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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. Zusätzlich bieten wir Ihnen SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily B, Member 1 Antikörper (131) und SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily B, Member 1 Kits (4) und viele weitere Produktgruppen zu diesem Protein an.
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Loss of SMARCB1/INI1 expression is considered to be a hallmark for childhood chordomas.
Of the 34 undifferentiated endometrial carcinomas examined, 17 (50%) exhibited SWI (zeige SMARCA1 Proteine)/SNF (zeige SNRPA Proteine) complex inactivation, with 11 tumors showing complete loss of both ARID1A and ARID1B, 5 showing complete loss of BRG1 (zeige SMARCA4 Proteine) 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 only with intact ARID1B, BRG1 (zeige SMARCA4 Proteine), and INI1 expression.
Our study, the first comprehensive analysis of RMC, supports a pivotal role for SMARCB1 in its development.
HRAS (zeige HRAS Proteine) mutations were more common in epithelial-myoepithelial carcinomas (EMCAs) with intact PLAG1 (zeige PLAG1 Proteine) 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 (zeige PLAG1 Proteine) and HMGA2 correlates with the presence of TP53 (zeige TP53 Proteine), FBXW7 (zeige FBXW7 Proteine) 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 (zeige ASH1L Proteine) 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 (zeige SMARCE1 Proteine), BAF60a (zeige SMARCD1 Proteine) 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 (zeige BANF1 Proteine) 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.
Data show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 (zeige NF2 Proteine) 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 (zeige EGFR Proteine) inhibitors in hindering the proliferation of human MRT cells and demonstrate that activation of EGFR (zeige EGFR Proteine) 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 (zeige SMARCA4 Proteine) leads to severe proliferation deficits of granule neuron precursors and a hypoplastic cerebellum.
results show that Smarcb1 is required for transcriptional activation of Igfbp7 (zeige IGFBP7 Proteine) and show that re-introduction of Igfbp7 (zeige IGFBP7 Proteine) alone can hinder tumor development; results define a novel mechanism for Smarcb1-mediated tumorigenesis
We find that inactivation of either Brg1 (zeige SMARCA4 Proteine) 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 (zeige SHH Proteine) signaling and that aberrant activation of GLI1 (zeige GLI1 Proteine) 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 (zeige CBX2 Proteine) gene EZH2 (zeige EZH2 Proteine).
SNF5 knockdown inhibits p53 (zeige TP53 Proteine) translation by eIF4E (zeige EIF4E Proteine) and replacement of eIF4E (zeige EIF4E Proteine) in SNF5 knockdown cells restores p53 (zeige TP53 Proteine) 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