Mammalian autophagy: core molecular machinery and signaling regulation

By Zhifen Yang, D. Klionsky. Current Opinion in Cell Biology, 2009

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Autophagy, a cellular catabolic pathway, is evolutionarily conserved from yeast to mammals. Central to this process is the formation of autophagosomes, double-membrane vesicles responsible for delivering long-lived proteins and excess or damaged organelle into the lysosome for degradation and reuse of the resulting macromolecules. In addition to the hallmark discovery of core molecular machinery components involved in autophagosome formation, complex signaling cascades controlling autophagy have also begun to emerge, with mTOR as a central but far from exclusive player. Malfunction of autophagy has been linked to a wide range of human pathologies, including cancer, neurodegeneration and pathogen infection. Here we highlight recent advances in identifying and understanding the core molecular machinery and signaling pathways that are involved in mammalian autophagy.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/f21c69f16481aa48d7e0a4b3c35556215de37a35

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Citations in the corpus

Glycogen and its metabolism: some new developments and old themes. (2012, background): “Autophagy comprises a family of processes initially described as a mechanism for random recycling of cellular materials under conditions of nutritional deprivation [214,215].”
Autophagy-deficient mice develop multiple liver tumors. (2011, background): “Among them, ATG genes that are required for macroautophagy are highly conserved in higher eukaryotes (Yang and Klionsky 2010).”
Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment (2013, background): “Several of the known tumor-suppressor genes (p53, PTEN, TSC1/TSC2) and tumor-associated genes (p21, AKT) also respectively stimulate or inhibit autophagy.(10,15) Autophagy is also induced by a variety of metabolic stresses such as endoplasmic reticulum (ER) stress, hypoxia, oxidative stress, express”
Activation of Autophagy by Inflammatory Signals Limits IL-1β Production by Targeting Ubiquitinated Inflammasomes for Destruction (2012, neutral): “Both starving cells of amino acids and treating cells with rapamycin trigger autophagy by inhibiting the nutrient and energy sensor mTO”
ER stress: Autophagy induction, inhibition and selection (2015, background): “Among those mechanisms, macroautophagy, the most widely studied mechanism, uses cytosolic double-membrane vesicles called autophagosomes to deliver cytosolic content to lysosomes.(67) In contrast, microautophagy, the least characterized mechanism, results in the isolation of cytoplasmic proteins and”
Differential regulation of distinct Vps34 complexes by AMPK in nutrient stress and autophagy (2013, background): “in Nutrient Stress and Autophagy”
The regulation of autophagy – unanswered questions (2011, background): “to autophagy induction, whereas ULK1 (or ULK2) still phosphorylates Atg13 and itself, and hyperphosphorylates FIP200 (Chang and Neufeld, 2010; Mizushima, 2010; Yang and Klionsky, 2010).”
Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “Autophagy also coincides with the proteasomal degradation of sequestome-1 (p62/SQSTM1) which binds autophagic target proteins and LC3-II (160, 174, 342) (FIGURE 7).”