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Validated All-in-One™ qPCR Primer for SMARCA4(NM_001128849.3) Search again
Product ID:
HQP161053
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BAF190, BAF190A, BRG1, CSS4, MRD16, RTPS2, SNF2, SNF2-beta, SNF2L4, SNF2LB, SWI2, hSNF2b
Gene Description:
SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4
Target Gene Accession:
NM_001128849.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- majority of tumor lines with germ line defects in BRG-1 were sensitive to RB-mediated cell cycle arrest
- generation and interconversion of multiple distinct nucleosomal states as a mechanism for catalyzing chromatin fluidity
- Functional involvement of the Brahma/SWI2-related gene 1 protein in cytochrome P4501A1 transcription mediated by the aryl hydrocarbon receptor complex
- BRG1 enzymes generate localized changes in DNA topology that drive formation of multiple, remodeled nucleosomal states.
- SWI/SNF complex interacts with tumor suppressor p53 and is necessary for the activation of p53-mediated transcription
- Interferon-gamma-induced chromatin remodeling at the CIITA locus is BRG1 dependent
- Data show that prohibitin recruits Brg-1/Brm to E2F-responsive promoters, and that this recruitment is required for the repression of E2F-mediated transcription by prohibitin.
- CIITA requires the ATPase subunit of an hSWI/SNF complex, brahma-related gene 1 (BRG-1), to activate transcription.
- REST repression of neuronal genes requires components of the hSWI.SNF complex
- BRG1 interacts with signal transducer and activator of transcription 2 (STAT2) - a transcription factor that regulates gene expression mediated by interferon-alpha.
- suggestion of an entirely novel function for BRG1 in modulating HP1alpha-containing heterochromatic structures
- human adrenal carcinoma cells can spontaneously transition between two subtypes by switching expression of BRG1 and Brm at the post-transcriptional level
- This report provides supportive evidence that BRG1 and BRM act as tumor suppressor proteins and implicates a role for their loss in the development of non-small cell lung cancers.
- The Brg1 subunit of SWI/SNF was shown to interact directly with RTA.
- BRG1 and BRM complexes may direct distinct cellular processes by recruitment to specific promoters through protein-protein interactions that are unique to each ATPase.
- Some mutations are found in prostate cancer, such as germline mutation, SNPs, but common mutations are excluded.
- the amino-terminal and carboxyl-terminal regions of Mi-2 beta have distinct transcriptional activities and bind to BRG1 and the RET finger protein, forming a multiprotein supercomplex involved in transcriptional regulation.
- BRG1 has a role in promoting cell proliferation by interacting with EVI1, which blocks its repression on E2F1 activity
- in human cells, SWI/SNF enzyme complex formation and the expression of many BRG1-dependent genes are independent of INI1.
- BRG1 is required for growth suppression by estrogen antagonists.
- BRM and BRG1 participate in two distinct chromosome remodeling complexes that are functionally complementary in non-small cell lung cancer
- Sta3 regulates chromatin remodeling and transcription elongation through its interaction with BRG1 and cdk9
- Somatic point mutations of the BRG1 gene are present in a small subset of lung tumors
- Somatic point mutations of the SMARCA4 gene are present in a small subset of lung tumors.
- Brg-1 plays a role in regulating the recruitment of Sp1, Sp3, AP-2, and polymerase II to the MMP-2 promoter.
- Brahma and Brahma/SWI2-related gene 1 have roles in hypoxic induction of the erythropoietin gene
- transcriptional activation of ZNF185 and CYP3A4 is mediated by direct association of BRG1 with their promoters and a decreased level of ZNF185 is a common feature of lung tumours
- BRG1 loss in pancreatic tumor cell lines induces an altered cell morphology and disruption in the organization of the actin cytoskeleton.
- Brg1 co-localized with NF1/CTF & RNAP II in HeLa cells. It is isolated together with NF1/CTF & RNAP II in ConA-stimulated, but not resting, T lymphocytes. BAF complexes interact with NF1/CTF & RNAP II, dependent on activation of gene transcription.
- BRG1 has an apical role in cytokine-induced promoter assembly, acting upstream of STAT complexes at multiple IFN target loci.
- Here antibody phage display technology is employed for development of an antibody specifically targeting BRG1.
- TG repeats are assembled in a positioned nucleosome in the silent colony-stimulating factor 1 (CSF1) promoter and that activation by BRG1 disrupts this nucleosome and results in Z-DNA formation.
- The SWI/SNF protein Brg1 is associated with a DNA-binding complex containing TAL1/SCL, E47, GATA-1, LMO2 and Ldb1 complex. Both the E box and GATA DNA-binding sites in these elements are required for Brg1 recruitment.
- These results thus demonstrate that BRG1, through the facilitation of Z-DNA formation and subsequent recruitment of RNA polymerase II, is critical in Nrf2-mediated inducible expression of HO-1.
- BRG1 facilitates REST repression by increasing the interaction between REST and chromatin
- Brg1 and HDAC2 have roles in GR trans-repression of the pituitary POMC gene and misexpression in Cushing disease
- Aberrant expression of BRG1 and BRM genes is associated with development and progression of prostate cancers and increased BRG1 expression may promote tumor growth and invasion.
- primary micromolar interaction is through the AT-hook motif
- BRG1 is constitutively present at IL-6-responsive promoters and is required for STAT3 recruitment, downstream histone modifications, and IL-6-induced chromatin remodeling.
- Study reports the solution structure of the Brg1 bromodomain determined by using NMR perturbation studies; it was shown that the Brg1 bromodomain binds acetyllysine in the context of histone tails, with no comparable affinity for unacetylated peptides
- IGF-1 induces phosphorylation and an increase of the AP1 complex, which is phosphorylated and binds to the pS2/TFF1 promoter, allowing recruitment of the chromatin remodeling factor Brg1 followed by binding of ERalpha via its interaction with c-Jun
- nuclear actin regulates CSF1 gene transcription in a BRG1 independent manner.
- Both PCAF and BRG1 are also involved in the activation of the myogenin gene in rhabdomyosarcoma
- By modeling the acetylated-lysine peptide into the BRG1 bromodomain structure, we were able to explain the weak binding of acetylated-lysine peptides to this bromodomain
- Brg1/Brm containing SWI/SNF complexes play a critical role in regulating expression of SRF/MRTFA-dependent smooth muscle-specific genes but not SRF/MRTFA-dependent early response genes.
- occurrence of an unusual TG 3' splice site in intron 29
- 30 bp DNA element required for mediating the activation of CRYAB by brahma-related gene 1 (BRG1).
- The onset of chromatin remodelling corresponds with the binding of activated STAT1 and the chromatin remodelling enzyme BRG1 at specific sites within the MHC, and is followed by RNA-polymerase recruitment and histone hyperacetylation.
- p53 activity is differentially regulated by Brm- and Brg1-containing SWI/SNF chromatin remodeling complexes
- Participation of BRG1 in TGFbeta action suggests a widespread yet differential involvement of BRG1 SWI/SNF remodeler in the transcriptional response of many genes to this cytokine.
- at the TERT gene locus in human tumour cells containing a functional SWI/SNF complex, Brm, and possibly BRG1, in concert with p54(nrb), would initiate efficient transcription and could be involved in the subsequent splicing of TERT transcripts
- These studies suggest BAF250a is a necessary facilitator of BRG1-mediated chromatin remodeling required for SWI/SNF-dependent transcriptional activation.
- These studies suggest the endogenous cyclin D1 promoter BRG-1 binding site functions as a molecular scaffold in the context of local chromatin upon which coactivators and corepressors are recruited to regulate cyclin D1.
- coordination of ERK signaling and NF-kappaB and Brg-1 activation are indispensable to regulation of Axl-dependent MMP-9 gene transcription
- alterations at BRG1 always occurred in the absence of MYC amplification, suggesting a common role in lung cancer development. In conclusion, our data strongly support that BRG1 is a bona fide tumor suppressor and a major factor in lung tumorigenesis
- BRG1 regulates CIITA through many interdependent remote enhancers, not through the promoter alone.
- Translational view of human pathologic physiology involving SWI/SNF2 superfamily in human hereditary diseases an cancers. [REVIEW]
- SMARCA4 expression was statistically significantly associated with prednisolone sensitivity. Prednisolone resistance was higher in SMARCA4 shRNA-transfected Jurkat cells than in control shRNA-transfected cells