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This locus encodes an AT-rich DNA interacting domain-containing protein. Additionally we are shipping ARID1B Kits (1) and and many more products for this protein.
Showing 10 out of 43 products:
Human Monoclonal ARID1B Primary Antibody for IF, IHC (p) - ABIN566118
Coatham, Li, Karnezis, Hoang, Tessier-Cloutier, Meng, Soslow, Blake Gilks, Huntsman, Stewart, Postovit, Köbel, Lee: Concurrent ARID1A and ARID1B inactivation in endometrial and ovarian dedifferentiated carcinomas. in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2016
Show all 2 Pubmed References
Human Monoclonal ARID1B Primary Antibody for IF, IHC (p) - ABIN528194
Flores-Alcantar, Gonzalez-Sandoval, Escalante-Alcalde, Lomelí: Dynamics of expression of ARID1A and ARID1B subunits in mouse embryos and in cells during the cell cycle. in Cell and tissue research 2011
Human Polyclonal ARID1B Primary Antibody for IHC, IP - ABIN252822
Sim, White, Fitzpatrick, Wilson, Gillies, Pope, Mountford, Torring, McKee, Vulto-van Silfhout, Jhangiani, Muzny, Leventer, Delatycki, Amor, Lockhart: Expanding the phenotypic spectrum of ARID1B-mediated disorders and identification of altered cell-cycle dynamics due to ARID1B haploinsufficiency. in Orphanet journal of rare diseases 2014
STAT3 (show STAT3 Antibodies)/Arid1b/beta-catenin (show CTNNB1 Antibodies) pathway is driving neurofibroma initiation.
The patterns of expression of ARID1A (show ARID1A Antibodies) and ARID1B genes through various mouse embryonic stages, was examined.
These data suggest that the BAF250B-associated SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) is essential for mouse embryonic stem cells to maintain their normal proliferation and pluripotency.
A subset of mammalian SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) complexes, specifically containing ARID1B, is required for efficient cell cycle re-entry and for association of activation factors with the c-myc (show MYC Antibodies) promoter.
we identified concurrent ARID1A (show ARID1A Antibodies) and ARID1B inactivating mutations with consequent loss of protein expression in the undifferentiated component of approximately one-quarter of dedifferentiated endometrial and ovarian carcinomas
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, 5 showing complete loss of BRG1 (show SMARCA4 Antibodies) and 1 showing complete loss of INI1 (show SMARCB1 Antibodies). 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, BRG1 (show SMARCA4 Antibodies), and INI1 (show SMARCB1 Antibodies) expression.
We report here the clinical, genetic, and proteomic phenotypes of an individual with a unique apparent de novo mutation of ARID1B due to an intragenic duplication
HSCR (show EDNRB Antibodies) was observed in a patient with a truncating mutation in ARID1B, further expanding the phenotypic spectrum of Coffin-Siris syndrome. This suggests that the BAF (show BANF1 Antibodies) complex does not only play a role in the enteric system of Drosophila, but also in humans.
Case Report: Melanotic Xp11 renal cell carcinoma (show MOK Antibodies) with ARID1B-TFE3 (show TFE3 Antibodies) gene fusion.
The clinical features of both patients are felt to be consistent with an ARID1B-related disorder. To our knowledge, this is the first report of a pathogenic mutation in ARID1B being passed from an affected parent to their offspring.
We report two teenagers with ID whose molecular diagnosis of a SMARC2A or ARID1B mutation, respectively, was established through clinical exome analysis.
The ARID1B gene, commonly mutated in multiple types of cancer, was identified as an additional ZNF384 (show ZNF384 Antibodies) gene fusion partner.
knockdown of the SWI/SNF component ARID1B prevents OIS and cooperates with RAS to induce liver tumors
Chromosome analysis by array-CGH revealed a small interstitial 6q deletion spanning approximately 1.1 Mb of DNA and containing only one coding gene, ARID1B. We suggest that ARID1B is the key gene behind 6q microdeletion syndrome, and we discuss its possible role in the phenotypic manifestations
This locus encodes an AT-rich DNA interacting domain-containing protein. The encoded protein is a component of the SWI/SNF chromatin remodeling complex and may play a role in cell-cycle activation. The protein encoded by this locus is similar to AT-rich interactive domain-containing protein 1A. These two proteins function as alternative, mutually exclusive ARID-subunits of the SWI/SNF complex. The associated complexes play opposing roles. Alternatively spliced transcript variants encoding different isoforms have been described.
AT rich interactive domain 1B (Swi1 like)
, AT-rich interactive domain-containing protein 1B
, transcription factor 1
, ARID domain-containing protein 1B
, BRG1-associated factor 250b
, BRG1-binding protein ELD/OSA1
, ELD (eyelid)/OSA protein