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Autophagy. 2021 Aug;17(8):1828-1840. doi: 10.1080/15548627.2020.1783833. Epub 2020 Jul 09.

Differential activation of eMI by distinct forms of cellular stress.

Autophagy

Ana Mesquita, James Glenn, Andreas Jenny

Affiliations

  1. Department of Developmental and Molecular Biology, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, New York, NY, US.
  2. Department of Genetics, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, New York, NY, US.
  3. Marion Bessin Liver Research Center, Albert Einstein College of Medicine, New York, NY, US.

PMID: 32559125 PMCID: PMC8386722 DOI: 10.1080/15548627.2020.1783833

Abstract

As one of the major, highly conserved catabolic pathways, autophagy delivers cytosolic components to lysosomes for degradation. It is essential for development, cellular homeostasis, and coping with stress. Reduced autophagy increases susceptibility to protein aggregation diseases and leads to phenotypes associated with aging. Of the three major forms of autophagy, macroautophagy (MA) can degrade organelles or aggregated proteins, and chaperone-mediated autophagy is specific for soluble proteins containing KFERQ-related targeting motifs. During endosomal microautophagy (eMI), cytoplasmic proteins are engulfed into late endosomes in an ESCRT machinery-dependent manner. eMI can be KFERQ-specific or occur in bulk and be induced by prolonged starvation. Its physiological regulation and function, however, are not understood. Here, we show that eMI in the

Keywords: Autophagy; DNA damage; ER stress; ROS; microautophagy; oxidative stress; proteostasis

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