The HMG20A Knockout Jurkat Polyclonal Cells represent a polyclonal population of immortalized human T lymphocytes engineered via CRISPR/Cas9-mediated disruption of the HMG20A gene. This product provides a pooled loss-of-function model, enabling the study of HMG20A deficiency without the selection biases of monoclonal isolates. The polyclonal format maintains genetic diversity while introducing targeted gene disruption, ensuring robust representation of knockout effects across the cell population.
Jurkat cells are derived from the peripheral blood of a 14-year-old male with acute T cell leukemia and serve as a widely employed model for T cell signaling, apoptosis, and HIV infection. Their continuous proliferation and well-characterized signaling pathways make them an ideal host for dissecting the epigenetic and transcriptional networks governed by HMG20A.
HMG20A is a core subunit of the BRAF35/HDAC repressor complex, where it facilitates transcriptional silencing of neuronal genes by coordinating LSD1/KDM1A-mediated histone H3K4 demethylation and HDAC1/HDAC2-mediated deacetylation. It directly interacts with RCOR1, PHF21A, and HMG20B, and is recruited by REST/NRSF to gene promoters. Additionally, HMG20A associates with BRCA2 to participate in DNA double-strand break repair. Upstream regulation by SP1 and downstream targets such as SCN2A, STMN2, SYN1, and miR-124 further embed HMG20A within networks controlling chromatin architecture and genome stability.
In the Jurkat T lymphocyte context, disruption of HMG20A offers a unique system to interrogate its contributions to REST-dependent gene repression and DNA repair. Given the role of REST in neuronal gene silencing and its emerging functions in immune cells, this model may illuminate how HMG20A modulates epigenetic landscapes to influence T cell activation, cytokine secretion, and apoptosis. Moreover, loss of HMG20A may compromise BRCA2-mediated repair pathways, providing insights into genomic instability mechanisms relevant to leukemogenesis and therapeutic resistance.
This polyclonal knockout product is suitable for a broad range of assays, including ChIP-qPCR to assess histone modification changes, Western blotting for protein complex integrity, RT-qPCR to quantify downstream target expression, flow cytometry for cell cycle and apoptosis profiling, and DNA damage assays to evaluate repair capacity. By enabling functional dissection of HMG20A in T cell epigenetics, REST complex dynamics, and DNA repair, these cells serve studies in cancer biology, neurodegeneration, and immune signaling. For further technical inquiries or to place an order, please contact Ascent Research.
