ATP5MJ Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cervical adenocarcinoma cell line, engineered to disrupt the ATP5MJ gene. This product provides a heterogeneous pool of knockout cells for studying mitochondrial ATP synthase dysfunction without clonal selection artifacts. The polyclonal format preserves diverse genomic editing outcomes, enabling robust assessment of ATP5MJ-dependent phenotypes in a physiologically relevant cellular context.
Host HeLa cells are an HPV18-positive, aneuploid, and immortalized epithelial line in which the viral oncoproteins E6 and E7 inactivate the tumor suppressors p53 and Rb. These characteristics have established HeLa as a foundational model for cancer biology, virology, and cell signaling. The aneuploid genome and altered cell cycle control make this line particularly valuable for examining metabolic vulnerabilities in cancer.
ATP5MJ encodes a membrane subunit of mitochondrial ATP synthase (Complex V), essential for proton-driven ATP synthesis during oxidative phosphorylation. It contributes to the structural integrity of the F0 sector and is regulated by metabolic sensors including PGC-1??, NRF1, TFAM, and HIF-1??. The protein interacts directly with other synthase subunits such as ATP5F1A, ATP5F1B, ATP5O, ATP5IF1, ATP5MG, and ATP5MK, as well as MICOS complex components. Disruption of ATP5MJ compromises ATP synthase assembly, impairs electron transport chain coupling, and alters downstream AMPK signaling and mitochondrial membrane potential.
In the HeLa background, ATP5MJ knockout creates a model of defective oxidative phosphorylation that parallels the Warburg effect observed in many cancers. The resulting metabolic shift toward glycolysis is exacerbated by the host cell??s HPV-driven oncogenic program, making this system ideal for dissecting the interplay between viral transformation and mitochondrial bioenergetics. Reduced ATP output and elevated ROS generation can be used to probe mechanisms of metabolic adaptation and therapy resistance.
Research applications include cancer metabolism studies, mitochondrial dysfunction modeling, and drug resistance assays. Researchers can assess ATP synthase subunit expression by Western blot, measure ATP levels via luminescent assays, evaluate mitochondrial membrane potential with TMRE or JC-1, and analyze oxygen consumption using Seahorse respirometry. ROS detection with DCFDA, mtDNA copy number qPCR, galactose viability tests, and metabolomic profiling via LC?MS/GC?MS are also well?suited. This polyclonal knockout cell pool is a versatile tool for investigating therapeutic vulnerabilities in oxidative phosphorylation-dependent tumors. For inquiries, contact Ascent Research.
