Journal
TRENDS IN CELL BIOLOGY
Volume 27, Issue 6, Pages 430-440Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2016.12.002
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Funding
- NIH [R01GM113188, R01DK105393]
- Juvenile Diabetes Research Foundation [1-SRA-2014-251-Q-R]
- American Diabetes Association (ADA) [1-12-CD-04, R01AI083252, R01AI064296, R01DK48280, R01DK40344, R01DK111174]
- University of Michigan Protein Folding Diseases Initiative
- Junior Faculty and Career Development Awards from the ADA
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Many human diseases are associated with mutations causing protein misfolding and aggregation in the endoplasmic reticulum (ER). ER-associated degradation (ERAD) is a principal quality-control mechanism responsible for targeting misfolded ER proteins for cytosolic degradation. However, despite years of effort, the physiological role of ERAD in vivo remains largely unknown. Several recent studies have reported intriguing phenotypes of mice deficient for ERAD function in specific cell types. These studies highlight that mammalian ERAD has been designed to perform a wide-range of cell-type-specific functions in vivo in a substrate-dependent manner.
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