ATP synthesis assays using membranes from the indicated strains demonstrates that exAtpB exhibits faster kinetics based on luminescence measurement​
Invention Summary:
Mitochondrial disease impacts thousands of children, presenting a significant health problem. Many of these conditions occur due to ATP synthase mutations; the most prevalent being the ATP6 gene. Mutations in this region cause severe disorders including Leigh syndrome. Current treatments for mitochondrial diseases are insufficient, primarily due to the challenges in modifying the mitochondrial genome.
Rutgers researchers have synthetically engineered ATP6 protein, inspired by the glacier ice worm, to enhance mitochondrial function in cells affected by diseases such as Leigh syndrome. By incorporating a unique C-terminal extension from the ice worm's ATP6 protein into the human version, this innovation aims to significantly boost ATP synthase activity, offering a novel avenue for treatment.
Market Applications:
Advantages:
Publications:
• Dunkley, T., Shain, D.H., and Klein, E.A. A histidine-rich extension of the mitochondrial F0 subunit ATP6 from the ice worm Mesenchytraeus solifugus increases ATP synthase activity in bacteria. FEBS Letters (2025). https://doi.org/10.1002/1873-3468.15100
Intellectual Property & Development Status: Provisional application filed. Patent pending. Available for licensing and/or research collaboration. For any business development and other collaborative partnerships, contact: marketingbd@research.rutgers.edu
