The ARHGAP10 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ARHGAP10 gene in the HAP1 cell line. This loss-of-function model enables the study of ARHGAP10-dependent regulation of cytoskeletal dynamics, cell adhesion, and migration. As a polyclonal pool, it provides a heterogeneous knockout population suitable for functional screening and pathway analysis.
The host cell line HAP1 is a near-haploid human cell line derived from a male patient with chronic myeloid leukemia (CML). Its haploid karyotype facilitates unambiguous genotype?Cphenotype correlation, making it a powerful tool for functional genomics. The CML origin positions HAP1 as a relevant hematopoietic cancer model for investigating leukemogenesis and metastasis-associated processes.
ARHGAP10 encodes a Rho GTPase-activating protein (RhoGAP) that negatively regulates Rho family GTPases (RhoA, Rac1, Cdc42) by accelerating their intrinsic GTP hydrolysis. ARHGAP10 activity is modulated by growth factor receptors (e.g., EGFR, PDGFR) and integrin engagement, with Src kinase acting as a key upstream mediator. At focal adhesions, ARHGAP10 interacts with actin and vinculin, linking it to adhesion complexes. Inactivation of Rho GTPases by ARHGAP10 suppresses downstream effectors including ROCK, PAK, and LIMK, thereby reducing cofilin-mediated actin polymerization and stabilizing the cytoskeleton.
Knockout of ARHGAP10 in HAP1 cells removes this negative regulation, leading to sustained Rho signaling, enhanced actin dynamics, and increased migratory capacity. Given the CML background, these phenotypic changes are directly relevant to aberrant adhesion and invasion mechanisms observed in leukemia progression. The haploid nature of HAP1 ensures that observed phenotypes are unambiguously linked to ARHGAP10 loss, providing a clean genetic model for dissecting Rho GTPase signaling in cancer.
Research applications include functional genomics screens, cancer cell migration and invasion studies, and Rho GTPase signaling pathway analysis. Representative assays comprise Rho activity pull-downs, western blotting for phosphorylated effectors, Transwell migration assays, immunofluorescence for F-actin, and co-immunoprecipitation of interacting partners. The model is also suitable for drug target validation and phenotypic screening with Rho pathway inhibitors. For further information or to request a quote, please contact Ascent Research.
