joint with Selective Autophagy
Organizer(s): Jodi Nunnari, Anu Suomalainen-Wartiovaara and Koji OkamotoDate: April 22 - 26, 2018
Location: Westin Miyako Kyoto, Kyoto, Japan
Mitochondria perform fundamental diverse functions in eukaryotic cells, including ATP production and ion and phospholipid homeostasis. They also serve as platforms to integrate signaling pathways and cellular processes, such as innate immunity and autophagy. Mitochondrial functions are tightly linked to mitochondrial form, which is established through coordinated machines that control dynamics, positioning, motility and mitochondrial DNA transmission. Contact sites between mitochondrial with diverse organelles have emerged as key and pervasive regulators of mitochondrial form and function. These contact sites, as well as metabolites, fully integrate mitochondria into the cell and organism. It is therefore not surprising that mitochondrial dysfunction has emerged as a key factor in a myriad of diseases, including neurodegenerative and metabolic disorders. This conference will provide a cutting-edge view of how mitochondrial form and function is controlled and how its myriad of functions impinge on health and disease.
We gratefully acknowledge additional support for this conference from:
We gratefully acknowledge the generous grant for this conference provided by:National Cancer Institute (NCI)
Grant No. 1R13CA228548-01
Funding for this conference was made possible (in part) by 1R13CA228548-01 from the National Institutes of Health. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.