The mitochondrion is the “powerhouse of the cell”. It is also a signaling hub that regulates cell growth, survival and stress responses. Mitochondrial dysfunction has been observed in a variety of disease conditions. There is, however, no therapy available up to date. We recently revealed a critical role of mitochondrial NAD(H) redox state in protein modification and stress tolerance. We are developing technology platforms with collaborators to investigate subcellular redox states and protein-protein interactions using novel biosensors and quantitative proteomics. Both basic and clinical research are ongoing to seek the molecular targets and therapeutic applications.
Mitochondria Complex I Deficiency Increases Protein Acetylation and Accelerates Heart Failure.
Karamanlidis G, Lee CF, Garcia-Menendez L, Kolwicz Jr. SC, Suthammarak W, Gong G, Sedensky MM, Morgan PG, Wang W, Tian R. Cell Metab. 2013 Aug 6;18(2):239-50. PMCID: PMC3779647.
Normalization of NAD+ Redox Balance as a Therapy for Heart Failure.
Lee CF, Chavez J, Garcia-Menendez L, Choi YS, Roe N, Chiao YA, Edgar J, Goo YA, Goodlett, Bruce J, Tian R. Circulation 2016 Sep 201; 34(12):883-94. doi: 10.1161/CIRCULATIONAHA.116.022495. Epub 2016 Aug 3. PMID:27489254
Mitochondrial Protein Interactome Elucidated by Chemical Cross-Linking Mass Spectrometry