The BRWD1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T-lymphoblastoid cells, designed for loss-of-function studies of the BRWD1 gene. This product provides a heterogeneous knockout cell pool, enabling functional genomics and epigenetic research without the constraints of clonal selection.
The Jurkat cell line (E6.1) is a well-established human T-lymphocyte model, widely used to study T-cell signaling, activation, and leukemogenesis. Derived from an acute T-cell leukemia patient, Jurkat cells recapitulate key aspects of T-cell acute lymphoblastic leukemia (T-ALL) and serve as a robust platform for investigating oncogenic pathways and therapeutic interventions.
BRWD1 encodes a bromodomain and WD repeat-containing protein that functions as an epigenetic reader and scaffold, recruiting Polycomb repressive complex 2 (PRC2) to specific chromatin loci. Through direct interaction with core PRC2 subunits EZH2, SUZ12, and EED, BRWD1 promotes trimethylation of histone H3 at lysine 27 (H3K27me3), a hallmark of transcriptional silencing. BRWD1 activity is regulated by upstream Notch and MYC signaling, and it governs the expression of downstream targets including HOX cluster genes and cell cycle regulators. This chromatin-organizing function positions BRWD1 at the intersection of PRC2-mediated gene silencing and Wnt/??-catenin signaling.
In Jurkat cells, BRWD1 is implicated in maintaining the repressive chromatin landscape that controls proliferation and differentiation programs. Disruption of BRWD1 by CRISPR/Cas9 is expected to alleviate PRC2-mediated silencing, potentially leading to derepression of tumour suppressor genes or developmental regulators, thereby altering cell growth, apoptosis, and T-ALL phenotypes. Thus, these polyclonal knockout cells offer a physiologically relevant model to dissect the epigenetic mechanisms underlying T-cell malignancies and to evaluate the role of chromatin remodeling in leukemia.
This knockout product is ideally suited for a variety of experimental workflows, including chromatin immunoprecipitation sequencing (ChIP-seq) to map H3K27me3 redistribution, quantitative RT-PCR profiling of PRC2 target gene expression, and western blot analysis of BRWD1 and histone modifications. Functional assays such as cell proliferation assessment and flow cytometry-based apoptosis detection further enable drug target validation and screening of epigenetic inhibitors. Researchers can exploit this system to investigate the Notch-MYC-BRWD1 signaling axis, to interrogate PRC2 dependency in T-ALL, and to identify synthetic lethal interactions. For further information, please contact Ascent Research.
