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The protein encoded by SMARCB1 is part of a complex that relieves repressive chromatin structures, allowing the transcriptional machinery to access its targets more effectively. Additionally we are shipping SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily B, Member 1 Proteins (9) and SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily B, Member 1 Kits (4) and many more products for this protein.
Showing 10 out of 133 products:
Human Monoclonal SMARCB1 Primary Antibody for IF, WB - ABIN968741
Bruder, Dumanski, Kedra: The mouse ortholog of the human SMARCB1 gene encodes two splice forms. in Biochemical and biophysical research communications 1999
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Human Monoclonal SMARCB1 Primary Antibody for IF, WB - ABIN968742
Guidi, Sands, Zambrowicz, Turner, Demers, Webster, Smith, Imbalzano, Jones: Disruption of Ini1 leads to peri-implantation lethality and tumorigenesis in mice. in Molecular and cellular biology 2001
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Human Polyclonal SMARCB1 Primary Antibody for ICC, IF - ABIN252863
Young, Jacks: Tissue-specific p19Arf regulation dictates the response to oncogenic K-ras. in Proceedings of the National Academy of Sciences of the United States of America 2010
Human Monoclonal SMARCB1 Primary Antibody for WB - ABIN393962
Wu, Ho, Lin, Lin: Rhabdoid papillary meningioma: a clinicopathologic case series study. in Neuropathology : official journal of the Japanese Society of Neuropathology 2011
Human Polyclonal SMARCB1 Primary Antibody for IF (p), IHC (p) - ABIN762566
McAndrew, Gjidoda, Tagore, Miksanek, Floer: Chromatin Remodeler Recruitment during Macrophage Differentiation Facilitates Transcription Factor Binding to Enhancers in Mature Cells. in The Journal of biological chemistry 2016
Human Polyclonal SMARCB1 Primary Antibody for WB - ABIN2778302
Lazrek, Goffard, Schanen, Karquel, Bocket, Lion, Devaux, Hedouin, Gosset, Hober: Detection of hepatitis C virus antibodies and RNA among medicolegal autopsy cases in Northern France. in Diagnostic microbiology and infectious disease 2006
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Human Monoclonal SMARCB1 Primary Antibody for IHC (p), ELISA - ABIN562912
Scurr, Pupo, Becker, Lai, Schrama, Haferkamp, Irvine, Scolyer, Mann, Becker, Kefford, Rizos: IGFBP7 is not required for B-RAF-induced melanocyte senescence. in Cell 2010
Human Polyclonal SMARCB1 Primary Antibody for ICC, IF - ABIN4354923
Singh, Archer: Analysis of the SWI/SNF chromatin-remodeling complex during early heart development and BAF250a repression cardiac gene transcription during P19 cell differentiation. in Nucleic acids research 2014
Of the 34 undifferentiated endometrial carcinomas examined, 17 (50%) exhibited SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) complex inactivation, with 11 tumors showing complete loss of both ARID1A (show ARID1A Antibodies) and ARID1B (show ARID1B Antibodies), 5 showing complete loss of BRG1 (show SMARCA4 Antibodies) and 1 showing complete loss of INI1. Ten of the remaining 17 undifferentiated carcinomas showed the following alterations: 5 tumors (15%) showed loss of ARID1A (show ARID1A Antibodies) only with intact ARID1B (show ARID1B Antibodies), BRG1 (show SMARCA4 Antibodies), and INI1 expression.
Our study, the first comprehensive analysis of RMC, supports a pivotal role for SMARCB1 in its development.
HRAS (show HRAS Antibodies) mutations were more common in epithelial-myoepithelial carcinomas (EMCAs) with intact PLAG1 (show PLAG1 Antibodies) and HMGA2. Most EMCAs arose ex pleomorphic adenoma (PA)and the genetic profile of EMCA varies with the absence or presence of preexisting PA and its cytogenetic signature. Progression to higher grade EMCA with intact PLAG1 (show PLAG1 Antibodies) and HMGA2 correlates with the presence of TP53 (show TP53 Antibodies), FBXW7 (show FBXW7 Antibodies) mutations, or SMARCB1 deletion.
Intronic hotspot variant of SMARCB1 was identified in atypical teratoid and rhabdoid tumors of two patients. This cryptic variant was absent in the germline DNA of both patients.
These highly mobile and invasive cells no longer depend on KRAS signaling and rely on the aberrant activation of mesenchymal programs regulated by the chromatin remodeling factor (show ASH1L Antibodies) SMARCB1. Mouse models showed that Smarcb1 ablation could intensify cancer spread; conversely, restoring Smarcb1 slowed tumor growth and restored the cells to their less invasive, epithelial form
BAF57 (show SMARCE1 Antibodies), BAF60a (show SMARCD1 Antibodies) and SNF5 might act as novel pro-senescence factors in both normal and tumor human skin cells
Low SNF5 expression is associated with Hepatocellular Carcinoma.
SMARCB1 is required for widespread BAF (show BANF1 Antibodies) complex-mediated activation of enhancers and bivalent promoters.
Interactions have been indicated between SMARCB1/INI1 protein and key proteins in various pathways related to tumor proliferation and progression.
The common loss of INI1 expression in rhabdoid and non-rhabdoid tumors will also open new therapeutic doors by developing targeted therapy strategies which may help to consolidate an initial treatment response to conventional radiochemotherapy.
Data show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 (show NF2 Antibodies) gene inactivation causes shwannomas.
The occurrence of intracranial rhabdoid tumours depends on control of Smarcb1 inactivation.
These results support recent findings regarding the effectivity of EGFR (show EGFR Antibodies) inhibitors in hindering the proliferation of human MRT cells and demonstrate that activation of EGFR (show EGFR Antibodies) signaling in Rhabdoid tumors is SMARCB1 dependent.
these findings uncover a novel role for Snf5 in oligodendrocyte generation and survival, and they offer evidence of the first genetically engineered mouse model for AT/RT in the CNS.
This study show here that loss of Smarcb1 and Smarca4 (show SMARCA4 Antibodies) leads to severe proliferation deficits of granule neuron precursors and a hypoplastic cerebellum.
results show that Smarcb1 is required for transcriptional activation of Igfbp7 (show IGFBP7 Antibodies) and show that re-introduction of Igfbp7 (show IGFBP7 Antibodies) alone can hinder tumor development; results define a novel mechanism for Smarcb1-mediated tumorigenesis
We find that inactivation of either Brg1 (show SMARCA4 Antibodies) or Smarcb1 leads to disruptions of specific nucleosome patterning combined with a loss of overall nucleosome occupancy at a large number of promoters, regardless of their association with CpG islands.
SNF5 is a key mediator of Hedgehog (show SHH Antibodies) signaling and that aberrant activation of GLI1 (show GLI1 Antibodies) is a previously undescribed targetable mechanism contributing to the growth of malignant rhabdoid tumor cells.
Loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb (show CBX2 Antibodies) gene EZH2 (show EZH2 Antibodies).
SNF5 knockdown inhibits p53 (show TP53 Antibodies) translation by eIF4E (show EIF4E Antibodies) and replacement of eIF4E (show EIF4E Antibodies) in SNF5 knockdown cells restores p53 (show TP53 Antibodies) expression and cell survival
The protein encoded by this gene is part of a complex that relieves repressive chromatin structures, allowing the transcriptional machinery to access its targets more effectively. The encoded nuclear protein may also bind to and enhance the DNA joining activity of HIV-1 integrase. This gene has been found to be a tumor suppressor, and mutations in it have been associated with malignant rhabdoid tumors. Two transcript variants encoding different isoforms have been found for this gene.
SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1
, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1
, matrix metalloproteinase 11 (stromelysin 3)
, BRG1-associated factor 47
, SNF5 homolog
, integrase interactor 1 protein
, malignant rhabdoid tumor suppressor
, sucrose nonfermenting, yeast, homolog-like 1
, SWI/SNF-related matrix associated protein