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This locus encodes an AT-rich DNA interacting domain-containing protein. Additionally we are shipping ARID1B Antibodies (43) and and many more products for this protein.
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STAT3 (show STAT3 ELISA Kits)/Arid1b/beta-catenin (show CTNNB1 ELISA Kits) pathway is driving neurofibroma initiation.
The patterns of expression of ARID1A (show ARID1A ELISA Kits) and ARID1B genes through various mouse embryonic stages, was examined.
These data suggest that the BAF250B-associated SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) is essential for mouse embryonic stem cells to maintain their normal proliferation and pluripotency.
A subset of mammalian SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) complexes, specifically containing ARID1B, is required for efficient cell cycle re-entry and for association of activation factors with the c-myc (show MYC ELISA Kits) promoter.
HSCR (show EDNRB ELISA Kits) 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 ELISA Kits) complex does not only play a role in the enteric system of Drosophila, but also in humans.
Case Report: Melanotic Xp11 renal cell carcinoma with ARID1B-TFE3 (show TFE3 ELISA Kits) 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 ELISA Kits) 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
Gonadal mosaicism in ARID1B gene causes intellectual disability and dysmorphic features in three siblings.
ARID1B potentially serves as a valuable prognostic and predictive biomarker as well as a therapeutic target in breast cancer.
This study demonstrate that ARID1B is required for neuronal differentiation in the developing brain, such as in dendritic arborization and synapse formation.
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