The ARHGAP18 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HAP1 cells harboring a disruption of the ARHGAP18 gene. This product provides a loss-of-function model to study ARHGAP18, a GTPase-activating protein (GAP) for Rho family GTPases. The polyclonal knockout format ensures a heterogeneous population with CRISPR/Cas9-mediated gene disruption, enabling robust functional studies without clonal isolation. This model is designed for researchers investigating ARHGAP18-dependent cellular processes in a near-haploid human cell background.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. It maintains a predominantly haploid chromosome complement, making it especially valuable for knockout studies as only one allele needs to be disrupted for complete loss of function. HAP1 cells exhibit adherent growth and retain key signaling pathways of hematopoietic cells. Their neoplastic origin and haploid nature make them a versatile platform for functional genomics, high-throughput genetic screens, and mechanistic cancer research.
ARHGAP18 functions as a GAP that stimulates GTP hydrolysis on RhoA, thereby inactivating this small GTPase. Through this activity, ARHGAP18 regulates actin cytoskeleton dynamics, cell migration, and adhesion. The protein is integrated into VEGF signaling, acting downstream of VEGFR2 to modulate RhoA-ROCK-MLC-mediated contractility and focal adhesion turnover. ARHGAP18 interacts with CDC42EP3/Borg2 and septins, and its activity leads to reduced actin stress fiber formation and focal adhesion kinase (FAK)/paxillin signaling. Thus, ARHGAP18 acts as a negative regulator of RhoA-driven cytoskeletal remodeling, influencing cell motility and angiogenic responses.
In the HAP1 context, ARHGAP18 disruption allows dissection of RhoA-dependent processes critical for leukemia cell biology and angiogenesis. Because HAP1 cells are neoplastic, this knockout model enables investigation of ARHGAP18??s role in cancer cell migration and invasion. The near-haploid background simplifies genetic analysis, facilitating the study of signaling pathways where ARHGAP18 intersects with VEGF and RhoA. This polyclonal knockout population is well-suited for screening factors that modify ARHGAP18-dependent phenotypes, linking GTPase regulation to oncogenic behaviors.
Typical applications include western blotting to confirm target protein loss, RhoA activation assays (e.g., G-LISA) to assess GTPase activity, scratch wound migration and transwell invasion assays to evaluate cell motility, and immunofluorescence staining for F-actin to visualize cytoskeletal changes. The product also supports angiogenesis tube formation assays and haploid genetic screens to identify interacting partners or synthetic lethal interactions. For additional details or to request a quotation, please contact Ascent Research.
