Lysosomal Turnover, but Not a Cellular Level, of Endogenous LC3 is a Marker for Autophagy

By I. Tanida, Naoko Minematsu-Ikeguchi, T. Ueno, E. Kominami. Autophagy, 2005

1,150 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0b28240a0597c546157837f2fb3739b45c71db72

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Citations in the corpus

Two Beclin 1-binding proteins, Atg14L and Rubicon, reciprocally regulate autophagy at different stages (2009, background): “LC3-II on the autophagosome inner membrane is finally degraded on fusion of autophagosomes and lysosome”
Atg8 controls phagophore expansion during autophagosome formation. (2008, background): “When the phagophore matures into an autophagosome, some Atg8 is trapped inside and eventually degraded (Kirisako et al., 1999; Huang et al., 2000; Kabeya et al., 2000; Tanida et al., 2005).”
Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-β Levels in a Mouse Model of Alzheimer's Disease (2010, background): “Thus, decreased LC3-II levels may be observed as a consequence of robust induction of autophagic flux[43,44].”
Autophagosome formation: core machinery and adaptations (2007, background): “Additionally, the expression level and turnover rate of Atg8 is elevated, a phenomenon observed in other eukaryotes as wel”
Beclin 1 forms two distinct phosphatidylinositol 3-kinase complexes with mammalian Atg14 and UVRAG. (2008, neutral): “We then performed autophagy flux assay (Tanida et al., 2005; Mizushima and Yoshimori, 2007).”
Nutrient-dependent mTORC1 association with the ULK1-Atg13-FIP200 complex required for autophagy. (2009, background): “Because LC3-II inside autophagosomes is degraded in autolysosomes, we could see accumulation of LC3-II more clearly if cells were treated with lysosome protease inhibitors (E64d and pepstatin A; Figure Vol. 20, April 1, 2009 1983 3A, lane 3; Tanida et al., 2005; Mizushima and Yoshimori, 2007).”
Autophagy Regulates Cholesterol Efflux from Macrophage Foam Cells via Lysosomal Acid Lipase (2011, neutral): “A further increase in LC3-II protein upon lysosomal inhibition was observed, indicative of a functional autophagic flux in these cells, as cellular LC3 levels per se are not a good marker for autophagy (Tanida et al., 2005).”
Protein turnover via autophagy: implications for metabolism. (2007, background): “Thus, to monitor the autophagic flux, it is necessary to measure the amount of LC3-II delivered to lysosomes by comparing LC3-II levels in the presence and absence of lysosomal protease inhibitors (114).”
ER stress (PERK/eIF2α phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation (2007, methodology): “and pepstatin A, an inhibitor of cathepsins D and E, under starvation conditions.(23) Lysosomal turnover of LC3-II reflects autophagic activity.”
Autophagy Induction and Autophagosome Clearance in Neurons: Relationship to Autophagic Pathology in Alzheimer's Disease (2008, background): “…(Chu, 2006), termed autophagic flux, and it is now known that terminal stages of autophagosomal degradation require uncompromised vesicular trafficking, heterotypic organelle fusion and lysosomal function (Kovács et al., 1982; Takeshige et al., 1992; Tanida et al., 2005; Kiselyov et al., 2007).”
An Overview of Autophagy: Morphology, Mechanism, and Regulation (2014, background): “SQSTM1 is also important for the clearance of ubiquitinated protein aggregates by acting as an adaptor protein that interacts with LC3-II to target aggregates for macroautophagy-specific degradation in a process termed aggrephagy (10, 115, 141).”