TY - JOUR
T1 - Autophagy Receptors and Neurodegenerative Diseases
AU - Deng, Zhiqiang
AU - Purtell, Kerry
AU - Lachance, Veronik
AU - Wold, Mitchell S.
AU - Chen, Shi
AU - Yue, Zhenyu
N1 - Funding information:
This work was partially supported by NIH grant R01 NS060123 and CHDI contract (Z.Y.); Young One Thousand Talent Program of China (S.C.); China Scholarship Council Fellowship (Z.D.); CIHR postdoctoral fellowship (V.L.); we are thankful to all members of the Yue laboratory for the critical reading of the manuscript.
Publisher copyright:
© 2017 Elsevier Ltd.
PY - 2017/7
Y1 - 2017/7
N2 - Previously thought of as a nonselective digestion process, autophagy is now known to specifically degrade aggregated proteins and damaged cellular organelles through the action of autophagy receptors, which provides cellular quality control and maintains homeostasis. Autophagy receptors recognize and recruit specific cargoes to the autophagosome–lysosome pathway for degradation in ubiquitin-dependent and -independent manners, and their functions (in selective autophagy) are regulated by protein modifications, for example, phosphorylation and ubiquitination. Growing evidence has linked the genetic variants of autophagy receptors to neurodegenerative diseases and multiple experimental systems have validated their roles in modulating the disease process. Here, we review the recent advances in understanding the physiology and pathophysiology of autophagy receptors in selective autophagy, and discuss their potentials as therapeutic targets for neurodegenerative diseases.
AB - Previously thought of as a nonselective digestion process, autophagy is now known to specifically degrade aggregated proteins and damaged cellular organelles through the action of autophagy receptors, which provides cellular quality control and maintains homeostasis. Autophagy receptors recognize and recruit specific cargoes to the autophagosome–lysosome pathway for degradation in ubiquitin-dependent and -independent manners, and their functions (in selective autophagy) are regulated by protein modifications, for example, phosphorylation and ubiquitination. Growing evidence has linked the genetic variants of autophagy receptors to neurodegenerative diseases and multiple experimental systems have validated their roles in modulating the disease process. Here, we review the recent advances in understanding the physiology and pathophysiology of autophagy receptors in selective autophagy, and discuss their potentials as therapeutic targets for neurodegenerative diseases.
UR - https://www.scopus.com/inward/record.uri?eid=2-s2.0-85011296348&doi=10.1016%2fj.tcb.2017.01.001&partnerID=40&md5=c3e8cf3de367b4af598ee291af11d751
U2 - 10.1016/j.tcb.2017.01.001
DO - 10.1016/j.tcb.2017.01.001
M3 - Review article
C2 - 28169082
SN - 0962-8924
VL - 27
SP - 491
EP - 504
JO - Trends in Cell Biology
JF - Trends in Cell Biology
IS - 7
ER -