Journal
CELL
Volume 176, Issue 1-2, Pages 11-42Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.09.048
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Funding
- NIH [RO1 CA109618, U19 AI109725]
- Cancer Prevention Research Institute of Texas (CPRIT) [RP120718]
- Fondation Leducq [15CBD04]
- Ligue contre le Cancer (equipe labelisee)
- Agence National de la Recherche (ANR) - Projets blancs
- ANR
- Association pour la recherche sur le cancer (ARC)
- Canceropole Ile-de-France
- Fondation pour la Recherche Medicale (FRM)
- European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR)
- European Research Council (ERC)
- Fondation Carrefour
- Inserm (HTE)
- Institut Universitaire de France
- LabEx Immuno-Oncology
- RHU Torino Lumiere
- Seerave Foundation
- SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
- SIRIC Cancer Research and Personalized Medicine (CARPEM)
- Institut National du Cancer (INCa)
- Chancelerie des universites de Paris (Legs Poix)
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The lysosomal degradation pathway of autophagy plays a fundamental role in cellular, tissue, and organismal homeostasis and is mediated by evolutionarily conserved autophagy-related (ATG) genes. Definitive etiological links exist between mutations in genes that control autophagy and human disease, especially neurodegenerative, inflammatory disorders and cancer. Autophagy selectively targets dysfunctional organelles, intracellular microbes, and pathogenic proteins, and deficiencies in these processes may lead to disease. Moreover, ATG genes have diverse physiologically important roles in other membrane-trafficking and signaling pathways. This Review discusses the biological functions of autophagy genes from the perspective of understanding-and potentially reversing-the pathophysiology of human disease and aging.
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