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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1

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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: SWI, CAN, HAD, AGE, BRG1
Papers using INI1 antibodies
Tilescope: online analysis pipeline for high-density tiling microarray data.
Copenhaver Gregory P., In PLoS Genetics, 2006
... were agitated overnight at 4°C with 20 µg of one of the following antibodies: 1) anti-Ini1 (C-20), Santa Cruz Biotechnology, sc-16189; 2) anti-BAF155 (H-76), ...
Papers on INI1
ALK-Rearranged Renal Cell Carcinomas in Children.
Perlman et al., Omaha, United States. In Genes Chromosomes Cancer, Feb 2016
In our review of 168 pediatric RCC prospectively registered on Children's Oncology Group AREN03B2 protocol, we identified six RCC (3.5%) that demonstrated a unique epithelioid morphology and a peculiar immunophenotypic profile that includes expression of ALK, TFE3 and retention of INI1.
SMARCB1/INI1 Genetic Alterations in Renal Medullary Carcinomas.
Montironi et al., Córdoba, Spain. In Eur Urol, Feb 2016
UNASSIGNED: Inactivation of the tumor suppressor gene SMARCB1 (also known as INI1) by interchromosomal balanced translocations is a molecular mechanism that characterizes renal medullary carcinoma and might be relevant for the development of more effective therapeutic strategies.
The importance of being Me: Magic methyls, methyltransferase inhibitors and the discovery of tazemetostat.
Chesworth et al., In J Med Chem, Feb 2016
Tazemetostat, an EHZ2 inhibitor in clinical development, has shown activity in both preclinical models of cancer as well as in patients with lymphoma or INI1-deficient solid tumors.
Atypical Teratoid/Rhabdoid Tumor (AT/RT) Arising From Ependymoma: A Type of AT/RT Secondarily Developing From Other Primary Central Nervous System Tumors.
Yokoo et al., Yamagata, Japan. In J Neuropathol Exp Neurol, Feb 2016
UNASSIGNED: Atypical teratoid/rhabdoid tumors (AT/RT) are rare, aggressive, embryonal brain tumors that occur most frequently in very young children; they are characterized by rhabdoid cells and loss of INI1 protein nuclear expression.
Atypical teratoid/rhabdoid tumors-current concepts, advances in biology, and potential future therapies.
Chi et al., Boston, United States. In Neuro Oncol, Feb 2016
The majority of AT/RTs demonstrate genomic alterations in SMARCB1 (INI1, SNF5, BAF47) or, to a lesser extent, SMARCA4 (BRG1) of the SWItch/sucrose nonfermentable chromatin remodeling complex.
A mutation in the Cc.arp9 gene encoding a putative actin-related protein causes defects in fruiting initiation and asexual development in the agaricomycete Coprinopsis cinerea.
Nakahori et al., Kyoto, Japan. In Curr Genet, Feb 2016
Dikaryon formation in agaricomycetes, which is followed by fruiting development, is governed by the mating type loci, A and B. Recently, mutations in the Cc.snf5 gene, which encodes a putative component of the chromatin remodeling complex switch/sucrose non-fermentable (SWI/SNF), were shown to cause defects in A-regulated clamp cell morphogenesis, as well as in fruiting initiation.
Adult Atypical Teratoid/Rhabdoid Tumors.
Dunn et al., Boston, United States. In World Neurosurg, Jan 2016
Due to the complex histology of AT/RTs, the differential diagnosis of these tumors is quite challenging and increasingly relies on demonstration of characteristic SMARCB1/INI1 inactivation in tumor cells.
Recently described neoplasms of the sinonasal tract.
Bishop, Baltimore, United States. In Semin Diagn Pathol, Jan 2016
This manuscript will review the clinicopathologic features of some of the recently described sinonasal tumor types: NUT midline carcinoma, HPV-related carcinoma with adenoid cystic-like features, SMARCB1 (INI-1) deficient sinonasal carcinoma, biphenotypic sinonasal sarcoma, and adamantinoma-like Ewing family tumor.
SMARCA4 inactivation defines a group of undifferentiated thoracic malignancies transcriptionally related to BAF-deficient sarcomas.
Tirode et al., Lyon, France. In Nat Genet, Oct 2015
To help define the nosological relationships of these tumors, we compared their transcriptomic profiles with those of SMARCA4-mutated small-cell carcinomas of the ovary, hypercalcemic type (SCCOHTs), SMARCB1-inactivated malignant rhabdoid tumors (MRTs) and lung carcinomas (of which 10% display SMARCA4 mutations).
Molecular subgroups of atypical teratoid rhabdoid tumours in children: an integrated genomic and clinicopathological analysis.
Huang et al., Toronto, Canada. In Lancet Oncol, May 2015
BACKGROUND: Rhabdoid brain tumours, also called atypical teratoid rhabdoid tumours, are lethal childhood cancers with characteristic genetic alterations of SMARCB1/hSNF5.
SWI/SNF chromatin remodeling and human malignancies.
Delattre et al., In Annu Rev Pathol, 2014
The first evidence of the involvement of these complexes in carcinogenesis was provided by the identification of biallelic, truncating mutations of the SMARCB1 gene in malignant rhabdoid tumors, a highly aggressive childhood cancer.
Biology and Treatment of Rhabdoid Tumor.
Biegel et al., Los Angeles, United States. In Crit Rev Oncog, 2014
SMARCB1 is a member of the SWI/SNF chromatin-remodeling complex and functions as a tumor suppressor in the vast majority of rhabdoid tumors.
Epithelioid Sarcoma: Opportunities for Biology-Driven Targeted Therapy.
Keller et al., Fort Collins, United States. In Front Oncol, 2014
In this review, we will summarize clinically relevant biomarkers (e.g., SMARCB1, CA125, dysadherin, and others) with respect to targeted therapeutic opportunities.
Germline loss-of-function mutations in LZTR1 predispose to an inherited disorder of multiple schwannomas.
Messiaen et al., Birmingham, United States. In Nat Genet, 2014
Constitutional SMARCB1 mutations at 22q11.23 have been found in ∼50% of familial and <10% of sporadic schwannomatosis cases.
Linking the SWI/SNF complex to prostate cancer.
Roberts et al., Boston, United States. In Nat Genet, 2013
Although mutations in SWI/SNF genes are uncommon in prostate cancer, a new study shows that SChLAP1, a long noncoding RNA frequently expressed in aggressive prostate tumors, drives cancer by directly disrupting SNF5, a core subunit of the SWI/SNF complex.
A remarkably simple genome underlies highly malignant pediatric rhabdoid cancers.
Roberts et al., Boston, United States. In J Clin Invest, 2012
Sequenced the exomes of 35 rhabdoid tumors, aggressive cancers characterized by biallelic loss of SMARCB1 of the chromatin remodeling complex. Identified an extremely low rate of mutation, with loss of SMARCB1 being essentially the sole recurrent event.
SMARCB1 deficiency in tumors from the peripheral nervous system: a link between schwannomas and rhabdoid tumors?
Bourdeaut et al., Roma, Italy. In Am J Surg Pathol, 2012
SMARCB1 inactivation, occasionally associated with NF2 deletion, might have oncogenic effects in peripheral nerves.
[BEX2 regulates cell cycle through the interaction with INI1/hSNF5].
Han et al., Shijiazhuang, China. In Yi Chuan, 2012
Both BEX2 and INI1/hSNF5 mainly localized in cell nucleus.
Epigenetic inactivation of the tumor suppressor BIN1 drives proliferation of SNF5-deficient tumors.
Roberts et al., Boston, United States. In Cell Cycle, 2012
SNF5 recruits the SWI/SNF complex to the BIN1 promoter, and that the marked reduction of BIN1 expression in RT correlates with decreased SWI/SNF occupancy.
Integrase interactor 1 regulates proliferation, apoptosis and invasion in gastric cancer cells.
Zhang et al., Shijiazhuang, China. In Chin Med J (engl), 2012
INI1 plays a key role in gastric carcinogenesis by affecting proliferation, apoptosis and invasion.
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