The CD2AP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the immortalized human T lymphocyte line, Jurkat. This product provides a loss-of-function model for the adaptor protein CD2AP, which plays a critical role in T cell receptor (TCR) signaling and cytoskeletal regulation. The polyclonal nature of the knockout population enables examination of heterogeneous gene disruption, closely resembling physiological variation, without the isolation of monoclonal lines, making it a versatile tool for studying CD2AP-dependent processes.
Jurkat cells are a widely accepted suspension cell model originally established from a patient with T cell leukemia. They robustly respond to TCR stimulation and are extensively used to dissect early T cell activation events, immune synapse formation, and downstream signal transduction. Their well-characterized signaling network and ease of genetic manipulation make them an ideal host for CRISPR/Cas9-mediated gene disruption, allowing functional interrogation of adaptor proteins in a human T cell context.
CD2AP functions as a scaffold adaptor that links transmembrane receptors such as CD2 to the actin cytoskeleton. Upon TCR engagement, CD2AP is activated downstream of CD2 and interacts with the PI3K p85 subunit, Cbl, and endophilin, while also associating with nephrin and podocin in specialized cell types. It orchestrates actin polymerization through Rac1 and the WAVE complex, and enhances PI3K-AKT signaling. Upstream regulators include TCR stimulation via CD3 and CD28, and the representative pathway involves ZAP70, LAT, SLP-76, and Vav, which converge on CD2AP to modulate cytoskeletal remodeling mediated by the Arp2/3 complex.
In Jurkat T cells, CD2AP knockout impairs TCR-mediated activation, evidenced by reduced surface expression of early activation markers CD69 and CD25. Loss of CD2AP disrupts actin dynamics at the immune synapse, attenuates PI3K-AKT signaling, and compromises receptor endocytosis. These cellular phenotypes mirror aspects of CD2AP-related pathologies, including T cell malignancies, Alzheimer??s disease, and focal segmental glomerulosclerosis (FSGS), where adaptor dysfunction contributes to aberrant signaling and cytoskeletal organization.
These polyclonal knockout cells are suitable for a range of applications, including analysis of TCR signaling kinetics via phospho-ZAP70 flow cytometry, validation of CD2AP interaction partners by co-immunoprecipitation, and visualization of actin cytoskeleton reorganization by immunofluorescence. They support endocytosis assays, proliferation and apoptosis studies, and high-throughput drug screening for immunomodulatory compounds. For further details on validation and customization options, please contact Ascent Research.
