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- W2804730003 abstract "As a stress-induced mechanism, autophagy provides energy and essential biomolecules through degradation of cellular cytoplasmic constituents, thus helping cells to adapt to nutrient scarcity. Autophagy regulation by nutrient availability has been evolutionarily conserved from the simplest eukaryotic organisms, as yeasts, to mammals or plants. Apart from this ancient energy-providing role, autophagy has evolved to act as a basal, constitutively-activated, catabolic route preventing accumulation of detrimental intracellular structures, thus keeping cells homeostasis and organism integrity. To better understand autophagy's roles in higher eukaryotes, a variety of autophagy-deficient mice have currently been generated. The study of these modes has provided clues on how basal autophagy sustains cellular health, tissue-specific functions and organismal response to environmental factors. We will describe how the study of autophagy-deficient animal models has improved our understanding on how this catabolic route protects cells, tissues and organisms either as a constitutive or inducible pathway. Finally, we will discuss the differences between animal models with either total or partial autophagy inactivation and explain the advantages for each of these complementary strategies." @default.
- W2804730003 created "2018-06-01" @default.
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- W2804730003 date "2018-05-01" @default.
- W2804730003 modified "2023-09-28" @default.
- W2804730003 title "Autophagy deficient mice as a model for studying stress-induced autophagy in vivo" @default.
- W2804730003 doi "https://doi.org/10.1016/j.freeradbiomed.2018.04.084" @default.
- W2804730003 hasPublicationYear "2018" @default.
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