EGFR Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T lymphocyte cell line. This product features targeted disruption of the epidermal growth factor receptor (EGFR) gene, generating a loss-of-function model for investigating EGFR-dependent signaling mechanisms. The polyclonal knockout format provides a heterogeneous knockout population, enabling robust functional studies without clonal selection bias.
The Jurkat cell line originates from the peripheral blood of a 14-year-old male with acute T cell leukemia and serves as a widely used model for T cell receptor (TCR) signaling, apoptosis, and leukemia biology. These suspension cells exhibit characteristic T lymphocyte features and respond to a variety of stimuli, making them suitable for dissection of signal transduction pathways.
EGFR functions as a receptor tyrosine kinase that, upon binding of ligands such as EGF, TGF-??, amphiregulin, and epiregulin, activates critical intracellular signaling cascades. Ligand-induced receptor dimerization and phosphorylation recruit adaptor proteins including GRB2, SHC, and GAB1, leading to activation of the RAS-RAF-MEK-ERK axis and the PI3K-AKT-mTOR pathway. Additionally, EGFR engages PLC??-PKC signaling. Downstream, these pathways regulate transcription factors such as MYC, FOS, and JUN to control cell proliferation, survival, and migration. Interacting factors like PTEN and CBL fine-tune signal output. CRISPR/Cas9-mediated disruption of EGFR in Jurkat cells abolishes EGF-induced signaling, thereby impairing MAPK/ERK and PI3K/AKT pathway activation and disrupting downstream cellular responses.
In the Jurkat T cell context, EGFR knockout provides a valuable model to study the interplay between growth factor receptor signaling and T cell-specific pathways. Because Jurkat cells endogenously express low to moderate levels of EGFR, this knockout system enables precise investigation of EGFR contributions to leukemic T cell biology, including potential crosstalk with TCR signaling networks. It also allows for assessment of EGFR-targeted agents in a lymphoid background, facilitating drug resistance studies and validation of therapeutic strategies.
Typical research applications include functional validation of EGFR inhibitors, analysis of EGF-stimulated signaling cascades by Western blotting for phosphorylated ERK and AKT, RT-qPCR for EGFR transcript levels, and flow cytometry for surface EGFR expression. Additional assays such as BrdU proliferation assays, annexin V apoptosis assays, and migration assays enable comprehensive phenotypic characterization. This knockout model is also suitable for drug sensitivity testing with EGFR inhibitors and exploring mechanisms of resistance in T lymphoid cells. For further information or to inquire about this product, please contact Ascent Research.
