The KIAA1217 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KIAA1217 gene in the near-haploid HAP1 cell line. This product provides a heterogeneous pool of cells with disrupted KIAA1217 alleles, generated via CRISPR/Cas9-mediated gene disruption, and is suitable for studies requiring a loss-of-function model without clonal isolation. The polyclonal format retains a representative range of genetic backgrounds and editing events, enabling robust population-level analyses in functional genomics and cancer biology.
HAP1 cells are a male-derived, near-haploid human cell line originating from the KBM-7 chronic myeloid leukemia line. Their fibroblastoid morphology and near-haploid karyotype make them an ideal host for genetic manipulation, as the presence of a single allele for most genes simplifies knockout generation and downstream phenotypic characterization. Widely adopted in haploid genetic screens and functional genomics, HAP1 cells allow efficient loss-of-function studies and genotype-phenotype correlation across diverse signaling pathways.
KIAA1217 encodes a CRAL-TRIO domain-containing protein proposed to function as a Rho guanine nucleotide exchange factor (GEF), linking upstream signals to cytoskeletal reorganization. It is activated by growth factors such as EGF and TGF-??, and by integrin-mediated adhesion and mechanical cues. It interacts with RhoA and Rac1, promoting their GTP-bound states, thereby regulating downstream effectors including ROCK, LIMK, cofilin, and the Arp2/3 complex to drive actin polymerization and actomyosin contractility. KIAA1217 influences focal adhesion dynamics through FAK, paxillin, and vinculin, impacting adhesion and migration. Its loss impairs actin cytoskeletal integrity and focal adhesion assembly.
In the HAP1 cellular context, KIAA1217 knockout is anticipated to compromise actin filament organization and cell-substrate adhesion, leading to altered morphology, reduced migration, and possibly enhanced proliferation due to loss of tumor-suppressive constraints. The near-haploid HAP1 genome amplifies phenotypic consequences, providing a sensitive system to dissect KIAA1217??s roles in Rho GTPase signaling and cytoskeletal remodeling. This model is a powerful tool for investigating the cellular functions of a putative tumor suppressor in cancers such as colorectal, hepatocellular, breast, and lung malignancies.
Researchers can employ this polyclonal knockout population in a wide array of assays, including western blotting, immunofluorescence for actin, scratch wound migration, proliferation and colony formation assays, adhesion assays, and Rho activity G-LISA. It supports applications in cancer biology, drug target validation, haploid genetic screens, and tumor suppressor gene analysis. This product enables rigorous exploration of actin-dependent processes and adhesion signaling. For further details, please contact Ascent Research.
