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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 Antibodies (133) and SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily B, Member 1 Proteins (20) and many more products for this protein.
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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.
Biallelic alterations in the INI1 gene were identified in 4 of the 5 cases of atypical teratoid/rhabdoid tumors. Three of the 4 cases harbored 2 different mutations, presumably on different alleles (compound heterozygous mutations), and 1 case of which had a splice-site mutation.
The epithelioid variant of schwannoma is rare, and loss of SMARCB1/INI1 expression has been observed in a subset of cases. Our aim was to further define the clinicopathologic features and to evaluate SMARCB1/INI1 deficiency in a large cohort of 65 epithelioid schwannomas diagnosed between 2002 and 2015
SMARCB1 is required for the integrity of SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) complexes.
INI1 loss occurs rarely in colorectal carcinoma, where it is associated with higher grade, larger tumor size, poorer survival, mismatch repair deficiency, and BRAFV600E mutation.
SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) complexes lacking SMARCB1 are vital determinants of drug sensitivity, not just to TOP2A (show TOP2A ELISA Kits)-targeted agents, but to the much broader range of cancer drugs effluxed by ABCB1 (show ABCB1 ELISA Kits).
SMARCB1-deficient sinonasal carcinoma represents an emerging poorly differentiated/undifferentiated sinonasal carcinoma.
Deletions in INI1 gene is associated with Small cell undifferentiated hepatoblastomas.
Our results confirm the pathogenic involvement of SMARCB1/INI1 in childhood chordoma
The occurrence of intracranial rhabdoid tumours depends on control of Smarcb1 inactivation.
These results support recent findings regarding the effectivity of EGFR (show EGFR ELISA Kits) inhibitors in hindering the proliferation of human MRT cells and demonstrate that activation of EGFR (show EGFR ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) and show that re-introduction of Igfbp7 (show IGFBP7 ELISA Kits) alone can hinder tumor development; results define a novel mechanism for Smarcb1-mediated tumorigenesis
We find that inactivation of either Brg1 (show SMARCA4 ELISA Kits) 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 ELISA Kits) signaling and that aberrant activation of GLI1 (show GLI1 ELISA Kits) 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 ELISA Kits) gene EZH2 (show EZH2 ELISA Kits).
SNF5 knockdown inhibits p53 (show TP53 ELISA Kits) translation by eIF4E (show EIF4E ELISA Kits) and replacement of eIF4E (show EIF4E ELISA Kits) in SNF5 knockdown cells restores p53 (show TP53 ELISA Kits) expression and cell survival
The loss of this protein, a core subunit of SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits), results in highly penetrant cancer predisposition with 100% of mice developing mature CD8 (show CD8A ELISA Kits)(+)T cell lymphoma or rare rhabdoid tumors with a median onset of only 11 weeks.
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