4.8 Review

Organelle-Specific Initiation of Autophagy

期刊

MOLECULAR CELL
卷 59, 期 4, 页码 522-539

出版社

CELL PRESS
DOI: 10.1016/j.molcel.2015.07.021

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资金

  1. Ligue contre le Cancer (equipe labelisee)
  2. Agence National de la Recherche (ANR) - Projets blancs
  3. ANR
  4. ERA-Net for Research on Rare Diseases
  5. Association pour la recherche sur le cancer (ARC)
  6. Canceropole Ile-de-France
  7. Institut National du Cancer (INCa)
  8. Fondation Bettencourt-Schueller
  9. Fondation de France
  10. Fondation pour la Recherche Medicale (FRM)
  11. European Commission (Art-Force)
  12. European Research Council (ERC)
  13. LabEx Immuno-Oncology
  14. SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
  15. SIRIC Cancer Research and Personalized Medicine (CARPEM)
  16. Paris Alliance of Cancer Research Institutes (PACRI)
  17. Ligue contre le Cancer (equipe labelisee)
  18. Agence National de la Recherche (ANR) - Projets blancs
  19. ANR
  20. ERA-Net for Research on Rare Diseases
  21. Association pour la recherche sur le cancer (ARC)
  22. Canceropole Ile-de-France
  23. Institut National du Cancer (INCa)
  24. Fondation Bettencourt-Schueller
  25. Fondation de France
  26. Fondation pour la Recherche Medicale (FRM)
  27. European Commission (Art-Force)
  28. European Research Council (ERC)
  29. LabEx Immuno-Oncology
  30. SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
  31. SIRIC Cancer Research and Personalized Medicine (CARPEM)
  32. Paris Alliance of Cancer Research Institutes (PACRI)

向作者/读者索取更多资源

Autophagy constitutes a prominent mechanism through which eukaryotic cells preserve homeostasis in baseline conditions and in response to perturbations of the intracellular or extracellular microenvironment. Autophagic responses can be relatively non-selective or target a specific subcellular compartment. At least in part, this depends on the balance between the availability of autophagic substrates (offer'') and the cellular need of autophagic products or functions for adaptation (demand''). Irrespective of cargo specificity, adaptive autophagy relies on a panel of sensors that detect potentially dangerous cues and convert them into signals that are ultimately relayed to the autophagic machinery. Here, we summarize the molecular systems through which specific subcellular compartments-including the nucleus, mitochondria, plasma membrane, reticular apparatus, and cytosol-convert homeostatic perturbations into an increased offer of autophagic substrates or an accrued cellular demand for autophagic products or functions.

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