The DPYSL2 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DPYSL2 gene, which encodes collapsin response mediator protein 2 (CRMP2). This loss-of-function model enables investigation of CRMP2??s roles in cytoskeletal dynamics and cell migration. The polyclonal format, generated via CRISPR/Cas9-mediated gene disruption, provides a heterogeneous pool of edited cells suitable for pooled functional assays without clonal selection, maintaining genetic diversity while achieving effective target-gene disruption.
The host cell line, NCI-H1299, is a p53-deficient human lung adenocarcinoma cell line derived from a lymph node metastasis, widely used to model non-small cell lung adenocarcinoma. With p53 deficiency, these cells exhibit enhanced survival and genomic instability, providing a permissive environment to study gene-specific contributions to tumor behavior. Its high metastatic potential and adherent epithelial-like morphology make it an relevant system for studying cancer cell invasion and migration.
DPYSL2/CRMP2 is a phosphoprotein that regulates microtubule polymerization and actin cytoskeleton reorganization, acting downstream of Semaphorin 3A signaling via Neuropilin-1/Plexin-A receptors. Phosphorylation by GSK3?? and CDK5, and modulation by Fyn kinase and Rho kinase, alters CRMP2??s interactions with tubulin, actin, vimentin, kinesin light chain, and Cav2.2. These interactions facilitate microtubule stability, vesicular transport, and cell shape changes. Knockout of DPYSL2 therefore disrupts these molecular connections, impairing microtubule assembly, actin dynamics, cell migration, and invasion.
In the NCI-H1299 background, DPYSL2 is hypothesized to drive invasive properties, as the parental cells are highly metastatic. Loss of CRMP2 is expected to reduce migration and invasion, providing a model to dissect its contribution to metastasis. This knockout population enables comparative studies with the parental line or with pharmacological inhibitors of upstream regulators like GSK3??, to delineate CRMP2-specific functions in lung adenocarcinoma progression.
The product is suitable for functional assays such as wound healing, transwell invasion, immunofluorescence, western blotting, and tubulin polymerization assays. Research applications encompass cancer invasion and metastasis modeling, neurobiology studies on axon guidance and neuronal development, and drug target validation targeting the semaphorin?CCRMP2 axis or GSK3??-mediated phosphorylation. The polyclonal knockout format is especially useful for pooled screens and population-level analyses. For additional technical details, please contact Ascent Research.
