GST fusion protein corresponding to 419 residues in the mid-portion of human BAF250a/ARID1a
Application
Anti-BAF250a/ARID1a Antibody, clone PSG3 is an antibody against BAF250a/ARID1a for use in WB, ChIP, IC & IHC.
Research Category Epigenetics & Nuclear Function
Research Sub Category Chromatin Biology
Transcription Factors
Quality
Routinely evaluated by immunoblot.
Target description
~270 kDa
Physical form
100 μg of Protein A purified mouse monoclonal IgG in 100μl of 1X PBS, pH 7.0, 0.1% Azide.
Format: Purified
Protein A purified
Storage and Stability
2 years at -20°C from date of shipment
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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The Journal of biological chemistry, 277(44), 41674-41685 (2002-08-30)
The mammalian SWI/SNF-related complexes facilitate gene transcription by remodeling chromatin using the energy of ATP hydrolysis. The recruitment of these complexes to promoters remains poorly understood and may involve histone modifications or direct interactions with site-specific transcription factors or other
Essential role of ARID2 protein-containing SWI/SNF complex in tissue-specific gene expression.
Molecular and cellular biology, 23(8), 2942-2952 (2003-04-01)
The SWI/SNF family of chromatin-remodeling complexes has been discovered in many species and has been shown to regulate gene expression by assisting transcriptional machinery to gain access to their sites in chromatin. Several complexes of this family have been reported
Genes encoding subunits of SWI/SNF (BAF) chromatin-remodeling complexes are collectively mutated in ∼20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here we demonstrate that
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