The DPYSL5 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the Jurkat T-lymphocyte background, generated to disrupt the human DPYSL5 gene (also known as CRMP5). This polyclonal product provides a genetically mixed pool of Jurkat cells harboring targeted gene disruption, enabling loss-of-function studies without clonal isolation or selection of a single knockout genotype. The product is suitable for applications requiring a heterogeneous population that retains the general characteristics of the parental Jurkat line while abolishing DPYSL5 expression.
The Jurkat cell line is an immortalized human T lymphocyte line originally derived from the peripheral blood of a patient with T-cell acute lymphoblastic leukemia. Widely utilized as a model for T-cell leukemia and T-cell signaling, Jurkat cells display key features of T-cell activation, including expression of the T-cell receptor (TCR) and downstream signaling components. Their robust growth in suspension culture and well-characterized signaling pathways make them a versatile platform for studying immune cell biology, cytoskeletal regulation, and cancer-related processes.
DPYSL5 encodes collapsin response mediator protein 5 (CRMP5), a member of the CRMP family that mediates semaphorin signal transduction, particularly Semaphorin 3A signaling through Plexin A and Neuropilin-1 receptor complexes. DPYSL5 functions downstream of semaphorin-plexin-neuropilin engagement, where it is phosphorylated and regulated by kinases such as Fyn tyrosine kinase, Cdk5, and GSK-3??. At the molecular level, DPYSL5 interacts with tubulin and other CRMP family proteins (e.g., DPYSL2/CRMP2) to modulate microtubule polymerization dynamics and actin cytoskeleton reorganization. Through these interactions, DPYSL5 influences RhoA signaling, cell morphology, and processes such as neurite outgrowth and growth cone collapse. In T cells, analogous cytoskeletal remodeling pathways are thought to govern cell polarization, migration, and immunological synapse formation.
The Jurkat T-cell model provides a unique system to interrogate the largely uncharacterized role of DPYSL5 in lymphocyte biology. While CRMP5 has been extensively studied in neuronal contexts, evidence suggests it may impact immune cell migration and morphology through conserved cytoskeletal regulatory mechanisms. The DPYSL5 knockout Jurkat polyclonal cells allow investigators to examine how loss of CRMP5 affects T-cell shape, adhesion, and directed movement, as well as potential crosstalk with TCR signaling. This model may also serve as a tool to explore the intersection of semaphorin-mediated guidance cues and immune cell function, offering insights into T-cell trafficking and disease states such as leukemia dissemination.
Typical research applications include, but are not limited to, characterization of DPYSL5-dependent changes in T-cell migration using Transwell assays, immunofluorescence-based analysis of microtubule and F-actin organization, and co-immunoprecipitation to confirm disrupted protein interactions, for example with tubulin or CRMP2. Additionally, the product can be employed to model neurodevelopmental disorder pathways in an immune cell context, investigate semaphorin signaling in tumor immunity, and study mechanisms of cancer cell motility relevant to metastasis. A wide range of downstream assays such as Western blotting for DPYSL5 protein validation, RT?qPCR to confirm transcript loss, and flow cytometry for activation markers can be integrated. For detailed product specifications, validation data, or technical support, please contact Ascent Research.
