Literature DB >> 17329252

Relative sensitivity of parkin and other cysteine-containing enzymes to stress-induced solubility alterations.

Esther S P Wong1, Jeanne M M Tan, Cheng Wang, Zhenshui Zhang, Shiam-Peng Tay, Norazean Zaiden, Han Seok Ko, Valina L Dawson, Ted M Dawson, Kah-Leong Lim.   

Abstract

Loss of parkin function is a predominant cause of familial Parkinsonism. Emerging evidence also suggests that parkin expression variability may confer a risk for sporadic Parkinson disease. We have recently demonstrated that a wide variety of Parkinson disease-linked stressors, including dopamine (DA), induce parkin solubility alterations and promote its aggregation within the cell, a phenomenon that may underlie the progressive susceptibility of the brain to degeneration. The vulnerability of parkin to stress-induced modification is likely due to its abundance of cysteine residues. Here, we performed a comprehensive mutational analysis and demonstrate that Cys residues residing both within and outside of the RING-IBR (in between RING fingers)-RING domain of parkin are important in maintaining its solubility. The majority of these Cys residues are highly conserved in parkin across different species and potentially fulfil important structural roles. Further, we found that both parkin and HHARI (human homologue of Drosophila ariadne), another RING-IBR-RING-type ubiquitin ligase, are comparably more susceptible to solubility alterations induced by oxidative and nitrosative stress when compared with other non-RING-IBR-RING Cys-containing enzymes. However, parkin appears to be uniquely sensitive to DA-mediated stress, the specificity of which is likely due to DA modification of 2 Cys residues on parkin (Cys-268 and Cys-323) that are distinct from other RING-IBR-RING members.

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Year:  2007        PMID: 17329252     DOI: 10.1074/jbc.M609466200

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  37 in total

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Review 2.  Redox reactions induced by nitrosative stress mediate protein misfolding and mitochondrial dysfunction in neurodegenerative diseases.

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Review 3.  The two faces of protein misfolding: gain- and loss-of-function in neurodegenerative diseases.

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4.  Drosophila overexpressing parkin R275W mutant exhibits dopaminergic neuron degeneration and mitochondrial abnormalities.

Authors:  Cheng Wang; Ruifeng Lu; Xuezhi Ouyang; Michelle W L Ho; William Chia; Fengwei Yu; Kah-Leong Lim
Journal:  J Neurosci       Date:  2007-08-08       Impact factor: 6.167

Review 5.  The role of parkin in familial and sporadic Parkinson's disease.

Authors:  Ted M Dawson; Valina L Dawson
Journal:  Mov Disord       Date:  2010       Impact factor: 10.338

Review 6.  Mitochondrial Redox Dysfunction and Environmental Exposures.

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Review 7.  Mitochondria and mitophagy: the yin and yang of cell death control.

Authors:  Dieter A Kubli; Åsa B Gustafsson
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Review 8.  Redox regulation of mitochondrial fission, protein misfolding, synaptic damage, and neuronal cell death: potential implications for Alzheimer's and Parkinson's diseases.

Authors:  Tomohiro Nakamura; Stuart A Lipton
Journal:  Apoptosis       Date:  2010-11       Impact factor: 4.677

Review 9.  An emerging role of PARK2 in cancer.

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Journal:  J Mol Med (Berl)       Date:  2013-12-03       Impact factor: 4.599

10.  Parkin reverses intracellular beta-amyloid accumulation and its negative effects on proteasome function.

Authors:  Kenneth M Rosen; Charbel E-H Moussa; Han-Kyu Lee; Pravir Kumar; Tohru Kitada; Gangjian Qin; Qinghao Fu; Henry W Querfurth
Journal:  J Neurosci Res       Date:  2010-01       Impact factor: 4.164

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