The IMPA2 Knockout HAP1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human IMPA2 gene in the HAP1 cell line. This heterogeneous pool of knockout cells is generated by CRISPR/Cas9-mediated gene disruption, providing a robust loss-of-function model without clonal selection. The polyclonal format ensures broad coverage of knockout mutations across the target locus, making it suitable for functional studies of inositol monophosphatase 2 in a near-haploid genetic background.
HAP1 cells are a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. They display an adherent, fibroblast-like morphology and are extensively employed for genetic knockout studies and functional genomics screening. The haploid karyotype simplifies gene editing and reduces genetic complexity, allowing clear interpretation of knockout phenotypes. HAP1 cells provide a well-characterized platform for interrogating signaling pathways and disease mechanisms in a human context.
IMPA2 encodes inositol monophosphatase 2, which catalyzes dephosphorylation of inositol monophosphate to free inositol, a critical step in phosphatidylinositol recycling. This enzyme is inhibited by lithium, thereby reducing inositol availability and dampening downstream phosphoinositide signaling. IMPA2 functions downstream of phosphatidylinositol synthesis and upstream of PLCB1 and ITPR1, modulating calcium mobilization and PRKCA activation. Representative pathway components include PIK3CA, PLCB1, ITPR1, and PRKCA. IMPA2-mediated inositol regeneration is essential for maintaining IP3 and DAG second messenger levels.
In the HAP1 cell line, IMPA2 knockout models lithium’s effect on inositol metabolism and provides insights into bipolar disorder and major depressive disorder pathophysiology. The near-haploid genome ensures that loss of IMPA2 function produces clear phenotypic consequences, facilitating studies of calcium signaling and PKC pathways. This cellular model allows dissection of the phosphoinositide cycle under controlled genetic conditions, effectively mimicking lithium-induced inositol depletion without pharmacological intervention.
This IMPA2 knockout population supports diverse applications, including investigation of lithium’s mechanism of action, mood disorder disease modeling, and screening of IMPA2 inhibitors. Compatible assays include inositol monophosphatase activity measurements, Western blotting, RT-qPCR, intracellular inositol quantification, calcium imaging, phospho-PKC detection, and lithium dose-response studies. The polyclonal knockout cells offer a reproducible system for phosphoinositide signaling research and functional genomics. For additional information or custom inquiries, please contact Ascent Research.
