The HABP4 Knockout Jurkat Polyclonal Cells are a population of Jurkat T-lymphocyte cells engineered via CRISPR/Cas9 to disrupt the HABP4 gene. This pooled polyclonal preparation provides a biologically representative loss-of-function model without clonal bias, enabling studies of HABP4-dependent processes across a heterogeneous cell population.
Jurkat cells, an immortalized human T-lymphocyte line derived from a 14-year-old male with acute T-cell leukemia, express CD3, CD4, and functional T-cell receptors. This well-characterized line is a cornerstone for investigating T-cell signaling, apoptosis, and viral pathogenesis, making it an ideal host for dissecting gene function in a malignant T-cell context.
HABP4 encodes an intracellular hyaluronan-binding protein that acts as a transcriptional regulator and modulator of cell cycle progression and apoptosis. The protein is transcriptionally induced by p53 in response to cellular stress and assembles into complexes containing chromatin remodeling factors such as CHD3 and the NuRD complex (including HDAC1/2 and MTA1), as well as topoisomerase II (TOP2A). Through these interactions, HABP4 influences the expression of downstream targets including the cyclin-dependent kinase inhibitor p21 and the pro-apoptotic factor BAX, thereby mediating p53-driven cell cycle arrest and apoptotic programs.
In the Jurkat T-cell leukemia background, HABP4 knockout permits precise interrogation of its role in p53-regulated growth control and death pathways. This model is particularly valuable for elucidating how hyaluronan signaling intersects with chromatin dynamics and transcriptional networks in lymphoid malignancies. It enables researchers to separate HABP4-dependent effects from other p53 targets and to assess contributions to leukemogenesis and drug sensitivity.
Typical applications include functional genomics using transcriptomic profiling (RNA-seq) and chromatin occupancy analysis (ChIP-qPCR), complemented by protein interaction studies via co-immunoprecipitation. Apoptosis and cell cycle alterations are readily quantified by flow cytometry, while proliferation assays and targeted gene expression measurements (RT-qPCR, Western blotting) provide mechanistic insights. The cells also serve in pharmacological studies evaluating responses to genotoxic agents or targeted therapies. For further details and batch-specific information, please contact Ascent Research.
