Affiliation: Tufts University
- Chaperone-mediated autophagyJ Fred Dice
Department of Cellular and Molecular Physiology, Tufts University School of Medicine, Boston, MA 02111, USA
Autophagy 3:295-9. 2007..These findings reveal a rich complexity of mechanisms to control CMA activity...
- Mechanisms of chaperone-mediated autophagyAmy E Majeski
Department of Physiology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA
Int J Biochem Cell Biol 36:2435-44. 2004..The exact roles of this lysosomal chaperone remain to be defined. The mechanisms of chaperone-mediated autophagy are similar to mechanisms of protein import into mitochondria, chloroplasts, and the endoplasmic reticulum...
- Ketone bodies stimulate chaperone-mediated autophagyPatrick F Finn
Department of Molecular and Cellular Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Biol Chem 280:25864-70. 2005..The induction of CMA by ketone bodies may provide an important physiological mechanism for the activation of CMA during prolonged starvation...
- Effects of small molecules on chaperone-mediated autophagyPatrick F Finn
Department of Cellular and Molecular Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
Autophagy 1:141-5. 2005..Finally we demonstrate that the glucose-6-phophate dehydrogenase inhibitor, 6-aminonicotinamide, and heat shock protein of 90 kilodaltons inhibitor, geldanamycin, have the ability to activate CMA...
- Proteolytic and lipolytic responses to starvationPatrick F Finn
Department of Molecular and Cellular Physiology, Tufts University School of Medicine, Boston, Massachusetts, USA
Nutrition 22:830-44. 2006..Tissues that cannot use ketone bodies for energy respond to these small molecules by activating chaperone-mediated autophagy. This is one form of interaction between proteolytic and lipolytic responses to starvation...
- Chaperone-mediated autophagy is defective in mucolipidosis type IVBhuvarahamurthy Venugopal
Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
J Cell Physiol 219:344-53. 2009..It is also possible that TRPML1 channel activity may be required for CMA. Understanding the role of TRPML1 in CMA will undoubtedly help to characterize the pathogenesis of MLIV...