The KIAA1191 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population targeting KIAA1191 in the HAP1 cell line. This loss-of-function model enables studies of KIAA1191, a putative oncogene that promotes proliferation and migration via PI3K/AKT signaling, in a near-haploid background suitable for genetic screens and drug discovery.
HAP1 cells are derived from the CML line KBM-7 and maintain a near-haploid karyotype with adherent fibroblast-like morphology. They retain the BCR-ABL oncogene, providing a model for kinase-driven signaling. The haploid genome simplifies functional genomics by ensuring unambiguous gene disruption, making HAP1 a preferred host for CRISPR knockout screens in oncogenesis, signal transduction, and drug resistance studies.
KIAA1191 functions as a putative oncogene by activating PI3K/AKT signaling. It is transcriptionally regulated by growth factor stimulation (EGF, HGF) and factors such as MYC and HIF1A, while promoting AKT1 phosphorylation and downstream mTOR and CCND1 activation, thereby enhancing proliferation and cell cycle progression. KIAA1191 also inhibits pro-apoptotic FOXO3. Interacting with ubiquitin-proteasome components (UBC, HSP90AA1, CUL3, PSMC1), it may modulate protein stability. In hepatocellular carcinoma and solid tumors, KIAA1191 upregulation is associated with aggressive phenotypes.
Disruption of KIAA1191 in HAP1 cells is expected to attenuate PI3K/AKT-driven proliferation and migration. The polyclonal knockout population, derived from a heterogeneous mix of edited cells, avoids clonal selection bias and is suited for high-throughput applications. The near-haploid background ensures that phenotypic effects are direct and unambiguous, allowing for robust correlation with molecular readouts such as phospho-AKT, cyclin D1, and mTOR activity.
This knockout product is ideal for functional genomics screens, drug target validation, and PI3K/AKT pathway studies. Representative assays include western blotting for phospho-AKT, cell proliferation (MTS, BrdU), migration/invasion assays, clonogenic survival, and drug sensitivity testing with PI3K inhibitors. Proteasome activity assays can assess ubiquitin-mediated signaling, and immunoprecipitation studies can explore KIAA1191 interactions with CUL3 and PSMC1. For further information, please contact Ascent Research.
