The ARID1B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line, engineered for target-gene disruption of ARID1B. This heterogeneous pool of gene-edited cells provides a powerful tool for studying loss-of-function phenotypes in an immunologically relevant background. The polyclonal format captures a spectrum of editing events, offering a robust model without clonal limitations. These cells are intended for research into ARID1B-dependent chromatin remodeling and T-cell biology.
Jurkat cells are a well-established model of human T-cell leukemia, originally derived from a patient with acute T-cell leukemia. They grow in suspension and are extensively used to study T-cell receptor signaling, apoptosis, and lymphocyte activation. Their rapid proliferation, genetic tractability, and intact expression of SWI/SNF complex components make them an ideal host for interrogating ARID1B function in a leukemic context.
ARID1B encodes a DNA-binding subunit of the SWI/SNF chromatin remodeling complex, which uses ATP hydrolysis to alter nucleosome positioning and regulate transcription. It interacts with ARID1A, SMARCA4 (BRG1), SMARCB1 (SNF5), and is regulated by TCF/LEF transcription factors, ??-catenin, and the NOTCH intracellular domain. ARID1B-containing complexes control expression of key targets such as MYC, CCND1, and CDKN1A, thereby linking Wnt, Notch, and T-cell receptor signaling to cell cycle progression and differentiation.
In Jurkat T-cells, ARID1B disruption impairs SWI/SNF-dependent chromatin remodeling, disrupting transcriptional programs required for T-cell receptor signaling and leukemic growth. This model provides a relevant system for investigating the molecular pathology of ARID1B-mutant cancers, including acute lymphoblastic leukemia, hepatocellular carcinoma, and colorectal cancer, as well as neurodevelopmental disorders like Coffin-Siris syndrome. It enables dissection of ARID1B??s role in oncogenic signaling and identification of synthetic lethal vulnerabilities.
These polyclonal knockout cells support a broad range of applications: functional analysis of SWI/SNF complex assembly in leukemia, high-throughput drug screening for chromatin modifier sensitivities, and epigenetic studies of T-cell activation. Representative techniques include Western blotting, RT-qPCR of MYC and CCND1, RNA-seq, ChIP-qPCR, flow cytometric assessment of apoptosis and cell cycle, co-immunoprecipitation of BAF subunits, and drug sensitivity testing. For further information, please contact Ascent Research.
