The ATPAF2 Knockout SK-HEP-1 Polyclonal Cells are a pooled population of SK-HEP-1 cells in which the ATPAF2 gene has been functionally disrupted using CRISPR/Cas9 genome editing. This polyclonal knockout product offers a cost-effective and robust loss-of-function model for investigating ATPAF2??s role in mitochondrial function. The mixed editing outcomes in the polyclonal pool minimize clonal artifacts, making it ideal for bulk biochemical and functional assays.
The SK-HEP-1 host cell line, derived from a liver adenocarcinoma patient??s ascitic fluid, is characterized by an endothelial-like phenotype and serves as a prominent model for liver sinusoidal endothelial cells. Its dual tumor and endothelial features provide a unique platform for studying mitochondrial biology in the context of hepatic cancer and endothelial dysfunction.
ATPAF2 is a mitochondrial matrix protein that functions as a dedicated assembly factor for the F1 catalytic domain of ATP synthase. It facilitates the insertion of ATP5A1 (??) and ATP5B (??) subunits into the F1 oligomer, cooperating with ATPAF1 and the chaperones HSP60 and HSP10. ATPAF2 expression is transcriptionally controlled by PGC-1??, NRF1, and NRF2, linking its regulation to mitochondrial biogenesis signaling. Disruption of ATPAF2 halts F1 assembly, resulting in crippled ATP synthase activity, diminished oxidative phosphorylation, reduced cellular ATP production, and loss of mitochondrial membrane potential.
Within SK-HEP-1 cells, the ATPAF2 knockout model is a valuable tool for exploring mitochondrial energy metabolism in a tumor-derived, endothelial-like environment. It is particularly suited for studying the molecular basis of diseases linked to ATP synthase deficiency, including mitochondrial complex V deficiency, Leigh syndrome, and lactic acidosis, as well as for investigating how mitochondrial impairment influences cancer cell metabolic reprogramming and endothelial cell function.
Typical research applications include mitochondrial ATP synthase assembly studies, mitochondrial disease modeling, cancer energy metabolism investigations, and drug screening for compounds targeting mitochondrial dysfunction. Common downstream assays include western blotting for ATP synthase subunit levels, ATP quantification, mitochondrial respiration analysis via Seahorse, complex V enzymatic activity measurement, immunoprecipitation of ATP synthase, and cell viability assessment under metabolic challenge. For additional product details and ordering information, please contact Ascent Research.
