EHD4 Knockout Jurkat Polyclonal Cells consist of a polyclonal population of Jurkat T lymphocytes engineered with CRISPR/Cas9 to disrupt the EHD4 gene, generating a heterogeneous knockout model for studying endocytic recycling and membrane trafficking. This product provides a ready-to-use, loss-of-function cellular tool derived from the Jurkat host line, with the polyclonal format preserving the functional diversity of multiple editing events without clonal isolation or selection for homozygous mutations.
The Jurkat cell line originates from a human acute T cell leukemia and serves as an immortalized T lymphocyte model system extensively employed in signal transduction research, immunological synapse studies, and leukemia biology. These suspension cells recapitulate key aspects of T cell receptor (TCR) signaling, cytokine response, and activation-induced gene expression, making them a versatile platform for dissecting pathways that govern adaptive immunity and oncogenic transformation.
EHD4 (Eps15 homology domain-containing protein 4) is an ATP-dependent membrane remodeling factor that regulates clathrin-mediated endocytosis, early endosomal fission, and receptor recycling. It interacts directly with adaptor proteins Eps15, Eps15R, intersectin, and syndapin, and cooperates with Rab GTPases (Rab11, Rab8) and Arf6 to orchestrate actin-dependent vesicle scission. Downstream targets include the transferrin receptor, EGFR, integrins, and various cytokine receptors, linking EHD4 to multiple endocytic recycling loops. Disruption of EHD4 expression impairs the return of internalized cargo to the plasma membrane, perturbing surface receptor homeostasis and clathrin-dependent trafficking.
In Jurkat cells, EHD4 plays a critical role in sustaining the recycling of immunoreceptors and adhesion molecules that shape T cell activation, immune synapse assembly, and signal propagation. Knockout of EHD4 in this T lymphocyte context leads to altered surface expression of key receptors, potential defects in sustained TCR signaling, and modified cytoskeletal dynamics, thereby providing a physiologically relevant model to investigate how endocytic recycling intersects with leukemic cell behavior and adaptive immune function.
This polyclonal knockout product is suitable for multiple research applications, including quantitative transferrin recycling assays, flow cytometric profiling of surface receptor turnover (e.g., CD3, CD28), phospho-flow analysis of TCR signaling cascades, and cell migration experiments to assess integrin-dependent motility. It also supports drug sensitivity screens that interrogate links between endocytic trafficking and chemotherapeutic response, as well as co-immunoprecipitation studies to map EHD4 interactomes. For further technical information, please contact Ascent Research.
