This product provides a CRISPR/Cas9-edited polyclonal knockout cell population of AGS human gastric adenocarcinoma cells with disrupted DPYSL5 gene expression, offering a heterogeneous loss-of-function model. The polyclonal format avoids biases of clonal selection and preserves genetic diversity for studying DPYSL5-dependent processes.
AGS cells, derived from a primary human gastric adenocarcinoma, serve as an established epithelial cancer model that retains proliferation, adhesion, and migration capabilities relevant to gastric carcinogenesis and metastasis. Their adherent morphology and well-characterized signaling landscape facilitate robust functional assays.
The DPYSL5 gene encodes collapsin response mediator protein 5 (CRMP5), a cytosolic phosphoprotein that functions at the intersection of semaphorin signaling, CRMP phosphorylation cascades, and Rho GTPase-mediated actin regulation. DPYSL5 is activated downstream of semaphorin-plexin receptor engagement and is phosphorylated by kinases including Cdk5, GSK3??, Rho kinase, and Fyn. It directly interacts with tubulin, actin, and other CRMP family members (CRMP1, CRMP2) and with the small GTPase RhoA. Through these interactions, DPYSL5 modulates microtubule dynamics, actin polymerization, and the cofilin pathway, ultimately governing cytoskeletal remodeling events such as growth cone collapse in neurons and cell migration in non-neuronal settings. The protein thus serves as a critical node in translating extracellular guidance cues into intracellular structural rearrangements.
In gastric cancer cells, DPYSL5 may promote migration and invasion by remodeling the actin and microtubule cytoskeleton. Knockout of DPYSL5 in AGS cells allows interrogation of its role in semaphorin-driven motility and metastasis-associated processes, circumventing clonal artifacts and better reflecting tumor heterogeneity.
This polyclonal knockout model supports a broad array of experimental workflows. Researchers can quantify DPYSL5 knockout efficiency via western blotting and RT-qPCR, examine functional consequences using transwell invasion, wound-healing migration, and cell viability assays, and visualize cytoskeletal alterations through immunofluorescence staining of microtubules (??-tubulin) and F-actin (phalloidin). Additional applications include semaphorin-induced collapse assays, cofilin activity assays, and drug sensitivity screens to discover synthetic lethal interactions or evaluate DPYSL5 as a druggable target. The cells are also amenable to studies investigating paraneoplastic neurological disorders and neurodevelopmental processes that intersect with DPYSL5 function. For further information, please contact Ascent Research.
