Ubiquitination of a New Form of α-Synuclein by Parkin from Human Brain: Implications for Parkinson's Disease
By H. Shimura, M. Schlossmacher, N. Hattori, Matthew P. Frosch, A. Trockenbacher, R. Schneider, Y. Mizuno, Kenneth S. Kosik, D. Selkoe. Science, 2001
1,104 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/7de0b64ebc615c0560c2398f54a879944e2f1762
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In Cellular and Molecular Neuroscience
- Leonidas Stefanis
- Valina L. Dawson
- M. Block
- T. Dawson
- Jau-Shyong Hong
- P. Jenner
- S. Przedborski
- A. Björklund
In Molecular Biology
- Valina L. Dawson
- T. Dawson
- Junying Yuan
- Jau-Shyong Hong
- M. Boyce
- Christopher A. Ross
- A. Björklund
- Jessica W. Wu
In Neurology
- Valina L. Dawson
- T. Dawson
- M. Block
- Leonidas Stefanis
- Jau-Shyong Hong
- P. Jenner
- S. Przedborski
- Vladimir N Uversky
Citations in the corpus
- Molecular pathophysiology of Parkinson's disease. (2005, background): “…and cell culture experiments, including CDCrel- 1 (Zhang et al. 2000), synphilin-1 (Chung et al. 2001b), a rare O-glycosylated form of α-synuclein (Shimura et al. 2001), the parkin-associated endothelin receptor-like receptor (Pael-R) (Imai et al. 2001), synaptotagmin XI (Huynh et al. 2003),…”
- Cellular response to endoplasmic reticulum stress: a matter of life or death (2006, background): “and the major constituent of Lewy inclusion bodies observed in the neurons of PD patients.(87) Parkin mutants associated with familial PD are unable to act on a-synuclein, suggesting that Parkin-mediated ERAD processing of a-synuclein is critical for avoiding PD.”
- Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States (2018, neutral): “are sufficient to cause early-onset PD (Shimura et al., 2001).”
- Parkinson's disease: genetics and pathogenesis. (2011, background): “Other data, such as (a) the finding that α-synuclein can be directly ubiquitinated by Parkin (118) or (b) evidence for potential interactions in animal models (discussed below) raise the possibility of an even more direct functional link between the mechanisms of PD and those of other genetic forms ”
- Parkinson's Disease Mechanisms and Models (2003, background): “Expression of this proline mutant form synuclein function (Shimura et al., 2001; Petrucelli et al., of DJ-1 appears to lead to its accumulation in mitochon2002) or aggregation (Chung et al., 2001).”
- Parkin ubiquitinates the α-synuclein–interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease (2001, background): “and affinity-purified antibodies against parkin recognize subsets of brainstem and cortical Lewy bodies in PD and dementia with Lewy-body brain”