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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 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
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
a HDAC3-SMARCA4-miR-27a-PAX3:FOXO1 circuit is a driver of chemoresistant alveolar rhabdomyosarcoma
Low BRG1 expression is associated with Cell Migration and Invasion in Colorectal Cancer.
Case Reports: BRG1 deficiency reflects underlying mutation in SMARCA4 gene in some but not all cases, suggesting that additional mechanisms may be causing BRG1 silencing.
The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.
BRG1 and INI1 loss were present in 14 of 26 cases of DDC/UDC, including 12 BRG1-deficient cases and 2 INI1-deficient cases, respectively
data unveil a novel epigenetic mechanism whereby a BRG1-centered complex mediates transcriptional activation of CSF1 by Ang II in vascular endothelial cells.
disruption of enhancer accessibility represents a key source of altered function in disorders with SMARCA4 mutations in a wide variety of tissues
Downregulation of SMARCAL1 and BRG1 results in downregulation of ATM and ATR and therefore, mitotic abnormalities
Study reports that BRG1 interacts with KDM3A to activate NOX transcription in endothelial cells. Endothelial-derived ROS, produced by elevated NOX expression, may contribute to cardiac ischemia-reperfusion injury.
Results found that Brg1 deficiency in hepatocytes protects liver injury and prolongs survival in the Acetaminophen (APAP) overdose model likely through interacting with the nuclear receptor HNF4 to promote Cyp3a11 transcription. These finding suggest that Brg1 might play an essential role mediating APAP induced liver injury in vivo.
In the Chinese Han study population, the mutant GT and TT genotypes and minor T allele of rs1122608 were positively correlated with the risk of acute myocardial infarction.
SMARCA4-deficient cells have a blunted transcriptional response to energy stress creating a therapeutically exploitable synthetic lethal interaction.
functional roles of the Q and I motifs in the human chromatin-remodeling enzyme BRG1
These findings demonstrate that BRG1 establishes specialized chromatin environments that define multiple classes of glucocorticoid receptor binding sites. This in turn predicts that glucocorticoid receptor and other transcriptional activators function via multiple distinct chromatin-based mechanisms to modulate the transcriptional response.
One of the newly validated CTCF interactors is BRG1, the major ATPase subunit of the chromatin remodeling complex SWI/SNF, establishing a relationship between two master regulators of genome organization.
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.
Together, Brg1 and Aire fine-tune the expression of tissue-specific genes at levels that prevent toxicity yet promote immune tolerance
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.
HDAC9, in cooperation with BRG1 and MALAT1, mediates a critical epigenetic pathway responsible for vascular smooth muscle cells dysfunction.
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.
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