The EHD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from Jurkat cells, featuring targeted disruption of the EHD2 gene. This product provides a mixed population of edited cells with loss-of-function mutations introduced by CRISPR/Cas9-mediated gene disruption, enabling the study of EHD2-dependent processes without clonal isolation.
The Jurkat host cell line is an immortalized human T lymphoblastoid cell line originally derived from a patient with acute T-cell leukemia. It serves as a well-characterized model for T-cell biology, leukemia research, and immunology, and is extensively used in studies of T-cell signaling, HIV pathogenesis, and lymphocyte activation. The Jurkat background offers a robust platform for investigating the roles of specific genes in T-cell function.
EHD2 is an ATPase that oligomerizes at membrane interfaces to drive tubulation and scission, playing a central role in caveolae stability and endocytic recycling. It is activated downstream of integrin signaling and the small GTPase Rac1, and is regulated by mechanical stress and MRTF transcription factors. EHD2 interacts directly with caveolin-1, dynamin-2, PACSIN2, the Arp2/3 complex, myosin-2, and actin to orchestrate focal adhesion dynamics and cell migration through actin cytoskeleton remodeling. Disruption of EHD2 thus perturbs membrane trafficking and cytoskeletal organization.
In Jurkat T lymphocytes, this knockout model is particularly valuable for dissecting the contributions of caveolae-mediated endocytosis and actin dynamics to T-cell migration, adhesion, and immune signaling. Since lymphocytes depend on precise cytoskeletal rearrangements for surveillance and activation, EHD2 loss enables researchers to explore how endocytic recycling influences T-cell functional responses and the interplay between membrane trafficking and cell motility.
Researchers can apply these polyclonal knockout cells in transwell migration assays to quantify T-cell invasiveness, immunofluorescence to visualize actin and focal adhesion architecture, and flow cytometry to monitor receptor recycling kinetics. The model also supports co-immunoprecipitation to probe EHD2-containing complexes and live-cell imaging to capture membrane dynamics. Typical applications include tumor metastasis research, immune cell trafficking studies, and drug target validation in cancer. For further information, please contact Ascent Research.