IPMK Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma line. This product provides a heterogeneous pool of IPMK-disrupted cells, enabling functional studies without clonal selection artifacts. The polyclonal format recapitulates population-level gene perturbation, offering a practical model for dissecting IPMK-dependent biological processes.
HeLa cells are an HPV18-positive, immortalized epithelial cell line originally isolated from a cervical carcinoma. Widely used in cancer biology, these cells exhibit robust growth and express key oncogenic signaling components. Their well-annotated genome and responsiveness to growth factors make them an ideal host for interrogating tumor-relevant pathways.
IPMK encodes an inositol polyphosphate multikinase that catalyzes the generation of IP4, IP5, IP6, and the critical lipid second messenger PIP3. Through PIP3 production, IPMK directly activates AKT, subsequently stimulating mTORC1 to promote cell growth and survival. Additionally, IPMK physically binds and stabilizes p53, mediated by interactions with CK2 and HSP90. Upstream regulators such as EGF, IGF-1, insulin, and PI3K converge on IPMK, while downstream targets include PDK1, FOXO transcription factors, and S6K, integrating metabolic and survival signals. Other interacting factors include Raptor, PTEN, and GSK3??, positioning IPMK at the intersection of growth factor, nutrient, and tumor suppressor networks.
Within the HeLa cancer context, IPMK disruption attenuates PI3K-AKT-mTOR signaling, potentially impacting the proliferative and metabolic advantages driven by HPV18 oncoproteins. This model allows dissection of p53-dependent and independent IPMK functions, revealing how inositol phosphate metabolism modulates tumor cell behavior. It also facilitates exploration of links between cellular energetics, insulin signaling, and Wnt pathways, with implications for cancer, metabolic disorders, and neurodegeneration.
Researchers can utilize these cells for Western blot analysis of phospho-AKT (S473), total AKT, p53, and phospho-S6, as well as RT-qPCR to confirm gene disruption. Functional assays include cell viability (MTT/CCK-8), apoptosis (Annexin V/PI), co-immunoprecipitation of IPMK complexes, and colony formation. Inositol phosphate profiling by mass spectrometry enables detailed metabolic studies. The polyclonal population is suited for drug target validation and high-throughput screening of pathway modulators. For technical inquiries or assay customization, please contact Ascent Research.
