Japan-Flag Korea-Flag China-Simplified-Flag China-Traditional-Flag  

Conference Menu

Day 1
Day 2
Download Brochure
Hotel & Travel
Sponsor & Exhibit
Request Brochure
Exhibit Contract

Book Offer!

Be one of the first ten registrants and receive a free copy of "The Science of Fitness," co-authored by legendary cyclist, three time Tour de France champion, and Mitochondrial Myopathy sufferer Greg LeMond and Mark Horn, MD.


Media Partners: 

Bentham Science Logo 

Bio-IT World Large 

Clinical Informatics News 


Genomeweb Logo 

Insight Pharma Reports 




Science AAAS 

The Scientist 

Thursday, March 19

Day 1 | Day 2 | Brochure  

8:00 am Short Course Registration

9:00 am – 12:00 pm SC1: Drug-Induced Mitochondrial Toxicity*

Chair: Yvonne Will, Ph.D., Senior Director & Head, Science and Technology Strategy, Drug Safety Research and Development, Pfizer R&D

Kendall B. Wallace, Ph.D., Professor, Biochemistry & Molecular Biology, University of Minnesota-Duluth

Rick G. Schnellmann, Ph.D., Professor, College of Pharmacy, Medical University of South Carolina

Mitochondria produce almost all the energy in cells, but also chronically expose the cell to cytotoxic free radicals. Mitochondrial disease and toxicity is a rapidly advancing field and the consequences of mitochondrial impairment should be appreciated by scientists in all disciplines. Numerous widely prescribed therapeutics can undermine mitochondrial function by interfering with DNA replication or expression, and more acutely, by uncoupling or inhibiting oxidative phosphorylation, leading to organ dysfunction and damage. This course will review fundamental concepts of mitochondrial biology and the many different mechanisms by which xenobiotics interfere with mitochondrial function. Both common and novel in vitro screening approaches will be described as well as lectures on mitochondrial dysfunction in the kidney, liver and heart.

* Separate registration required

1:00 Registration for Main Conference

2:00 Chairperson’s Opening Remarks

Elizabeth Lamb, Senior Conference Director, CHI

2:10 KEYNOTE PRESENTATION: Genetic Approaches to Identify Mitochondria-to-Nucleus Retrograde Targets Involved in Drug Toxicity

Keshav K. Singh, Ph.D., Departments of Genetics, Pathology, and Environmental Health; Center for Free Radical Biology, Center for Aging and UAB Comprehensive Cancer Center, University of Alabama at Birmingham

Mitochondria contain multiple copies of mtDNA, varying from 100-1000 copies per cell among different tissues. mtDNA content is reduced by a variety of drugs resulting in toxicity. We have developed genetic approaches to identify nuclear targets involved in retrograde signaling involved in communicating the mitochondrial state to the nucleus, resulting in altered nuclear gene expression, cell physiology, and metabolism mediating drug toxicity.


2:50 Next-Generation Mitochondrial Medicine Platform: Integrated Bioenergetic Phenotyping in Oncology as a Case Study

Anne Diers, Ph.D., Program Leader, Cancer Biology, Berg

A next-generation mitochondrial medicine platform was developed that allows for identification of unique bioenergetic facets that predict cellular responses to stress (e.g., therapeutics, microenvironmental conditions). Using whole-cell integrated energy metabolism parameters coupled with mitochondrial substrate-level oxidation measurements, predictive phenotypic signatures for anti-cancer responses can be identified and molecular adaptive therapy strategies devised. Here, we report the use of this approach to identify the phenotypic signature for sensitivity to BPM 31510, an ubidecarenone-containing formulation that alters mitochondrial metabolism currently in clinical trials for treatment of solid tumors, and highlight the clinical correlates from patients treated with this compound.

3:20 AIF Mediates Cell Survival, but Not Death, in Lymphocytes by Regulating Complex I Integrity

Sandra Milasta, Ph.D., Staff Scientist, Immunology, St. Jude Children’s Research Hospital

Apoptosis inducing factor (AIF) is a mitochondrial inter-membrane space protein initially described to mediate cell death that proceeds in the absence of caspase activity. More recent studies revealed that AIF is required for the efficient assembly of complex I of the respiratory chain and thus plays a role in maintaining normal oxidative phosphorylation (OXPHOS).  Thymocytes and B cells lacking AIF displayed normal caspase-dependent and –independent cell death. These studies suggest that the primary role of AIF in lymphocytes relates to complex I function and not to mediating cell death. Therefore, a cell`s dependence on AIF is dictated by its reliance on OXPHOS to generate ATP.

3:50 Refreshment Break in the Exhibit Hall with Poster Viewing

4:30 A New Answer to an Old Problem: The Energization of Brain Mitochondria is Regulated by Cytosolic Calcium via the “Mitochondrial Gas Pedal” and Does Not Require the Mitochondrial Ca Uptake via the Ca Uniporter

Frank Gellerich, Ph.D., Head, Bioenergetic Laboratory, Neurological University Hospital, Otto-von Guericke-University Magdeburg

In contrast to the classic opinion that the mitochondrial activity is regulated by Ca2+ after its uptake via the Ca2+ uniporter, we found that the energization of mitochondria is realized by the “mitochondrial gas pedal” and is strongly regulated by cytosolic Ca2+ but not by matrix Ca2+. The “mitochondrial gas pedal” realizes the mitochondrial pyruvate supply via oxidizing reactions of pyruvate formation as LDH and GAPDH both generating NADH together with the malate/aspartate shuttle (MAS) or glycero-3-phosphate shuttle (G3PS) both oxidizing NADH. Our model predicts that at sufficiently low Ca2+cyt mitochondria (e.g. in neurons and red muscle) switch into a substrate-limited state preventing dangerous large ROS.

5:00 Mitochondrial Immobilization Mediated by Syntaphilin Facilitates Survival of Demyelinated Axons

Bruce D. Trapp, Ph.D., Department Head, Department of Neurosciences, Lerner Research Institute, Cleveland Clinic

The purpose of this study was to define the roles of mitochondrial volume and distribution in axonal degeneration following acute CNS demyelination. We show that the axonal mitochondrial volume increase following acute demyelination of WT CNS axons does not occur in demyelinated axons deficient in syntaphilin, an axonal molecule that immobilizes stationary mitochondria to microtubules. These findings were supported by time-lapse imaging of WT and syntaphilin-deficient axons in vitro. These results support the concept that syntaphilin-mediated immobilization of mitochondria to microtubules is required for the volume increase of axonal mitochondria following acute demyelination and protects against axonal degeneration in the CNS.

5:30 Welcome Reception in the Exhibit Hall with Poster Viewing

6:30 End of Day 1

Day 1 | Day 2 | Brochure