EHD3 Knockout Jurkat Polyclonal Cells provide a polyclonal population of Jurkat cells with CRISPR/Cas9-mediated disruption of the EHD3 gene, offering a loss-of-function model for investigating EHD3-dependent cellular processes. As a polyclonal knockout, this product consists of a heterogeneous pool of edited cells, suitable for bulk functional assays and screening applications. The gene disruption is generated using CRISPR/Cas9 technology, and the cells are provided as a ready-to-use population for downstream experimental workflows.
Jurkat cells are an immortalized human CD4+ T lymphocyte line derived from acute T cell leukemia. They contain integrated human T-lymphotropic virus-1 (HTLV-1) sequences and serve as a well-established model for T cell receptor (TCR) signaling, apoptosis, and cytokine production. Their robust proliferative capacity and extensively characterized signaling networks make them a preferred system for studying lymphocyte biology and immune function.
EHD3 encodes a membrane-remodeling ATPase that functions in endocytic recycling by binding phosphatidylinositol phospholipids and ATP to induce membrane tubulation and fission. It cooperates with the scaffolding proteins EHBP1 and MICAL-L1, and small GTPases such as Rab4 and Rab11, to regulate the recycling of transferrin receptor, GLUT4, and ??1 integrins back to the plasma membrane. Upstream, insulin signaling and receptor tyrosine kinase activation stimulate EHD3-mediated trafficking, while downstream, EHD3 influences actin cytoskeleton dynamics and integrin-dependent adhesion and migration.
In Jurkat T cells, endocytic recycling is integral to TCR signal transduction, immune synapse assembly, and cytokine secretion. Disruption of EHD3 impairs the trafficking of receptors and integrins, potentially compromising T cell activation, adhesion, and migratory responses. This knockout model allows researchers to dissect EHD3-specific contributions to membrane trafficking without interference from other EHD family members such as EHD1, and to compare polyclonal knockout pools against parental Jurkat cells to elucidate EHD3’s role in lymphocyte signaling and immune regulation.
This polyclonal knockout cell population enables a range of research applications, including cancer biology, immunology, and drug discovery. Representative assays include flow cytometry for transferrin receptor recycling and TCR surface expression, immunofluorescence for endosomal markers, cell adhesion and migration studies, and T cell activation assays measuring IL-2 secretion and calcium flux. Co-immunoprecipitation and phospho-signaling analyses can be used to characterize EHD3 interaction networks and downstream signaling effects. These cells are suitable for mechanistic studies and genetic screens in lymphocyte trafficking. For additional information, please contact Ascent Research.
