James Franklin, Ph.D.

Pharmaceutical and Biomedical Sciences
Associate Professor

Pharmaceutical and Biomedical Sciences

  • Education

    Ph.D. Physiology, University of North Carolina at Chapel Hill 1990

    B.S. Zoology, North Carolina State University 1976

  • More About

    Dr. Franklin’s research is on the mechanisms underlying neuronal apoptosis with a focus on the basic cellular mechanism by which mitochondria contribute to this type of neuronal death, as well as the role of mitochondria in Alzheimer’s disease.

  • Honors, Awards, and Achievements

    Nominated as a candidate for Reynold’s Chair in Developmental Neuroscience, Biology Department, Wake Forest University, 2002

  • Affiliations
  • Research Interests

    Dr. Franklin’s research is on the mechanisms underlying neuronal apoptosis with a focus on the basic cellular mechanism by which mitochondria contribute to this type of neuronal death, as well as the role of mitochondria in Alzheimer’s disease. He is also studying drug discovery for treatment of filaria infections in humans, animals and plants in collaboration with Dr. Adrian Wolstenholme at the UGA Veterinary College.

  • Selected Publications

    Megan J. McManus and James L. Franklin* (2016) Dissociation of JNK Activation from Elevated Levels of Reactive Oxygen Species, Cytochrome c Release, and Cell Death in NGF-Deprived Sympathetic Neurons. Molecular Neurobiology. DOI 10.1007/s12035-016-0332-2.

    Ali A. Alshamrani, James L. Franklin, Aaron M. Beedle and Mandi M. Murph* (2016) Inhibiting Lactate Dehydrogenase A Enhances the Cytotoxicity of the Mitochondria Accumulating Antioxidant, Mitoquinone, in Melanoma Cells. Human Skin Cancer, Potential Biomarkers and Therapeutic Targets Chapter 6: 125-139.

    Kirkland, R. A. and Franklin, J. L. (2015). Bax and caspases regulate increased production of mitochondria-derived reactive species in neuronal apoptosis: Lack of A role for depletion of cytochrome c from the mitochondrial electron transport chain. Biochemistry and Biophysics Reports, 4, 158-168. doi:10.1016/j.bbrep.2015.09.004

    M. J. McManus, M. Murphy, and J.L. Franklin (2014). Mitochondria-derived reactive oxygen species mediate the progression of caspase-dependent and –independent neuronal death. Molecular and Cellular Neuroscience 63: 13-23.

    M. J. McManus, M. Murphy, and J.L. Franklin (2011).  The  mitochondria-targeted antioxidant, MitoQ, prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease. Journal of Neuroscience. 31: 15703-15715.

    J. L. Franklin. (2011). Redox regulation of the intrinsic pathway in neuronal apoptosis.Antioxidants and Redox Signaling, 15: 1437-48.

    R. A. Kirkland, G. M. Saavedra, B. S. Cummings, and J. L. Franklin. (2010). Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases.Journal of Neuroscience, 30: 16114-16127.

    D. J. Lomb, L. A. Desouza,  J. L. Franklin, and R. S. Freeman. (2009). Prolyl hydroxylase inhibitors depend on extracellular glucose and HIF-2a to inhibit cell death caused by NGF deprivation: evidence that HIF-2a has a role in NGF-promoted survival of sympathetic neurons. Molecular Pharmacology, 75: 198-209.

    B. Peterson, K. Stovall, P. T. Monian, J. L. Franklin, and B. S. Cummings. (2008). Alterations in phospholipid and fatty acid lipid profiles in primary neocortical cells during oxidant-induced cell injury. Chemico-Biological Interactions, 174: 163-176.

    R. A. Kirkland, G. M. Saavedra, and J. L. Franklin. (2007). Rapid activation of antioxidant defenses by nerve growth factor suppresses reaactive oxygen sepces during neuronal apoptosis: evidence for a role in cytochrome c redistribution. Journal of Neuroscience, 27: 11315-11326.

  • Grant Support

    Bax, Caspases, and Oxidative Stress in the Aging Brain” James Franklin (PI), NIH, R03AG051205-01, Aug 2015-Aug 2017