility and transcriptional programs that control cellular differentiation and development^[1][2]. Mechanistically, SMARCC2 functions within the BAF complex to influence gene expression through chromatin remodeling, and transcriptomic analyses have linked SMARCC2-dependent regulation to genes involved in neuronal development and function^[1]. Consistent with this role, pathogenic SMARCC2 variants cause a neurodevelopmental disorder characterized by intellectual disability, developmental delay, speech impairment, hypotonia, feeding difficulties, and growth abnormalities, establishing SMARCC2 as a critical regulator of nervous system development^[1][3][4]. Disease-associated variants are enriched in conserved DNA-interacting domains, including the SANT and SWIRM regions, and are associated with more severe clinical phenotypes^[1]. In experimental cancer models, SMARCC2 has also been reported to suppress glioblastoma cell proliferation through chromatin-remodeling-dependent regulation of DKK1, further supporting its role as a transcriptional regulator with context-dependent effects on cell fate and growth control^[5]. Compared with related SWI/SNF subunits, SMARCC2 represents a core structural component that is consistently incorporated into BAF complexes and has been directly linked to a distinct SMARCC2-associated neurodevelopmental syndrome within the broader spectrum of BAF-complex disorders^[1][3]. No selective SMARCC2 agonists or inhibitors were identified in the cited literature, and current research primarily uses genetic and disease-associated variant models to investigate SMARCC2 function^[1][3][4].