The HDGF Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line, engineered to disrupt the HDGF (hepatoma-derived growth factor) gene. This loss-of-function model enables investigations into the roles of HDGF in T cell biology, signal transduction, and leukemogenesis. The polyclonal nature of the knockout cells provides a heterogeneous population with diverse genetic edits, suitable for studying gene function without the clonal selection biases inherent in single-cell?Cderived lines.
Jurkat cells are an immortalized human T lymphocyte line originally established from the peripheral blood of a patient with acute T cell leukemia. These cells are extensively utilized in immunology and cancer biology research for examining T cell activation, proliferation, apoptosis, and signal transduction pathways, including T cell receptor?Cmediated signaling. Their leukemic origin makes them a relevant model for studying hematological malignancies, particularly acute lymphoblastic leukemia. The well-characterized genetic background and robust growth characteristics of Jurkat cells render them an ideal host for CRISPR-mediated gene editing applications.
HDGF is a mitogenic growth factor with heparin-binding and DNA-binding activities. It promotes cell proliferation and survival by activating multiple intracellular signaling cascades. Mechanistically, HDGF functions through interactions with membrane receptors and intracellular partners such as nucleolin and integrins, leading to activation of the MAPK/ERK and PI3K/AKT pathways. Upstream regulators include E2F transcription factors, NF-??B, hypoxia-inducible factors, and epidermal growth factor. Upon activation, HDGF transcriptionally regulates downstream targets such as Cyclin D1, Bcl-2, VEGF, and c-Myc. In the MAPK/ERK cascade, HDGF signaling engages HRas, Raf, MEK, and ERK, while in the PI3K/AKT pathway, it involves PI3K and AKT, and it also intersects with the NF-??B pathway through IKK. This network mediates enhanced cell cycle progression, survival, and angiogenesis.
Aberrant expression of HDGF has been implicated in multiple cancers, including hepatocellular carcinoma, lung cancer, and leukemia. In the context of Jurkat leukemic T cells, HDGF knockout provides a powerful tool to dissect its contribution to uncontrolled proliferation and survival. The loss of HDGF can alter downstream signaling, resulting in reduced expression of pro-survival factors like Bcl-2 and Cyclin D1, and dampened MAPK/ERK and AKT phosphorylation. This model is therefore significant for understanding the molecular underpinnings of T cell leukemia and evaluating the potential of HDGF as a therapeutic target.
Researchers can employ these HDGF Knockout Jurkat Polyclonal Cells in a variety of applications, including mechanistic studies on T cell proliferation and survival, investigation of leukemia progression, target validation for HDGF-focused therapies, and high-throughput screening for HDGF pathway modulators. Representative assays include Western blotting for HDGF and key signaling effectors such as phospho-ERK and phospho-AKT, RT-qPCR for downstream target gene expression, MTT and Annexin V assays for proliferation and apoptosis, RNA sequencing for transcriptomic profiling, and drug sensitivity tests. For further information or to discuss your experimental needs, please contact Ascent Research.
