The HDAC2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the human Jurkat T lymphocyte line. This product features targeted disruption of the HDAC2 gene, producing a heterogeneous pool of cells with loss of HDAC2 function. This polyclonal format preserves genetic diversity, minimizing clonal artifacts and making it suitable for studying epigenetic regulation, T-cell biology, and leukemia.
Jurkat cells are an immortalized human T lymphocyte line derived from acute T-cell leukemia, widely employed as a model for T-cell receptor signaling, cytokine production, and apoptosis. These suspension cells express CD3 and CD4 and are used to dissect pathways such as NF-??B, NOTCH, and TGF-??. Their rapid proliferation and amenability to genetic manipulation make them an ideal host for HDAC2 knockout, enabling focused investigations of epigenetic mechanisms in T-cell leukemia.
HDAC2 is a class I histone deacetylase that represses transcription by removing acetyl groups from histone lysine residues and non-histone substrates such as p53 and SP1. It functions within the NuRD complex, interacting with SIN3A, CoREST, and MBD2 to target specific genomic loci. Upstream regulators include p53, MYC, and NF-??B, while downstream targets encompass CDKN1A (p21), BCL2, BIM, and CCND1. These interactions link HDAC2 to p53, Wnt, TGF-??, NOTCH, and NF-??B signaling, governing cell cycle progression, apoptosis, and differentiation in T cells.
HDAC2 knockout in Jurkat cells provides a model to study the epigenetic basis of T-ALL. Loss of HDAC2 activity leads to derepression of pro-apoptotic genes like BIM and cell cycle inhibitors like p21, affecting leukemic cell survival. The model also permits analysis of HDAC2-dependent transcriptional regulation by SP1 and NF-??B and crosstalk with the p53 and NOTCH pathways, which are frequently altered in T-ALL.
Applications include ChIP-qPCR to map histone modifications, reporter assays to measure transcriptional activity, and flow cytometry for apoptosis and proliferation. The polyclonal knockout population is ideal for HDAC inhibitor screening, providing a critical control for drug specificity. Western blotting and RT-qPCR can validate HDAC2 knockout and downstream expression. Co-immunoprecipitation can probe HDAC2 complexes. For further technical details, please contact Ascent Research.
