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AT rich interactive domain 3A

This gene encodes a member of the ARID (AT-rich interaction domain) family of DNA binding proteins. It was found by homology to the Drosophila dead ringer gene, which is important for normal embryogenesis. Other ARID family members have roles in embryonic patterning, cell lineage gene regulation, cell cycle control, transcriptional regulation, and possibly in chromatin structure modification. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, SWI, FGFR3, CAN, AGE
Papers using BRIGHT antibodies
Components of the human SWI/SNF complex are enriched in active chromatin and are associated with the nuclear matrix.
Blagosklonny Mikhail V., In PLoS ONE, 1996
... Immunoblotting was performed with the following antibodies: rabbit DRIL1 and mouse T7 from Bethyl laboratory, mouse SUMO1 and ...
Papers on BRIGHT
The safety and effectiveness of bivalirudin in female patients with acute myocardial infarction undergoing primary angioplasty: A subgroup analysis of the BRIGHT trial.
Han et al., Shenyang, China. In Catheter Cardiovasc Interv, Feb 2016
METHODS: The present study was a subgroup analysis of the randomized Bivalirudin in Acute Myocardial Infarction vs. Heparin and GPI plus Heparin (BRIGHT) trial.
Interstitial 6q25 microdeletion syndrome: ARID1B is the key gene.
Milani et al., Milano, Italy. In Am J Med Genet A, Feb 2016
region containing the genes ARID1B and ZDHHC14.
Genome Sequencing of Autism-Affected Families Reveals Disruption of Putative Noncoding Regulatory DNA.
Eichler et al., Seattle, United States. In Am J Hum Genet, Feb 2016
This effect was only observed within 50 kb of genes that have been previously associated with autism risk, including genes where dosage sensitivity has already been established by recurrent disruptive de novo protein-coding mutations (ARID1B, SCN2A, NR3C2, PRKCA, and DSCAM).
Dynamic recrystallization behavior of a biomedical Ti-13Nb-13Zr alloy.
Madhu et al., Hyderābād, India. In J Mech Behav Biomed Mater, Jan 2016
UNASSIGNED: The dynamic recrystallization (DRX) behavior of a biomedical titanium Ti-13Nb-13Zr alloy has been investigated using the high temperature compression tests under wide range of strain rates (0.001-1/s) and temperatures 900-1050°C.
Genome-Wide Transcriptional Regulation Mediated by Biochemically Distinct SWI/SNF Complexes.
Magnuson et al., Chapel Hill, United States. In Plos Genet, Dec 2015
ARID1B and ARID2 participate in wide-spread cooperation to repress hundreds of genes.
Bivalirudin vs heparin with or without tirofiban during primary percutaneous coronary intervention in acute myocardial infarction: the BRIGHT randomized clinical trial.
BRIGHT Investigators et al., Shenyang, China. In Jama, May 2015
IMPORTANCE: The safety and efficacy of bivalirudin compared with heparin with or without glycoprotein IIb/IIIa inhibitors in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are uncertain.
ARID1B-mediated disorders: Mutations and possible mechanisms.
Lockhart et al., Melbourne, Australia. In Intractable Rare Dis Res, Feb 2015
Mutations in the gene encoding AT-rich interactive domain-containing protein 1B (ARID1B) were recently associated with multiple syndromes characterized by developmental delay and intellectual disability, in addition to nonsyndromic intellectual disability.
Coffin-Siris syndrome and related disorders involving components of the BAF (mSWI/SNF) complex: historical review and recent advances using next generation sequencing.
Carey et al., In Am J Med Genet C Semin Med Genet, 2014
In 2012, 42 years after the first description of CSS in 1970, five causative genes (SMARCB1, SMARCE1, SMARCA4, ARID1A, ARID1B), all encoding components of the BAF complex, were identified as being responsible for CSS through whole exome sequencing and pathway-based genetic screening.
The ARID1B phenotype: what we have learned so far.
ARID1B-CSS consortium et al., In Am J Med Genet C Semin Med Genet, 2014
Evidence is now accumulating from a number of sequencing studies that ARID1B not only appears to be one of the most frequently mutated intellectual disability (ID) genes, but that the range of phenotypes caused by ARID1B mutations seems to be extremely wide.
ARID1B is a specific vulnerability in ARID1A-mutant cancers.
Roberts et al., Boston, United States. In Nat Med, 2014
Here, using a broad screening approach, we identify ARID1B, an ARID1A homolog whose gene product is mutually exclusive with ARID1A in SWI/SNF complexes, as the number 1 gene preferentially required for the survival of ARID1A-mutant cancer cell lines.
Clinical correlations of mutations affecting six components of the SWI/SNF complex: detailed description of 21 patients and a review of the literature.
Matsumoto et al., Matsumoto, Japan. In Am J Med Genet A, 2013
Mutations in the components of the SWItch/sucrose nonfermentable (SWI/SNF)-like chromatin remodeling complex have recently been reported to cause Coffin-Siris syndrome (CSS), Nicolaides-Baraitser syndrome (NCBRS), and ARID1B-related intellectual disability (ID) syndrome.
Integrated genomic analyses identify ARID1A and ARID1B alterations in the childhood cancer neuroblastoma.
Hogarty et al., Baltimore, United States. In Nat Genet, 2013
Among genes not previously known to be involved in neuroblastoma, chromosomal deletions and sequence alterations of the chromatin-remodeling genes ARID1A and ARID1B were identified in 8 of 71 tumors (11%) and were associated with early treatment failure and decreased survival.
Bendamustine in indolent non-Hodgkin's lymphoma: a practice guide for patient management.
Ghielmini et al., Villingen-Schwenningen, Germany. In Oncologist, 2012
For patients with advanced indolent non-Hodgkin's lymphoma (NHL) or elderly patients with mantle cell lymphoma (MCL), the recently reported results of the German StiL NHL-1 2003 and the international BRIGHT phase III trials showed that, as first-line treatment, the combination of bendamustine and rituximab is at least as effective as rituximab/cyclophosphamide/doxorubicin/vincristine/prednisone or rituximab/cyclophosphamide/vincristine/prednisone, possibly with a better therapeutic index.
Whole-genome sequencing of liver cancers identifies etiological influences on mutation patterns and recurrent mutations in chromatin regulators.
Nakagawa et al., Yokohama, Japan. In Nat Genet, 2012
Multiple chromatin regulators, including ARID1A, ARID1B, ARID2, MLL and MLL3, were mutated in ∼50% of the tumors.
The landscape of cancer genes and mutational processes in breast cancer.
Stratton et al., Sanger, United States. In Nature, 2012
Driver mutations were identified in several new cancer genes including AKT2, ARID1B, CASP8, CDKN1B, MAP3K1, MAP3K13, NCOR1, SMARCD1 and TBX3.
E2F1, ARID3A/Bright and Oct-2 factors bind to the Epstein-Barr virus C promoter, EBNA1 and oriP, participating in long-distance promoter-enhancer interactions.
Rymo et al., Göteborg, Sweden. In J Gen Virol, 2012
These findings support the hypothesis that Epstein-Barr virus EBNA1 initiates transcription at the C promoter via interactions between multiple EBNA1 homodimers and cellular transcription such as E2F1, ARID3A and Oct-2.
Mutations in SWI/SNF chromatin remodeling complex gene ARID1B cause Coffin-Siris syndrome.
Kriek et al., Leiden, Netherlands. In Nat Genet, 2012
these results indicate that haploinsufficiency of the ARID1B gene, which encodes an epigenetic modifier of chromatin structure, is an important cause of CSS and is potentially a common cause of intellectual disability and speech impairment.
Haploinsufficiency of ARID1B, a member of the SWI/SNF-a chromatin-remodeling complex, is a frequent cause of intellectual disability.
Reis et al., Nürnberg, Germany. In Am J Hum Genet, 2012
Haploinsufficiency of ARID1B, a member of the SWI/SNF-A chromatin-remodeling complex, is a common cause of ID.
Cooperation between ARID3A and p53 in the transcriptional activation of p21WAF1 in response to DNA damage.
Ikeda et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2012
These results indicate both cooperative and interdependent roles for ARID3A and p53 in the transcriptional activation of p21(WAF1) in response to DNA damage.
E2FBP1 antagonizes the p16(INK4A)-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability.
Nakajima et al., United States. In Int J Oral Sci, 2011
functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating promyelocytic leukemia protein stability
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