The IQGAP2 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in the HAP1 near-haploid human cell line, engineered for targeted IQGAP2 gene disruption. This format preserves genetic diversity across the population, enabling pooled functional genomics screens and phenotypic assays that benefit from averaging over multiple editing events while minimizing clonal bias.
HAP1 is a near-haploid cell line derived from the KBM-7 chronic myeloid leukemia model, characterized by a stable haploid karyotype in many chromosomes. This genetic simplicity makes it ideal for CRISPR-based functional genomics, as single-allele disruption directly produces a null phenotype, facilitating unambiguous genotype-phenotype correlations. The line is extensively used to study cancer-relevant pathways, including cell adhesion, migration, and signal transduction.
IQGAP2 is a scaffold protein that organizes actin dynamics, cell-cell adhesion, and migration by linking plasma membrane receptors to the cytoskeleton. It directly interacts with calmodulin, ??-catenin, E-cadherin, and actin, and modulates the small GTPases Rac1 and Cdc42. Upstream, IQGAP2 responds to Wnt ligands and EGF; downstream, it influences the ??-catenin/TCF transcriptional complex, ERK1/2, and PAK. Through APC binding, IQGAP2 participates in the ??-catenin destruction complex, integrating Wnt and adhesion signals. Knockout therefore disrupts actin assembly, weakens adherens junctions, and dysregulates ??-catenin-dependent transcription.
In the HAP1 haploid background, IQGAP2 knockout models its tumor suppressor roles in hepatocellular, gastric, and colorectal cancers. The absence of a second allele ensures robust phenotypic readouts of impaired adhesion, migration, and invasion. This system is well-suited for dissecting crosstalk between Wnt/??-catenin and Rac1/Cdc42 signaling, and for genome-wide screens to uncover synthetic lethal partners or drug sensitivities in IQGAP2-deficient tumors.
Key applications include tumor suppressor gene functional genomics, Wnt pathway analysis using ??-catenin luciferase reporters, and protein interaction mapping by co-immunoprecipitation. Compatible assays encompass western blotting, RT-qPCR, immunofluorescence, migration assays, and RNA-seq. This cell population accelerates drug target validation and metastasis research. For further technical inquiries, contact Ascent Research.
