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Mouse Monoclonal Anti-BRG1 antibody (STJ99234)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, ELISA
Recommended dilution: WB 1:500-2000; ELISA 1:10000-20000
Recommended protocols: check protocols
Click or hover above images to see image description for Anti-BRG1 antibody.
Check alternative names for the antibodyExpand
|ATP dependent helicase SMARCA4 antibody|SWI2 antibody|Transcription activator BRG1 antibody|Anti-BRG1 antibody [EPNCIR111A] (ab110641)
SCBT cat No: sc-17796|sc-374197|sc-10768|sc-8749|
|Catalogue No.|| |
Anti-BRG1 antibody detects endogenous levels of BRG1 and does not cross-react with related proteins.
Purified recombinant human BRG1 protein fragments expressed in E.coli.
|Recommended dilution|| |
WB 1:500-2000; ELISA 1:10000-20000
|Molecular weight|| |
Anti-BRG1 antibody was tube-contained in liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Anti-BRG1 antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
ATP dependent helicase SMARCA4 antibody, SWI2 antibody, Transcription activator BRG1 antibody
|Database links|| |
|Protein function|| |
Transcriptional coactivator cooperating with nuclear hormone receptors to potentiate transcriptional activation. Component of the CREST-BRG1 complex, a multiprotein complex that regulates promoter activation by orchestrating a calcium-dependent release of a repressor complex and a recruitment of an activator complex. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, which leads to release of the repressor complex. At the same time, there is increased recruitment of CREBBP to the promoter by a CREST-dependent mechanism, which leads to transcriptional activation. The CREST-BRG1 complex also binds to the NR2B promoter, and activity-dependent induction of NR2B expression involves a release of HDAC1 and recruitment of CREBBP. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth. SMARCA4/BAF190A may promote neural stem cell self-renewal/proliferation by enhancing Notch-dependent proliferative signals, while concurrently making the neural stem cell insensitive to SHH-dependent differentiating cues (By similarity). Acts as a corepressor of ZEB1 to regulate E-cadherin transcription and is required for induction of epithelial-mesenchymal transition (EMT) by ZEB1. .
|Protein tissue specificity|| |
Colocalizes with ZEB1 in E-cadherin-negative cells from established lines, and stroma of normal colon as well as in de-differentiated epithelial cells at the invasion front of colorectal carcinomas (at protein level). .
|Involvement in disease|| |
Rhabdoid tumor predisposition syndrome 2 (RTPS2) [MIM:613325]: A familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Coffin-Siris syndrome 4 (CSS4) [MIM:614609]: A form of Coffin-Siris syndrome, a congenital multiple malformation syndrome with broad phenotypic and genetic variability. Cardinal features are intellectual disability, coarse facial features, hypertrichosis, and hypoplastic or absent fifth digit nails or phalanges. Additional features include malformations of the cardiac, gastrointestinal, genitourinary, and/or central nervous systems. Sucking/feeding difficulties, poor growth, ophthalmologic abnormalities, hearing impairment, and spinal anomalies are common findings. Both autosomal dominant and autosomal recessive inheritance patterns have been reported. . Note=The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the SNF2/RAD54 helicase family. ; Contains 1 bromo domain. ; Contains 1 helicase ATP-binding domain. ; Contains 1 helicase C-terminal domain. ; Contains 1 HSA domain. ; Contains 1 QLQ domain.
|Protein cellular localization|| |
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St John’s Laboratory Ltd.
|Product type|| |
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