Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy.

By A. Cuervo, Leonidas Stefanis, R. Fredenburg, P. Lansbury, D. Sulzer. Science, 2004

1,033 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/01345d98e36e2fb21d58e0b7c4d44ee38cf7aaff

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Citations in the corpus

Autophagy Induction and Autophagosome Clearance in Neurons: Relationship to Autophagic Pathology in Alzheimer's Disease (2008, background): “Dysfunction within either of two proteolytic pathways, involved in clearing abnormal or obsolete cellular proteins, the ubiquitin– proteasome system (UPS) and the autophagic–lysosomal system, have been increasingly implicated in proteinopathies of Alzheimer’s disease (AD), Huntington’s disease, Park”
Guidelines for the use and interpretation of assays for monitoring autophagy (2012, background): “Finally, inhibition of a particular degradative pathway is typically accompanied by an increase in a separate pathway as the cell attempts to compensate for the loss of degradative capacity.(158,478,493) This compensation might interfere with control measurements under conditions that attempt to inh”
Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway (2008, background): “Virgin female flies of the genotype y w; gmr-httNterm(1-171)Q120 (gmrQ120)(22) were allowed to mate with male flies from an isogenised w(1118) stock(23) in food vials for 48 h.”
Autophagy, amyloidogenesis and Alzheimer disease (2007, unknown): “Notably APP and synuclein, a protein implicated in Parkinson disease, contain this targeting sequence (Massey et al., 2004), and impaired CMA-mediated degradation contributes to accumulation of mutant -synuclein in the disease (Cuervo et al., 2004).”
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, unknown): “the cell attempts to compensate for the loss of degradative capacity.(229,666) This compensation might interfere with control”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, unknown): “…mutated a-syn (Vogiatzi et al., 2008) CMA degrades wild-type a-syn (Cuervo et al., 2004; Vogiatzi et al., 2008) CMA is inhibited by mutated a-syn (Cuervo et al., 2004) CMA activity is reduced in the brain of PD patient (Alvarez-Erviti et al., 2010) Rapamycin (Dehay et al., 2010; Mendelsohn and…”
TFEB-mediated autophagy rescues midbrain dopamine neurons from α-synuclein toxicity (2013, background): “However, in case of α-syn overload, it has been shown that processing by the ALP becomes the dominant pathway for α-syn removal (12, 13).”
Pathogenic Lysosomal Depletion in Parkinson's Disease (2010, background): “While alterations in CMA have been linked to PD because of the ability of mutant and posttranslationally modified -synuclein to block CMA in vitro (Cuervo et al., 2004; Martinez-Vicente et al., 2008), macroautophagy dysregulation is increasingly recognized as a potential pathogenic factor in neurode”
Acetylation Targets the M2 Isoform of Pyruvate Kinase for Degradation through Chaperone-Mediated Autophagy and Promotes Tumor Growth (2011, methodology): “Both lysosome binding and uptake assays were carried out as described previously (Cuervo et al., 2004).”
Direct Observation of the Interconversion of Normal and Toxic Forms of α-Synuclein (2012, unknown): “It is interesting to note in this regard that this slow structural conversion is on the same timescale as the half-life for aS turnover in vivo reported previously (Cuervo et al., 2004; Okochi et al., 2000).”