The UCH-L1 gene encodes two opposing enzymatic activities that affect-synuclein degradation and Park
By Yichin Liu, Lara Fallon, H. Lashuel, P. Lansbury. 2002
789 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/f0f65e1cba25622a4a05d5fc5689fcb9bedf0f61
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Citations in the corpus
- Molecular pathophysiology of Parkinson's disease. (2005, background): “UCH-L1 can also promote the accumulation of α-synuclein in cultured cells presumably through the addition of Lys63linked poly-ubiquitin chains that are not associated with proteasomal degradation (Liu et al. 2002).”
- The roles of intracellular protein-degradation pathways in neurodegeneration (2006, background): “UCHL1 might function not only as a ubiquitin hydrolase (hydrolysing ubiquitin chains to free ubiquitin monomers) but also as a ubiquitin ligas”
- Parkinson's Disease Mechanisms and Models (2003, background): “…this E3 ligase activity, suggesting that the accumula- L1 ligase activity is decreased by the pathogenic I93M tion of misfolded parkin substrates could be responsible mutation and increased by the protective S18Y polymorfor the demise of SNpc dopaminergic neurons in PD. phism (Liu et al., 2002).”
- Pathogenesis of parkinson's disease: dopamine, vesicles and α-synuclein (2002, background): “Recent findings indicate that UCHL1 might have dual and opposing functions in the degradation of α-synuclein by the UPP, and that polymorphisms in PARK5 can even lead to a reduced risk of Parkinson's diseas”
- Origin and Function of Ubiquitin-like Protein Conjugation (2009, background): “In one of these models, a ubiquitin hydrolase was proposed to be able not only to cleave ubiquitin from substrates but also to work backwards, in effect, and ligate ubiquitin to a protei”
- A genomic and functional inventory of deubiquitinating enzymes. (2005, background): “Mutations in UCH-L1 (a UCH specifically expressed in neurons) that reduce its DUB activity have been described in two siblings with Parkinson’s disease (PD), and a polymorphism in this gene has been linked to reduced PD risk (Leroy et al., 1998; Liu et al., 2002).”
- Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, unknown): “One of the substrates of ERAD ubiquitinated by Parkin is the Pael receptor, a homologue of endothelin receptor type B (54).”