Interpretation of bafilomycin, pH neutralizing or protease inhibitor treatments in autophagic flux experiments: novel considerations
G Juhász - Autophagy, 2012 - Taylor & Francis
Autophagy, 2012•Taylor & Francis
Recent publications showed that the kinase MTOR localizes to lysosomes and its activation
depends on amino acids inside the lysosomal lumen, implying that autophagic protein
degradation is a positive regulator of MTOR in this setting. Since decreased MTOR activity
results in autophagy induction, drug treatments that block autolysosomal degradation (a
commonly used technique to estimate autophagic flux) may actually interfere not only with
lysosomal breakdown, but also increase autophagosome generation through impaired …
depends on amino acids inside the lysosomal lumen, implying that autophagic protein
degradation is a positive regulator of MTOR in this setting. Since decreased MTOR activity
results in autophagy induction, drug treatments that block autolysosomal degradation (a
commonly used technique to estimate autophagic flux) may actually interfere not only with
lysosomal breakdown, but also increase autophagosome generation through impaired …
Recent publications showed that the kinase MTOR localizes to lysosomes and its activation depends on amino acids inside the lysosomal lumen, implying that autophagic protein degradation is a positive regulator of MTOR in this setting. Since decreased MTOR activity results in autophagy induction, drug treatments that block autolysosomal degradation (a commonly used technique to estimate autophagic flux) may actually interfere not only with lysosomal breakdown, but also increase autophagosome generation through impaired MTOR signaling.
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