AGK Knockout HeLa Polyclonal Cells are a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the AGK gene in HeLa cells. This product provides a loss-of-function model for studying AGK in a widely used cervical adenocarcinoma epithelial cell line. The polyclonal population consists of a heterogeneous pool of edited cells, avoiding clonal selection artifacts and maintaining genetic diversity.
HeLa cells are an immortalized human cervical adenocarcinoma line that is HPV18 positive and extensively employed in cancer biology, signal transduction, and drug discovery. Their robust proliferation and well-characterized signaling networks make them an ideal host for dissecting the roles of lipid kinases such as AGK in cancer-relevant contexts.
AGK encodes a mitochondrial lipid kinase that catalyzes the phosphorylation of monoacylglycerol and diacylglycerol to produce lysophosphatidic acid (LPA) and phosphatidic acid (PA). These lipid mediators are pivotal for glycerophospholipid biosynthesis, mitochondrial cardiolipin remodeling, and lipid signaling cascades. AGK activity is regulated by upstream factors including PPAR??, PPAR??, and mitochondrial stress signals, and its products activate downstream pathways such as LPA receptor (LPAR)-mediated signaling and PA-dependent mTOR and PKC activation. Additionally, AGK interacts with the adenine nucleotide translocator ANT1 (SLC25A4) and the MICOS complex, linking lipid metabolism to mitochondrial architecture and function.
In HeLa cells, AGK knockout disrupts the synthesis of LPA and PA, leading to aberrant glycerophospholipid profiles and compromised mitochondrial integrity. This disruption is particularly relevant given HeLa cells?? dependence on lipid metabolism for membrane biogenesis and energy homeostasis. The model recapitulates key aspects of AGK-related mitochondrial dysfunction observed in Sengers syndrome and provides a tractable system to examine how AGK deficiency influences cancer cell proliferation, survival, and metabolic reprogramming.
Typical research applications include investigation of mitochondrial lipid homeostasis, modeling of Sengers syndrome-associated defects, analysis of LPA signaling in cancer, drug screening for mitochondrial disorders, and metabolic profiling studies. Researchers can assess downstream effects using western blotting, RT-qPCR, lipidomics, ATP assays, Seahorse metabolic flux analysis, immunofluorescence, flow cytometry, and LPA quantification. For further technical details and ordering information, please contact Ascent Research.
