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Cited by 4,458 publications
(4,140 citation statements)
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References 2,165 publications
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“…Thus, the above results are not surprising. However, what remains to be determined is how the acetylation of Atg9a on K359 and K363 within the lumen of the ER can activate the core of the autophagy machinery, which is mainly cytosolic (Klionsky et al, 2016). Interestingly, the above two lysine residues are flanked by two coiled regions that could be involved with protein–protein interactions (Pehar et al, 2012).…”
Section: Resultsmentioning
confidence: 99%
“…Thus, the above results are not surprising. However, what remains to be determined is how the acetylation of Atg9a on K359 and K363 within the lumen of the ER can activate the core of the autophagy machinery, which is mainly cytosolic (Klionsky et al, 2016). Interestingly, the above two lysine residues are flanked by two coiled regions that could be involved with protein–protein interactions (Pehar et al, 2012).…”
Section: Resultsmentioning
confidence: 99%
“…Autophagic flux was measured by immunoblot for LC3‐II and p62 (Klionsky, 2016) or by imaging with tandem reporter mCherry‐GFP‐LC3 (for in bulk autophagy) or mt‐Keima (Katayama et al., 2011; for mitophagy). Inhibition of lysosomal proteolysis for the flux assays was attained using 20 m m NH 4 Cl and 100 μ m leupeptin that we determined were saturating concentrations for blockage of LC3 degradation both in young and in old cells.…”
Section: Methodsmentioning
confidence: 99%
“…This observation suggested that MAPK8/9 deficiency caused no major change in autophagy as a result of MTOR inhibition. This conclusion was confirmed by measurement of autophagic flux by monitoring the formation of phosphatidylethanolamine-conjugated LC3B-II in response to MTOR inhibition in the presence of a lysosomal inhibitor [36] (Figure. 1(c) and S1B) and reduced accumulation of the autophagic substrate SQSTM1/p62 (sequestosome 1) (Figure.…”
Section: Resultsmentioning
confidence: 67%
“…Control studies demonstrated that rapamycin inhibited phosphorylation of the TORC1 substrate RPS6KB1 at Thr389, but not the TORC2 substrate AKT (thymoma viral proto-oncogene) at target site Ser473 (Figure 1(e)). We found that treatment of WT and mapk8 −/- mapk9 −/- immortalized MEFs with rapamycin caused a similar increase in autophagic flux that was measured by monitoring the accumulation of LC3B-II in the presence of a lysosomal inhibitor [36] (Figure. 1(f) and S1D).…”
Section: Resultsmentioning
confidence: 67%
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