The BRD3 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population in which the BRD3 gene has been disrupted across a pool of Jurkat cells. This polyclonal format captures a spectrum of editing outcomes, providing a robust loss-of-function model without clonal bias. The population is generated through CRISPR/Cas9-mediated gene disruption, enabling functional interrogation of BRD3 in a human T lymphocyte leukemia background.
Jurkat cells are an immortalized human T lymphocyte line derived from an acute T cell leukemia patient. Widely used to study T cell receptor signaling, activation, and leukemogenesis, they provide a biologically relevant host for investigating genes involved in proliferation and survival of T cells. The hematopoietic malignancy origin makes Jurkat cells particularly suited for examining epigenetic regulators in T-cell acute lymphoblastic leukemia.
BRD3 is a BET family bromodomain protein that functions as an epigenetic reader of acetylated histones, preferentially binding H3K27ac and H4ac marks. At promoters and enhancers, BRD3 recruits the P-TEFb complex (CDK9/Cyclin T1) to phosphorylate RNA Polymerase II, facilitating transcriptional elongation of targets such as MYC, CDK6, BCL2, CCND1, and CDK4. Upstream, BRD3 is regulated by histone acetyltransferases p300 and CBP and integrates NF-??B signaling. It interacts with BRD4 and other coactivators to sustain oncogenic gene expression programs, linking acetylation signals to RNA Pol II activity.
In the Jurkat T-ALL context, BRD3 knockout polyclonal cells enable study of epigenetic control over leukemic growth. Disruption of BRD3 allows assessment of BET-dependent transcriptional networks and the resulting effects on proliferation and survival pathways. This model supports investigation of BET inhibitor mechanisms, including JQ1 sensitivity, and the role of MYC and cell cycle regulators in T cell leukemia maintenance. The polyclonal nature ensures representation of diverse genetic alterations, reflecting population-level responses.
These cells are applicable to functional genomics, epigenetic regulation, and drug target validation assays. Common readouts include Western blotting, RT-qPCR, and RNA-seq for expression profiling, ChIP-qPCR for chromatin mark analysis, and functional assays such as MTT proliferation, apoptosis detection, and drug sensitivity screens. Flow cytometry and immunofluorescence facilitate protein-level signaling studies, while reporter gene assays monitor BRD3-dependent transcription. The polyclonal knockout cells are an ideal tool for BET protein research and preclinical evaluation of epigenetic therapies. For further information, please contact Ascent Research.
