Chu Laboratory

Charleen T. Chu, MD, PhD

Charleen T. Chu, MD, PhD

Professor of Pathology and A. Julio Martinez Chair of Neuropathology
E-mail Website


My laboratory studies neuronal autophagy, protein kinases and mitochondrial pathobiology, with an emphasis on genetic and toxin models of Parkinson’s disease. I have >26 years of research experience with cell signaling, proteolysis and post-translational protein modifications, with additional expertise in immunochemical image analysis as a practicing neuropathologist. A central area of interest involves the regulation of mitochondrial function and turnover, studied with respect to: 1) toxins that affect mitochondrial function, and 2) kinases whose mutations cause familial Parkinson’s disease. Using cell biologic, molecular imaging and mass spectrometry approaches, my team identified novel phosphorylation sites of the major autophagy protein LC3, and of the mitochondrial transcription factor A (TFAM A), which modulate dendritic/post-synaptic neuron injury. We also discovered a basic mechanism by which damaged mitochondria are recognized by the autophagy system for clearance, based on redistribution of the inner membrane phospholipid cardiolipin. Current efforts are directed at the interplay of aging and calcium dysegulation in the LRRK2 model, mechanisms that regulate PINK1 processing and the subcellular compartmentalization of its function in neurons, and transcriptional (mtDNA and nDNA) mechanisms that underlie the catabolic-anabolic imbalance leading to neurodegeneration.

Dr. Charleen Chu is Professor in the Department of Pathology, University of Pittsburgh School of Medicine, where she holds the A. Julio Martinez Chair in Neuropathology. She is a Faculty Member of the Center for Neuroscience at the University of Pittsburgh, and a member of the Mitochondria, Aging and Metabolism working group. In addition, Dr. Chu is the Director of Ophthalmic Pathology and serves on the Medical Staff of several UPMC hospitals. Dr. Chu is Co-Director of the Pathologist Investigator Residency-Research Training Program.
Dr. Chu graduated summa cum laude from Harvard University with an AB degree in Biology in 1987. She went on to receive a PhD in Pathology-Biochemistry and an MD from Duke University in the years 1993 and 1994, respectively, in the Medical Scientist Training Program. Following graduation, Dr. Chu continued training in Anatomic Pathology, Neuropathology, and Ophthalmic Pathology fellowships at Duke University, receiving a Neuro-Oncology Postdoctoral Research Fellowship, before joining the faculty at the University of Pittsburgh in 1998.


AB Biology Harvard University 1987
PhD Pathology-Biochemistry Duke University 1993
MD Medicine Duke University 1994

Honors and awards

Among other honors, Dr. Chu was the recipient of the Julie Martin Mid-Career Award in Aging Research (Ellison Medical Foundation/AFAR, 2009-2013), the Emerging Female Scientist Award Winner of the 14th Annual Carnegie Science Awards (2010), the American Society for Clinical Investigation (ASCI) Honor Society (elected 2010), the ASIP Outstanding Investigator Award (2010), and the American Association of University Pathologists – The Pluto Society (elected 2014).


Selected Publications

CT Chu, J Ji, RK Dagda, JF Jiang, YY Tyurina, AA Kapralov, VA Tyurin, N Yanamala, IH Shrivastava, D Mohammadyani, KZQ Wang, J Zhu, J Klein-Seetharaman, K Balasubramanian, AA Amoscato, G Borisenko, Z Huang, AM Gusdon, A Cheikhi, EK Steer, R Wang, C Baty, S Watkins, I Bahar, H Bayır & VE Kagan (2013) Cardiolipin externalization to the outer mitochondrial membrane acts as an elimination signal for mitophagy in neuronal cells. Nature Cell Biol 15:1197-1205.PMC3806088. F1000 Cell Biology, Neuroscience and Microbiology Recommended.

RK Dagda, I Pien, R Wang, J Zhu, KZQ Wang, J Callio, TD Banerjee, RY Dagda & CT Chu (2014) Beyond the mitochondrion: cytosolic PINK1 remodels dendrites through Protein Kinase A. J Neurochem 128: 864-877. PMC3951661

E Plowey, JW Johnson, D Eisenberg, NM Valentino, YJ Liu & CT Chu. (2014) Mutant LRRK2 overexpression in cultured cortical neurons elicits glutamatergic synapse activity and excitotoxic neurite degeneration.Biochim. Biophys. Acta (Molecular Basis of Disease) 1842: 1596-1603. PMC4144018

VP Patel & CT Chu. (2014) Decreased SIRT2 activity leads to altered microtubule dynamics in oxidatively-stressed neuronal cells: Implications for Parkinson’s disease. Exp. Neurol. 257: 170-181. PMC4141566

KZQ Wang, J Zhu, RK Dagda, G Uechi, SJ Cherra III, AM Gusdon, M Balasubramani & CT Chu. (2014) ERK-mediated phosphorylation of TFAM downregulates mitochondrial transcription.Mitochondrion, 17: 132-140. PMC4134365

More publications

Lab Members

  • Jason Callio

    Research Specialist and Lab Manager

    Mouse models of Parkinsonian injury and neuroprotection

  • Jianhui Zhu, MD, PhD

    Research Assistant Professor

    Autophagy and mitophagy in toxin models of Parkinson's disease

  • Kent Zhi Qiang Wang, PhD

    Research Instructor

    Post-translational regulation of mitochondrial dynamics, molecular biology

  • Erin Steer

    Graduate Student

    PINK1 in neurite outgrowth and dendritogenesis

  • Manish Verma, PhD

    Postdoctoral Fellow

    Calcium dysregulation in mutant LRRK2 pathogenesis

  • Lily Francis

    Volunteer Scholar

    Regulation of mitochondria in iPSC-derived neurons