The EHD1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte line, with targeted disruption of the EHD1 gene. This loss-of-function model enables investigation of EHD1-dependent endocytic recycling and membrane trafficking. The polyclonal format preserves the heterogeneous knockout pool, suitable for functional genomics studies and drug discovery applications requiring pooled cell analysis.
The Jurkat host cell line is an immortalized human T lymphocyte line originally isolated from peripheral blood of a 14-year-old male with acute T cell leukemia. Widely used in T cell biology, signal transduction, and cancer research, they provide a relevant context for studying endocytic trafficking pathways that regulate immune receptor surface expression and T cell function.
EHD1 encodes an ATPase that oligomerizes on endosomal membranes to facilitate recycling of internalized receptors to the plasma membrane. It is recruited by Rab GTPases such as Rab4a, Rab5, and Rab11a, and collaborates with MICAL-L1, syndapin I/II, and Eps15 to drive cargo sorting and vesicle scission. EHD1 interacts with rabenosyn-5 and pacsin, and functions downstream of EGF and transferrin signaling. Its activity controls recycling of the transferrin receptor, EGFR, and integrins, thereby regulating surface receptor levels and downstream pathways including mTOR signaling and GLUT4 translocation. Disruption of EHD1 thus impairs receptor trafficking and associated cellular responses.
In Jurkat T cells, EHD1 critically regulates recycling of T cell receptors and integrins, processes essential for immune synapse formation and leukocyte adhesion. Loss of EHD1 disrupts surface expression dynamics of these receptors, altering antigen recognition and signal transduction. Given the leukemic origin, this model also offers insights into how endocytic trafficking defects may contribute to T cell malignancy.
This product is suited for studying receptor trafficking, immune cell signaling, and leukemia biology. Researchers can measure TCR and integrin surface levels by flow cytometry, perform transferrin recycling assays, visualize endosomes via immunofluorescence, and analyze protein interactions by co-immunoprecipitation and western blot. Cell migration and adhesion assays are enabled by impaired integrin recycling. The combination of Jurkat host and EHD1 knockout facilitates dissection of T cell activation and tumorigenesis. For technical inquiries, contact Ascent Research.
