The ARID1B Knockout HEK293T Polyclonal Cells are a genetically heterogeneous population generated by CRISPR/Cas9-mediated disruption of the ARID1B gene in the human embryonic kidney HEK293T cell line. This polyclonal knockout model consists of a diverse pool of edited cells harboring a range of loss-of-function mutations, providing a robust system for investigating ARID1B-dependent pathways without the limitations of clonal selection.
HEK293T is a derivative of the HEK293 cell line that stably expresses the SV40 large T antigen, enhancing episomal replication and enabling high-level transient protein expression. Originating from human embryonic kidney tissue transformed with adenovirus 5, HEK293T retains epithelial characteristics relevant to kidney development and differentiation, making it a widely adopted platform for chromatin biology and signal transduction studies.
ARID1B encodes a non-catalytic core subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex. It directly interacts with essential SWI/SNF components including SMARCA4 (BRG1), SMARCA2 (BRM), ARID1A, SMARCB1 (SNF5), and ACTL6A, and is targeted to chromatin by transcription factors such as ??-catenin, REST, and SOX2. Through these interactions, ARID1B regulates the expression of key downstream targets like CDKN1A (p21), CCND1 (cyclin D1), NEUROD1, NGN2, and multiple HOX genes. ARID1B is itself regulated by upstream kinases (CDK1) and ubiquitin ligases (TRIM37), and its activity is critical for the proper function of developmental signaling cascades, including Wnt/??-catenin, TGF-??/SMAD, and Notch. Disruption of ARID1B in the polyclonal HEK293T knockout population leads to impaired SWI/SNF complex assembly and altered chromatin occupancy, causing transcriptional dysregulation of these pathways.
In the HEK293T epithelial background, loss of ARID1B perturbs both cell cycle progression and differentiation-associated gene programs, mirroring aspects of the Coffin-Siris syndrome neurodevelopmental phenotype and cancer-related processes. The HEK293T system, while not neuronal, offers a genetically tractable model to dissect conserved SWI/SNF-dependent regulatory mechanisms. These polyclonal knockout cells enable investigation of how ARID1B coordinates key transcription factor complexes, such as TCF/LEF downstream of Wnt, SMAD2/3 in TGF-?? signaling, and the Notch intracellular domain, thereby influencing proliferation, apoptosis, and lineage commitment.
This polyclonal knockout product is suitable for diverse applications, including mechanistic studies of chromatin remodeling, high-content screening for small-molecule modulators of the SWI/SNF complex, and functional rescue experiments with mutant ARID1B constructs. Representative assays include Western blotting for SWI/SNF subunit levels, RT-qPCR and RNA-seq for transcriptome profiling, ChIP-seq for genome-wide chromatin occupancy, co-immunoprecipitation for complex integrity, and flow cytometry for cell cycle analysis. Neurodifferentiation and proliferation assays further expand its utility in neurodevelopmental and cancer research. For additional information or custom applications, please contact Ascent Research.
