The DPYSL5 Knockout HEK293T Polyclonal Cells product provides a polyclonal cell population generated by CRISPR/Cas9-mediated disruption of the human DPYSL5 gene in HEK293T cells. This knockout model offers a robust loss-of-function system for investigating the functional roles of DPYSL5 in signal transduction and cellular regulation. The polyclonal format ensures a heterogeneous pool of knockout cells, allowing bulk analysis without the selection of a single clonal isolate.
HEK293T cells, a derivative of HEK293 human embryonic kidney epithelium, stably express SV40 large T antigen. Originally transformed with adenovirus 5 DNA, these cells enable high-level protein expression and viral production. Their ease of transfection and well-characterized signaling pathways make them ideal for studying diverse biological processes.
DPYSL5 encodes CRMP5, a member of the collapsin response mediator protein family that controls axonal growth and guidance by modulating microtubule dynamics. In the semaphorin 3A pathway, ligand binding to neuropilin-1 and plexin-A1 activates the kinases Fyn, CDK5, and GSK-3??, which phosphorylate CRMP5 to suppress its microtubule assembly activity, thereby triggering growth cone collapse. CRMP5 also interacts with actin and tubulin, and multimerizes with related CRMP proteins (CRMP1, CRMP2, CRMP4) to orchestrate cytoskeletal remodeling. Additionally, CRMP5 participates in Reelin and Wnt signaling pathways implicated in neuronal development.
In HEK293T cells, this DPYSL5 polyclonal knockout provides a simplified platform to dissect CRMP5-specific functions without interference from neuronal background. The cells retain core semaphorin pathway components and allow analysis of CRMP5 phosphorylation, protein interactions, and microtubule-related phenotypes. High transfection efficiency enables complementation with mutant constructs for structure-function studies. The polyclonal nature avoids clonal artifacts and reflects population-level knockout effects.
This knockout product supports studies of semaphorin 3A/CRMP5 signaling, axon guidance, and CRMP family crosstalk. Typical assays include western blotting for total and phospho-CRMP5, co-immunoprecipitation with tubulin, immunofluorescence for microtubule organization, microtubule polymerization assays, and RhoA activation assays. It is also suitable for modeling paraneoplastic neurological syndromes associated with anti-CRMP5 autoantibodies and for drug screening in neuroregeneration or cancer contexts. For further information, please contact Ascent Research.
