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Human Polyclonal SMARCA4 Primary Antibody for ChIP, ICC - ABIN4285245
Miyamoto, Pasque, Jullien, Gurdon: Nuclear actin polymerization is required for transcriptional reprogramming of Oct4 by oocytes. in Genes & development 2011
Show all 4 Pubmed References
Human Polyclonal SMARCA4 Primary Antibody for WB - ABIN686122
Chen, Han, Wei, Zhang, Shi, Duan, Li, Zhou, Pu, Zhang, Kang: SNORD76, a box C/D snoRNA, acts as a tumor suppressor in glioblastoma. in Scientific reports 2015
Human Monoclonal SMARCA4 Primary Antibody for ICC, IF - ABIN2668499
Ohkawa, Harada, Nakamura, Yoshimura, Tachibana: Production of a rat monoclonal antibody against Brg1. in Hybridoma (2005) 2009
Human Monoclonal SMARCA4 Primary Antibody for ICC, IF - ABIN2668498
de la Serna, Ohkawa, Higashi, Dutta, Osias, Kommajosyula, Tachibana, Imbalzano: The microphthalmia-associated transcription factor requires SWI/SNF enzymes to activate melanocyte-specific genes. in The Journal of biological chemistry 2006
LncFZD6 interacts and recruits BRG1 to FZD6 promoter to initiate transcription in liver cancer cells.
the results of this study suggest that high BRG1 expression was associated with high SNAI expression and was significantly correlated with poor prognosis in colorectal cancer
Mechanism of TRbeta repression of oncogenic gene expression: TRbeta recruitment of BRG1 induces chromatin compaction and diminishes RUNX2 expression. Therefore, BRG1-mediated chromatin remodeling may be obligatory for TRbeta transcriptional repression and tumor suppressor function in thyroid tumorigenesis.
Seven deleterious mutations in the HSA domain of BRG1 were identified based on the functional screening of cancer-associated mutations in the COSMIC database.
Brg1 is a bona fide ubiquitin substrate of SCF(FBW7). In keeping with a tumor suppressive role of FBW7 in human gastric cancer, we find an inverse correlation between FBW7 and Brg1 expression in human gastric cancer clinical samples. Mechanistically, we find that stabilization of Brg1 in gastric cancer cells suppresses E-cadherin expression, subsequently promoting gastric cancer metastasis.
The sensitivity of SWI/SNF-deficient cells to DNA damage induced by UV irradiation and cisplatin treatment depends on GTF2H1 levels.
The Brg1 promotes liver fibrosis by activating HSCs and may represent a potential target for anti-fibrotic therapies.
association of the BRG1/hBRM bromodomain with nucleosomes plays a regulatory rather than targeting role
BRG1, the essential ATPase subunit of the SWI/SNF chromatin-remodelling complex, is required for expression of Wilms' tumour 1 (Wt1), fetal epicardium-derived cell activation and subsequent differentiation into coronary smooth muscle, and restoration of Wt1 activity upon myocardial infarction.
High expression of SMARCA4 is associated with aggressive tumors.
This study showed that AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring SMARCA4/BRG1-inactivating mutations.
describe the approaches and methods used to identify SMARCA4 mutations, which drive development of the rare ovarian cancer, small cell carcinoma of the ovary, hypercalcemic type (SCCOHT), and point to the broader relevance of this paradigm for future research in rare cancers.
Here, the authors show that C-terminally truncated forms of both SMARCA2 and SMARCA4, produced by caspase-mediated cleavage, accumulate in cells infected with different RNA or DNA viruses. The levels of truncated SMARCA2 or SMARCA4 strongly correlate with the degree of cell damage and death observed after virus infection.
at genes where BRG1 and BRM antagonize one another we observe a nearly complete rescue of gene expression changes in the combined BRG/BRM double knockdown
Depletion of Brg1 improves the integrity of airway epithelium in asthma by regulating E-cadherin expression in lung epithelial cells. Knockdown of Brg1 increased the cell proliferation and migration by human bronchial epithelial 16HBE cells.
High BRG1 expression is associated with leukemia and lymphoma.
HDAC9, in cooperation with BRG1 and MALAT1, mediates a critical epigenetic pathway responsible for vascular smooth muscle cells dysfunction.
SMARCA4-deficient thoracic sarcomas constitute a unique, highly lethal entity that requires full recognition and differentiation from other epithelioid malignancies involving the thoracic region.
The outcome following a diagnosis of any of these tumors is often poor, and the value of surveillance is unknown. International efforts to determine surveillance protocols are underway, and preliminary recommendations are made for carriers of SMARCB1 and SMARCA4 mutations.
Study identified DNA methylation (DNAm) site, cg07786668 in ZFHX3 that is independently and significantly associated with myocardial infarction (MI) along with cg17218495 in SMARCA4. These results suggest that the development of MI might be influenced by changes in DNAm at these sites via a pathway that differs from that affected by cardiovascular disease-associated SNPs in these genes.
The study highlights a potential role of Brg1 in regulating cerebral ischemia/reperfusion injury in vivo.
BRG1 knockdown in the vascular endothelium suppressed neutrophil infiltration and down-regulated the levels of inflammation mediators in cardiac ischemia-reperfusion injury.
An increase in Brg1 and a decrease in the PI3K/Akt/mTOR pathway activity were detected in asthmatic mice, but not in control mice. When Brg1 was knocked out, the asthma severity was ameliorated and the PI3K/Akt/mTOR pathway was activated.
The results suggest that BRG1 and STAT3 coordinately regulate gene clustering and up-regulate Gfap and Osmr transcription in astrocytes.
Study using conditional Brg1 knockout mice showed that Brg1 interacted with and was recruited by SREBP1c to the promoters of SREBP target genes and optimized the chromatin structure to facilitate SREBP1c binding. Therefore, a previously unrecognized role for Brg1 in hepatic lipid metabolism by portraying Brg1 as an essential epigenetic co-factor for SREBP1c was identified.
Brg1 expression is up-regulated by pro-non-alcoholic steatohepatitis stimuli in vitro and in vivo. Hepatocyte-specific Brg1 deletion alleviates non-alcoholic steatohepatitis in mice.
results suggest that miR-144-3p contributes to OGD/R-induced neuronal injury in vitro through negatively regulating Brg1/Nrf2/ARE signaling.
Data found that Brg1 played important roles in hair cells (HCs) intrinsic polarity maintenance, anchoring outer hair cells base to the Deiter's cells and scar formation of the auditory epithelium. These results demonstrated a requirement for Brg1 activity in development and suggested a role for Brg1 in the proper cellular structure formation of HCs.
The results demonstrated that restoration of Brg1 during reperfusion could enhance Nrf2-mediated inducible expression of HO-1 during hepatic ischemia-reperfusion injury to effectively increase antioxidant ability to combat against hepatocytes damage.
BAF (BRG1/BRM-Associated Factor) chromatin-remodeling complex may adaptively respond to ethanol exposure to protect against a complete loss of miR-9-2 in fetal neural stem cells.
Chromatin accessibility at OCT4-bound sites requires the chromatin remodeller BRG1, which is recruited to these sites by OCT4 to support additional transcription factor binding and expression of the pluripotency-associated transcriptome.
Data (including data from studies using knockout mice) suggest that Brg1 is phosphorylated by casein kinase 2 (Ck2; Ck2alpha1 and Ck2alpha-prime are catalytic subunits) in proliferating skeletal myoblasts; Brg1 is catalytic subunit of SWI/SNF chromatin-remodeling enzymes; Ck2-mediated phosphorylation of Brg1 appears to regulate myoblast proliferation. (Brg1 = Brahma-related gene 1 protein)
BRG1 is a SOX10 co-activator, required to establish the melanocyte lineage and promote expression of genes important for melanocyte function.
n keratinocytes, the promoter-enhancer anchoring regions in the gene-rich transcriptionally active TADs are enriched for the binding of chromatin architectural proteins CTCF, Rad21 and chromatin remodeler Brg1. In contrast to gene-rich TADs, gene-poor TADs show preferential spatial contacts with each other, do not contain active enhancers and show decreased binding of CTCF, Rad21 and Brg1 in keratinocytes
Data demonstrate that Brg1 plays an essential role in development and homeostasis, including morphogenesis, stem cell differentiation and cell survival in the duodenum.
Point mutations in SMARCA4 (also known as BRG1) mapping to the ATPase domain cause loss of direct binding between BAF and PRC1.
BRG1 promotes transcription of endothelial Mrtfa and Mrtfb, which elevates expression of SRF and SRF target genes that establish embryonic capillary integrity.
RB is necessary for the recruitment of the BRG1 ATPase to DNA double-strand breaks, which stimulates DNA end resection and homologous recombination
Cdx members interact with the SWI-SNF complex and make direct contact with Brg1, a catalytic member of SWI-SNF. Both Cdx2 and Brg1 co-occupy a number of Cdx target genes, and both factors are necessary for transcriptional regulation of such targets. Finally, Cdx2 and Brg1 occupancy occurs coincident with chromatin remodeling at some of these loci.
The protein encoded by this gene is a member of the SWI/SNF family of proteins and is similar to the brahma protein of Drosophila. 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. The encoded protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin. In addition, this protein can bind BRCA1, as well as regulate the expression of the tumorigenic protein CD44. Mutations in this gene cause rhabdoid tumor predisposition syndrome type 2. Multiple transcript variants encoding different isoforms have been found for this gene.
SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4
, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin a4
, transcription activator BRG1-like
, ATP-dependent helicase SMARCA4
, BRG1-associated factor 190A
, BRM/SWI2-related gene 1
, SNF2-like 4
, brahma protein-like 1
, global transcription activator homologous sequence
, homeotic gene regulator
, mitotic growth and transcription activator
, nuclear protein GRB1
, protein BRG-1
, protein brahma homolog 1
, sucrose nonfermenting-like 4
, transcription activator BRG1
, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 4
, SWI/SNF related transcriptional activator
, WI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4