The ARHGAP17 Knockout HAP1 Polyclonal Cells product provides a pooled population of HAP1 cells carrying CRISPR/Cas9-mediated disruption of the ARHGAP17 gene. This polyclonal knockout cell population enables loss-of-function studies of the RhoGAP protein in a near-haploid human background, facilitating functional analysis of ARHGAP17 in actin dynamics, cell polarity, and tight junction regulation.
HAP1 cells are fibroblast-like, near-haploid human cells derived from the KBM-7 chronic myeloid leukemia line, with a male karyotype and disomy only for chromosome 8. Their hematopoietic progenitor origin and leukemic background offer a simplified genetic context for studying Rho GTPase signaling. The haploid genome allows efficient gene editing and clear genotype?Cphenotype coupling, making HAP1 a powerful system for functional genomics and cancer research.
ARHGAP17 encodes a RhoGAP that negatively regulates RAC1 and CDC42 by stimulating GTP hydrolysis, leading to actin depolymerization and cytoskeletal rearrangement. The protein is recruited to tight junctions via interactions with AMOT and PALS1 (MPP5) and associates with Patj, occludin, and ZO-1. Upstream inputs include SRC kinase, cell?Ccell contact, and TGF-beta. Downstream, ARHGAP17 influences the SRF pathway and the RAC1/CDC42?CPAK?CMLCK?Cactin contractility axis, thereby coordinating junctional stability and cell polarity.
In the HAP1 background, disruption of ARHGAP17 dysregulates RAC1 and CDC42 activity, altering actin organization, adhesion, and polarity. Given the leukemic origin, this model is relevant for exploring Rho GTPase defects in hematopoietic malignancies. The polyclonal population captures diverse editing outcomes, supporting robust population-level assays and reducing clonal artifacts. It is suitable for mechanistic studies of tight junction integrity and directional cell migration.
These ARHGAP17 knockout cells can be used in transwell migration/invasion, G-LISA, and immunofluorescence assays to dissect Rho GTPase-mediated processes. The model supports drug target validation for cancers such as hepatocellular carcinoma and breast cancer. Transcriptomic and proteomic profiling via RNA-seq and western blotting further extend its utility. For further information or to discuss custom applications, please contact Ascent Research.
