Cellular Mechanisms of Protein Degradation Among Tissues - Archive ouverte HAL Accéder directement au contenu
Chapitre D'ouvrage Année : 2016

Cellular Mechanisms of Protein Degradation Among Tissues

Lydie Combaret
Daniel Taillandier
Cécile Polge
Daniel Bechet

Résumé

Very little is known on the tissue-specific features of proteolytic systems in the body, mainly because we are lacking appropriate techniques to study protein breakdown in different tissues and organs. Experimental evidence has been provided in only skeletal muscle and liver where proteolysis can be studied in incubated muscles or myotubes and hepatocytes, respectively. These data have demonstrated that proteolysis is mainly ubiquitin-proteasome-dependent in skeletal muscle and lysosomal in liver. This led to the assumption that such tissue-specific differences mainly reflect the very different rates of protein turnover in these tissues (ie, slow in muscle and rapid in the liver). Although there is a correlation between the two parameters, our current understanding of proteolysis now shows that the situation is much more complex. In particular, autophagy is not only responsible for proteolysis, but also for the breakdown of any macromolecule. For example, recent data have shown that the breakdown of lipids is tightly connected to energy metabolism in the liver. Several lines of evidence strongly suggest that this might be the case in other tissues and organs, and that our knowledge of the precise role of each proteolytic pathway is far to be understood. This review focuses on some tissue-specific and more general features of proteolysis that are currently contributing to a better understanding of metabolism
Fichier non déposé

Dates et versions

hal-01581594 , version 1 (04-09-2017)

Identifiants

Citer

Lydie Combaret, Daniel Taillandier, Cécile Polge, Daniel Bechet, Didier Attaix. Cellular Mechanisms of Protein Degradation Among Tissues. The Molecular Nutrition of Amino Acids and Proteins, 3, Academic Press - Elsevier, 368 p., 2016, 9780128021675. ⟨10.1016/B978-0-12-802167-5.00003-7⟩. ⟨hal-01581594⟩
39 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More