Chaperone-mediated autophagy.

Research output: Contribution to journalArticle

Abstract

Chaperone-mediated autophagy (CMA) is the only type of autophagy in mammalian cells able to selectively degrade cytosolic proteins in lysosomes. CMA is maximally activated in response to stressors such as prolonged starvation, exposure to toxic compounds, or oxidative stress. We have found that CMA activity decreases in aging and in some age-related disorders such as Parkinson's disease. Impaired CMA under these conditions may be responsible for the accumulation of damaged proteins inside cells and for their higher vulnerability to stressors. In contrast to other forms of autophagy, where substrates are engulfed or sequestered along with other cytosolic components, CMA substrates are translocated one-by-one across the lysosomal membrane. Changes in the levels/activity of the lysosomal components required for substrate translocation can be used to stimulate CMA activity. However, the most unequivocal method to measure CMA is by directly tracking the translocation of substrate proteins into isolated lysosomes.

Original languageEnglish (US)
Pages (from-to)227-244
Number of pages18
JournalMethods in molecular biology (Clifton, N.J.)
Volume445
StatePublished - 2008

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Autophagy
Lysosomes
Poisons
Protein Transport
Starvation
Parkinson Disease
Proteins
Oxidative Stress
Membranes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

Cite this

Chaperone-mediated autophagy. / Kaushik, S.; Cuervo, A. M.

In: Methods in molecular biology (Clifton, N.J.), Vol. 445, 2008, p. 227-244.

Research output: Contribution to journalArticle

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