The ARID4A Knockout Jurkat Polyclonal Cells are a heterogeneous population of Jurkat T lymphocytes with CRISPR/Cas9-mediated disruption of the ARID4A gene. This polyclonal knockout pool provides a loss-of-function model for studying ARID4A-dependent transcriptional regulation without selection for a single clone. Ready-to-use, these cells enable investigation of ARID4A ablation effects in a leukemia-relevant background.
The Jurkat host cell line is an immortalized human T-lymphocyte line derived from a patient with acute T-cell leukemia. Widely used as a model for T-cell receptor signaling and leukemogenesis, Jurkat cells offer a characterized system for CRISPR-based gene disruption to dissect oncogenic and tumor-suppressive pathways in T-cell malignancies.
ARID4A functions as a transcriptional corepressor bridging the RB1 tumor suppressor pathway and SIN3A-HDAC chromatin remodeling complex. It directly interacts with RB1, SIN3A, HDAC1, HDAC2, and SAP30 to repress E2F target genes such as CCNE1 and CDC25A, while also modulating the apoptosis regulator BCL2L11. Upstream signals including TGF-??, Notch1, and E2F1 influence ARID4A activity, and p16INK4a (CDKN2A) sustains RB1-mediated repression. This network integrates mitogenic and anti-proliferative cues at the chromatin level.
In Jurkat T-lymphoblastic leukemia cells, disruption of ARID4A is expected to relieve transcriptional repression of E2F target genes, accelerating G1/S transition and promoting unchecked proliferation. Loss of ARID4A may also sensitize cells to apoptotic stimuli by altering the balance of BCL2L11 and other BCL-2 family members. This polyclonal knockout model provides a physiologically relevant platform to explore the tumor-suppressive role of ARID4A in acute lymphoblastic leukemia, revealing how epigenetic dysregulation contributes to hematopoietic cancers. The heterogeneous editing events in the population offer a more comprehensive view of loss-of-function consequences compared to single clones.
The ARID4A Knockout Jurkat Polyclonal Cells are well suited for chromatin immunoprecipitation (ChIP-qPCR) to assess corepressor complex positioning, RNA-seq to map global transcriptional changes, and RT-qPCR for quantifying derepression of E2F target genes such as CCNE1 and CDC25A. Functional phenotyping can be performed via cell proliferation assays, flow cytometry-based cell cycle profiling, and apoptosis detection. Additionally, this model supports drug target screening campaigns aimed at identifying synthetic lethal interactions or evaluating epigenetic therapies directed at T-cell leukemia. For further details or customized products, please contact Ascent Research.
