SMARCE1/BAF57 (E6H5J) Rabbit mAb

Product Usage Information

Storage

Specificity / Sensitivity

Species Reactivity:

Human, Mouse, Rat, Monkey

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu34 of human SMARCE1/BAF57 protein.

Background

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).

SMARCE1/BAF57 is a core component of the SWI/SNF complex and directly binds other transcription factors and co-factors, including androgen receptor and estrogen receptor. Binding of SMARCE1/BAF57 can directly affect the transcriptional activity of nuclear receptors, influencing the expression of target genes (9-12). Mutations of SMARCE1/BAF57 have been described in Coffin-Siris syndrome (13). SMARCE1/BAF57 has also been shown to contribute to invasion of some early-stage breast lesions by forming a complex with ILF3, an event independent of the SWI/SNF complex (14).