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SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 1

This gene encodes a member of the SWI/SNF family of proteins. Members of this family have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: BRG1, Histone, ATPase, CAN, INI1
Papers using SWI antibodies
UBF levels determine the number of active ribosomal RNA genes in mammals
Hannan Ross D. et al., In The Journal of Cell Biology, 1994
... Anti–trimethyl H3K9, anti–dimethyl H3K9, anti–trimethyl H3K4, anti–dimethyl H3K4, anti-H4, and anti-SNF2H antibodies were obtained from Abcam.
Papers on SWI
Regulation of antisense transcription by NuA4 histone acetyltransferase and other chromatin regulatory factors.
Bhaumik et al., Carbondale, United States. In Mol Cell Biol, Feb 2016
Like NuA4 KAT, histone H3 K4/36 methyltransferases and histone H2B ubiquitin conjugase facilitate GAL10 antisense transcription, while the Swi/Snf and SAGA chromatin remodeling/modification factors are dispensable for antisense, but not sense, transcription of GAL10.
A mutation in the Cc.arp9 gene encoding a putative actin-related protein causes defects in fruiting initiation and asexual development in the agaricomycete Coprinopsis cinerea.
Nakahori et al., Kyoto, Japan. In Curr Genet, Feb 2016
Dikaryon formation in agaricomycetes, which is followed by fruiting development, is governed by the mating type loci, A and B. Recently, mutations in the Cc.snf5 gene, which encodes a putative component of the chromatin remodeling complex switch/sucrose non-fermentable (SWI/SNF), were shown to cause defects in A-regulated clamp cell morphogenesis, as well as in fruiting initiation.
Loss of switch/sucrose non-fermenting complex protein expression is associated with dedifferentiation in endometrial carcinomas.
Lee et al., Vancouver, Canada. In Mod Pathol, Feb 2016
We performed targeted sequencing of eight dedifferentiated carcinomas and identified somatic frameshift/nonsense mutations in SMARCA4, a core ATPase of the switch/sucrose non-fermenting (SWI/SNF) complex, in the undifferentiated components of four tumors.
Novel missense mutations in a conserved loop between ERCC6 (CSB) helicase motifs V and VI: Insights into Cockayne syndrome.
Sutton et al., Newcastle upon Tyne, United Kingdom. In Am J Med Genet A, Feb 2016
Indeed, the amino acid sequence of this loop is more highly conserved than the adjacent helicase motifs V and VI, suggesting that this is a crucial structural component of the SWI/SNF family of proteins, to which ERCC6 (CSB) belongs.
FOXD3 Regulates Pluripotent Stem Cell Potential by Simultaneously Initiating and Repressing Enhancer Activity.
Blelloch et al., San Francisco, United States. In Cell Stem Cell, Feb 2016
It recruited the SWI/SNF chromatin remodeling complex ATPase BRG1 to promote nucleosome removal while concurrently inhibiting maximal activation of the same enhancers by recruiting histone deacetylases1/2.
SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2.
Roberts et al., Boston, United States. In Nat Med, Dec 2015
Human cancer genome sequencing has recently revealed that genes that encode subunits of SWI/SNF chromatin remodeling complexes are frequently mutated across a wide variety of cancers, and several subunits of the complex have been shown to have bona fide tumor suppressor activity.
Histone modification and chromatin remodeling during NER.
Reed et al., Cardiff, United Kingdom. In Dna Repair (amst), Dec 2015
Factors influencing this Gcn5-mediated event are considered which include Rad16, a GG-NER specific SWI/SNF factor and the yeast histone variant of H2AZ (Htz1).
Loss of Tumor Suppressor ARID1A Protein Expression Correlates with Poor Prognosis in Patients with Primary Breast Cancer.
Lee et al., Ch'ŏnan, South Korea. In J Breast Cancer, Dec 2015
PURPOSE: Somatic mutations of the chromatin remodeling AT-rich interactive domain 1A (SWI-like) gene (ARID1A) have been identified in many human cancers, including breast cancer.
DNA methylome analysis in Burkitt and follicular lymphomas identifies differentially methylated regions linked to somatic mutation and transcriptional control.
Radlwimmer et al., Leipzig, Germany. In Nat Genet, Nov 2015
Integrative pathway analyses of regions differentially methylated in Burkitt and follicular lymphomas implicated DNA methylation as cooperating with somatic mutation of sphingosine phosphate signaling, as well as the TCF3-ID3 and SWI/SNF complexes, in a large fraction of Burkitt lymphomas.
The helicase-like transcription factor (HLTF) in cancer: loss of function or oncomorphic conversion of a tumor suppressor?
Belayew et al., Mons, Belgium. In Cell Mol Life Sci, Nov 2015
UNASSIGNED: The Helicase-like Transcription Factor (HLTF) belongs to the SWI/SNF family of proteins involved in chromatin remodeling.
The role of TRIB1 in lipid metabolism; from genetics to pathways.
Nakayama et al., Tochigi, Japan. In Biochem Soc Trans, Nov 2015
Furthermore, novel binding partner, Sin3A (Swi-independent 3A)-associated protein, 18 kDa, was identified, which activates microsomal TG transfer protein (MTTP) expression by binding with MTTP regulatory elements in co-ordination with mSin3A and TRIB1.
G1/S Inhibitors and the SWI/SNF Complex Control Cell-Cycle Exit during Muscle Differentiation.
van den Heuvel et al., Utrecht, Netherlands. In Cell, Aug 2015
Combined lineage-specific gene inactivation and genetic screening revealed extensive redundancies between previously identified cell-cycle inhibitors and the SWI/SNF chromatin-remodeling complex.
The long noncoding RNA lncTCF7 promotes self-renewal of human liver cancer stem cells through activation of Wnt signaling.
Fan et al., Beijing, China. In Cell Stem Cell, May 2015
Mechanistically, lncTCF7 recruits the SWI/SNF complex to the promoter of TCF7 to regulate its expression, leading to activation of Wnt signaling.
RNF20-SNF2H Pathway of Chromatin Relaxation in DNA Double-Strand Break Repair.
Komatsu et al., Kyoto, Japan. In Genes (basel), 2014
Moreover, the connection between H2B ubiquitylation and the chromatin remodeling activity of SNF2H has been elucidated.
ADNP: in search for molecular mechanisms and innovative therapeutic strategies for frontotemporal degeneration.
Ivashko-Pachima et al., Tel Aviv-Yafo, Israel. In Front Aging Neurosci, 2014
ADNP is a member of the SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeling complex also associated with alternative splicing, including tau transcript splicing.
Histone H3 lysine 36 methylation targets the Isw1b remodeling complex to chromatin.
Howe et al., Vancouver, Canada. In Mol Cell Biol, 2012
Histone H3 lysine 36 methylation promoted the chromatin interaction of the Isw1b chromatin-remodeling complex in Saccharomyces cerevisiae.
Chromatin remodelers Isw1 and Chd1 maintain chromatin structure during transcription by preventing histone exchange.
Workman et al., Kansas City, United States. In Nat Struct Mol Biol, 2012
Deletion of ISW1 and CHD1 causes widespread intragenic transcription.
Nucleosome remodeler SNF2L suppresses cell proliferation and migration and attenuates Wnt signaling.
Becker et al., München, Germany. In Mol Cell Biol, 2012
The effect of SNF2L depletion on gene expression portray the cell in a state of activated Wnt signaling with increased proliferation and locomotion. High levels of SNF2L expression in normal melanocytes contrast with undetectable expression in melanoma.
Human CCAAT/enhancer-binding protein β interacts with chromatin remodeling complexes of the imitation switch subfamily.
Gutiérrez et al., Concepción, Chile. In Biochemistry, 2012
Functional interaction is characterized between C/EBPbeta and SNF2H/ACF1, involving mainly suppression of C/EBPbeta transactivation activity in the presence of SNF2H and ACF1.
Convergent structural alterations define SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeler as a central tumor suppressive complex in pancreatic cancer.
Pollack et al., Stanford, United States. In Proc Natl Acad Sci U S A, 2012
expression profiling analyses revealed that SWI/SNF likely antagonizes Polycomb repressive complex 2, implicating this as one possible mechanism of tumor suppression
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