ACTL6/BAF53 Antibody #43910

The modulation of chromatin structure is an essential component in the regulation of transcriptional activation and repression. Modifications can be made by at least two evolutionarily conserved strategies, through the disruption of histone-DNA contacts by ATP-dependent chromatin remodelers, or by histone tail modifications including methylation and acetylation. One of the four classes of ATP-dependent histone remodelers is the SWI/SNF complex, the central catalytic subunit of which is Brg1 or the highly related protein hBRM (1). This SWI/SNF complex contains varying subunits but its association with either Brg1 or hBRM remains constant (1). SWI/SNF complexes have been shown to regulate gene activation, cell growth, the cell cycle, and differentiation (1). Brg1/hBRM have been shown to regulate transcription through enhancing transcriptional activation of glucocorticoid receptors (2). Although usually associated with transcriptional activation, Brg1/hBRM have also been found in complexes associated with transcriptional repression, including HDACs, Rb, and Tif1β (3-5). Brg1/hBRM plays a vital role in the regulation of gene transcription during early mammalian embryogenesis. In addition, Brg1/hBRM also plays a role as a tumor suppressor and Brg1 is mutated in several tumor cell lines (6-8).

ACTL6/BAF53 proteins are highly homologous, actin-related proteins found in the SWI/SNF complex (9). In addition to the canonical SWI/SNF complex, ACT6LA/BAF53A is also a member of the embryonic SWI/SNF complex, known as esBAF, which plays a role in pluripotency and development (10-12). ACTL6B/BAF53B is a member of the neural-specific SWI/SNF complex that facilitates binding to target genes and is involved in memory and synaptic plasticity (13-15). ACTL6/BAF53 has been shown to interact with c-Myc, where it functions as a cofactor and is important in the transformation process (16). Further studies have shown ACTL6/BAF53 is associated with EMT and transformation in various cancers (17,18).