Prouduct: We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality SMARCA4 Antibody. Functiong: Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. 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 post-mitotic 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 post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron- specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self- renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Also involved in vitamin D-coupled transcription regulation via its association with the WINAC complex, a chromatin-remodeling complex recruited by vitamin D receptor (VDR), which is required for the ligand-bound VDR-mediated transrepression of the CYP27B1 gene. Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial- mesenchymal transition (EMT) by ZEB1. Summary: 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 histoneDNA contacts by ATPdependent chromatin remodelers, or by histone tail modifications including methylation and acetylation. One of the four classes of ATPdependent histone remodelers is the SWI/SNF complex, the central catalytic subunit of which is Brg1 or the highly related protein hBRM. This SWI/SNF complex contains varying subunits but its association with either Brg1 or hBRM remains constant. SWI/SNF complexes have been shown to regulate gene activation, cell growth, the cell cycle and differentiation. Brg1/hBRM has been shown to regulate transcription through enhancing transcriptional activation of glucocorticoid receptors. Although usually associated with transcriptional activation, Brg1/hBRM have also been found in complexes associated with transcriptional repression including with HDACs, Rb and Tif1β. 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 suppressors and Brg1 is mutated in several tumor cell lines.
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