Specifications
Species Reactivity
Mouse; Rat; Human
Immunogen
Mouse BRM/ SMARCA2 fusion protein derived from within residues 48-214 of the corresponding human sequence.(Note: Please see Muchardt C et al. EMBO J 15:3394-402 (1996) for further details).
Applications
Application Notes
WB: 0.95 μg/ml;
Target
Alternative Names
SMARCA2; SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2; BRM; SNF2; SWI2; hBRM; NCBRS; Sth1p; BAF190; SNF2L2
Product Background
Antigen Description
A transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. SMARCA2 / BRM belongs to the SNF2/RAD54 helicase family, is a homologue of the Saccharomyces cerevisiae SWI2/SNF2 and Drosophila brahma proteins. It contains a methyl lysine containing bromo domain and an HSA domain. The yeast protein SNF2, also known as SWI2, is involved in transcriptional activation of numerous genes. It contains a domain that is highly conserved among several known helicases and is required for transcriptional activity. SNF2/SWI2 is highly homologous to the Drosophila protein brahma (brm). Muchardt and Yaniv (1993) demonstrated a homolog of SNF2/SWI2 and brm in human cells. This human protein is 56% identical and 72% homologous to Drosophila brm. See also SNF2L1 (300012). Muchardt et al. (1996) found that the human homolog of brm and another protein, BRG1 (603254), are phosphorylated during mitosis. Although the 2 proteins show nuclear localization during interphase, they are excluded from the condensed chromosomes during mitosis. They found that the level of BRM, but not BRG1, was strongly reduced during mitosis. Phosphorylation of hbrm and BRG1 did not disrupt their association with SNF5 but correlated with a decreased affinity for the nuclear structure in early M phase. The authors suggested that chromosomal exclusion of the human SNF/SWI complex at the G2-M transition is part of the mechanism leading to transcriptional arrest during mitosis.
Pathway
C-MYB transcription factor network; RB in Cancer;
Citations
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