期刊
JOURNAL OF CELL BIOLOGY
卷 217, 期 3, 页码 813-822出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201706157
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资金
- National Institutes of Health [CA126792, CA201849, CA188404, AG057462, HL123340, DK093668, DK103788, AI121244]
- Department of Defense Breast Cancer Research Program [W81XWH-11-1-0130]
- Samuel Waxman Cancer Research Foundation
- QB3/Calico Longevity Fellowship
- Cystic Fibrosis Foundation Pilot Grant
- Howard Hughes Medical Institute
- Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Diseases Award
- Rainin Foundation Innovator Award
- Merieux Institute Advanced Research Grant
- Colton Center Pilot Grant
- Stony Wold-Herbert Fund
The identification of conserved autophagy-related proteins (ATGs) that mediate bulk degradation of cytosolic material laid the foundation for breakthroughs linking autophagy to a litany of physiological processes and disease conditions. Recent discoveries are revealing that these same ATGs orchestrate processes that are related to, and yet clearly distinct from, classic autophagy. Autophagy-related functions include secretion, trafficking of phagocytosed material, replication and egress of viral particles, and regulation of inflammatory and immune signaling cascades. Here, we define common processes dependent on ATGs, and discuss the challenges in mechanistically separating autophagy from these related pathways. Elucidating the molecular events that distinguish how individual ATGs function promises to improve our understanding of the origin of diseases ranging from autoimmunity to cancer.
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