Photo of Michael Forte, Ph.D.

Michael Forte Ph.D.

  •      (503) 494-5454
    • Professor Vollum Institute
    • Senior Scientist Vollum Institute
    • OHSU Knight Cancer Institute School of Medicine
    • OHSU Knight Cardiovascular Institute School of Medicine
    • Program in Molecular and Cellular Biosciences School of Medicine
    • Jungers Center for Neurosciences Research

Michael Forte, Ph.D. is a senior scientist at the Vollum Institute and a professor in the Departments of Molecular and Medical Genetics, Cell, Developmental and Cancer Biology, and Physiology and Pharmacology in the School of Medicine. After being awarded his B.S. from the University of Notre Dame in 1973, Forte earned his Ph.D. in Genetics from the University of Washington in 1978. He then went to the University of Wisconsin for four years of postdoctoral research in Molecular Biology. In 1982, Forte became an assistant professor at Case Western Reserve University, where he remained until his appointment to the Vollum in 1986.

Dr. Forte's lab is investigating the role of mitochondria in the overall regulation of cellular calcium.

Areas of interest

  • mitochondria
  • ischemic cell death
  • neurodegeneration
  • cardiac disease
  • small molecule therapies

Education

  • B.S., University of Notre Dame 1973
  • Ph.D., University of Washington 1978

Memberships and associations

  • Genetics Society of America
  • Federation of American Societies for Experimental Biology
  • Biophysical Society

Publications

  • "The unique histidine in OSCP subunit of F-ATP synthase mediates inhibition of the permeability transition pore by acidic pH." EMBO Reports  In: , Vol. 19, No. 2, 01.02.2018, p. 257-268.
  • "Ca binding to F-ATP synthase β subunit triggers the mitochondrial permeability transition." EMBO Reports  In: , Vol. 18, No. 7, 01.07.2017, p. 1065-1076.
  • "Commentary : The m-AAA protease associated with neurodegeneration limits MCU activity in mitochondria." Frontiers in Physiology  In: , Vol. 7, No. NOV, 583, 25.11.2016.
  • "N-Phenylbenzamides as Potent Inhibitors of the Mitochondrial Permeability Transition Pore." ChemMedChem  In: , Vol. 11, No. 3, 04.02.2016, p. 283-288.
  • "Shutting down the pore : The search for small molecule inhibitors of the mitochondrial permeability transition." Biochimica et Biophysica Acta - Bioenergetics  In: , 09.01.2016.
  • "The mitochondrial permeability transition pore : Channel formation by F-ATP synthase, integration in signal transduction, and role in pathophysiology." Physiological Reviews  In: , Vol. 95, No. 4, 01.10.2015, p. 1111-1155.
  • "Discovery, Synthesis, and Optimization of Diarylisoxazole-3-carboxamides as Potent Inhibitors of the Mitochondrial Permeability Transition Pore." ChemMedChem In: , Vol. 10, No. 10, 01.10.2015, p. 1655-1671.
  • "F-ATPase of drosophila melanogaster forms 53-picosiemen (53-pS) channels responsible for mitochondrial Ca-induced Ca release." Journal of Biological Chemistry  In: , Vol. 290, No. 8, 20.02.2015, p. 4537-4544.
  • "Commentary : SPG7 is an essential and conserved component of the mitochondrial permeability transition pore." Frontiers in Physiology  In: , Vol. 6, No. NOV, 320, 2015.
  • "Channel formation by yeast F-ATP synthase and the role of dimerization in the mitochondrial permeability transition." Journal of Biological Chemistry  In: , Vol. 289, No. 23, 06.06.2014, p. 15980-15985.
  • "Regulation of the mitochondrial permeability transition pore by the outer membrane does not involve the peripheral benzodiazepine receptor (translocator protein of 18 kDa (TSPO))." Journal of Biological Chemistry  In: , Vol. 289, No. 20, 16.05.2014, p. 13769-13781.
  • "BH3-only proteins Noxa, Bik, Bmf, and Bid activate Bax and Bak indirectly when studied in yeast model." FEMS Yeast Research  In: , Vol. 13, No. 8, 12.2013, p. 747-754.
  • "Dimers of mitochondrial ATP synthase form the permeability transition pore." Proceedings of the National Academy of Sciences of the United States of America  In: , Vol. 110, No. 15, 09.04.2013, p. 5887-5892.
  • "Mitochondrial dysfunction and neurodegeneration in multiple sclerosis." Frontiers in Physiology  In: , Vol. 4 JUL, Article 169, 2013.
  • "Focal increases of axoplasmic Ca 2+, aggregation of sodium-calcium exchanger, N-type Ca 2+ channel, and actin define the sites of spheroids in axons undergoing oxidative stress." Journal of Neuroscience  In: , Vol. 32, No. 35, 29.08.2012, p. 12028-12037.
  • "Genetic inactivation of the p66 isoform of ShcA is neuroprotective in a murine model of multiple sclerosis." European Journal of Neuroscience  In: , Vol. 35, No. 3-4, 02.2012, p. 562-571.
  • "Genetic inactivation of mitochondria-targeted redox enzyme p66shcA preserves neuronal viability and mitochondrial integrity in response to oxidative challenges." Frontiers in Physiology  In: , Vol. 3 JUL, 2012, p. 1-9.
  • "Properties of Ca 2+ transport in mitochondria of Drosophila melanogaster." Journal of Biological Chemistry  In: , Vol. 286, No. 48, 02.12.2011, p. 41163-41170.
  • "BH3-only protein Bim inhibits activity of antiapoptotic members of Bcl-2 family when expressed in yeast." FEBS Letters  In: , Vol. 585, No. 17, 02.09.2011, p. 2709-2713.
  • "Mitochondrial calcium and its regulation in neurodegeneration induced by oxidative stress." European Journal of Neuroscience  In: , Vol. 34, No. 3, 08.2011, p. 437-447.
  • "Reconstitution of interactions of Murine gammaherpesvirus 68 M11 with Bcl-2 family proteins in yeast." Biochemical and Biophysical Research Communications  In: , Vol. 407, No. 4, 22.04.2011, p. 783-787.
  • "Activation of the mitochondrial permeability transition pore modulates Ca2+ responses to physiological stimuli in adult neurons." European Journal of Neuroscience  In: , Vol. 33, No. 5, 03.2011, p. 831-842.
  • "Cyclophilin D in mitochondrial pathophysiology." Biochimica et Biophysica Acta - Bioenergetics  In: , Vol. 1797, No. 6-7, 06.2010, p. 1113-1118.
  • "The mitochondrial permeability transition from yeast to mammals." FEBS Letters  In: , Vol. 584, No. 12, 06.2010, p. 2504-2509.
  • "Cyclophilin D modulates mitochondrial F0F1-ATP synthase by interacting with the lateral stalk of the complex." Journal of Biological Chemistry  In: , Vol. 284, No. 49, 04.12.2009, p. 33982-33988.
  • "GM1-Ganglioside Accumulation at the Mitochondria-Associated ER Membranes Links ER Stress to Ca2+-Dependent Mitochondrial Apoptosis." Molecular Cell  In: , Vol. 36, No. 3, 13.11.2009, p. 500-511.
  • "Developmental shift of cyclophilin D contribution to hypoxic-ischemic brain injury." Journal of Neuroscience  In: , Vol. 29, No. 8, 25.02.2009, p. 2588-2596.
  • "Axonal degeneration in multiple sclerosis : The mitochondrial hypothesis." Current Neurology and Neuroscience Reports  In: , Vol. 9, No. 5, 2009, p. 411-417.
  • "Genetic ablation of cyclophilin D rescues mitochondrial defects and prevents muscle apoptosis in collagen VI myopathic mice." Human Molecular Genetics  In: , Vol. 18, No. 11, 2009, p. 2024-2031.
  • "Phosphate is essential for inhibition of the mitochondrial permeability transition pore by cyclosporin A and by cyclophilin D ablation." Journal of Biological Chemistry  In: , Vol. 283, No. 39, 26.09.2008, p. 26307-26311.

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