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Hongxia Wang, Pingping Song,
Lei Du,
Weili Tian,
Wen Yue,
Min Liu,
Dengwen Li,
Bin Wang,
Yushan Zhu,
Cheng Cao,
Jun Zhou,
Quan Chen
[show abstract]
[hide abstract]
ABSTRACT: Mutations in Parkin, an E3 ubiquitin ligase that regulates protein turnover, represent one of the major causes of familial
Parkinson disease, a neurodegenerative disorder characterized by the loss of dopaminergic neurons and impaired mitochondrial
functions. The underlying mechanism by which pathogenic Parkin mutations induce mitochondrial abnormality is not fully understood.
Here, we demonstrate that Parkin interacts with and subsequently ubiquitinates dynamin-related protein 1 (Drp1), for promoting
its proteasome-dependent degradation. Pathogenic mutation or knockdown of Parkin inhibits the ubiquitination and degradation
of Drp1, leading to an increased level of Drp1 for mitochondrial fragmentation. These results identify Drp1 as a novel substrate
of Parkin and suggest a potential mechanism linking abnormal Parkin expression to mitochondrial dysfunction in the pathogenesis
of Parkinson disease.
Journal of Biological Chemistry 03/2011; 286(13):11649-11658. · 4.77 Impact Factor
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Hongxia Wang, Pingping Song,
Lei Du,
Weili Tian,
Wen Yue,
Min Liu,
Dengwen Li,
Bin Wang,
Yushan Zhu,
Cheng Cao,
Jun Zhou,
Quan Chen
[show abstract]
[hide abstract]
ABSTRACT: Mutations in Parkin, an E3 ubiquitin ligase that regulates protein turnover, represent one of the major causes of familial Parkinson disease, a neurodegenerative disorder characterized by the loss of dopaminergic neurons and impaired mitochondrial functions. The underlying mechanism by which pathogenic Parkin mutations induce mitochondrial abnormality is not fully understood. Here, we demonstrate that Parkin interacts with and subsequently ubiquitinates dynamin-related protein 1 (Drp1), for promoting its proteasome-dependent degradation. Pathogenic mutation or knockdown of Parkin inhibits the ubiquitination and degradation of Drp1, leading to an increased level of Drp1 for mitochondrial fragmentation. These results identify Drp1 as a novel substrate of Parkin and suggest a potential mechanism linking abnormal Parkin expression to mitochondrial dysfunction in the pathogenesis of Parkinson disease.
Journal of Biological Chemistry 02/2011; 286(13):11649-58. · 4.77 Impact Factor
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Zhongguo fei ai za zhi = Chinese journal of lung cancer 05/2009; 12(5):456-9.
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Xiaojun Zhong,
Jinming Yu,
Baijiang Zhang,
Dianbin Mu,
Weidi Zhang,
Daotang Li,
Anqin Han, Pingping Song,
Hui Li,
Guoren Yang,
Feng-Ming Kong,
Zheng Fu
[show abstract]
[hide abstract]
ABSTRACT: To determine the optimal method of using (18)F-fluorodeoxyglucose positron emission tomography (FDG-PET) to estimate gross tumor length in esophageal carcinoma.
Thirty-six patients with esophageal squamous cell carcinoma treated with radical surgery were enrolled. Gross tumor volumes (GTVs) were delineated using three different methods: visual interpretation, standardized uptake value (SUV) 2.5, and 40% of maximum standard uptake value (SUV(max)) on FDG-PET imaging. The length of tumors on PET scan were measured and recorded as Length(vis), Length(2.5), and Length(40), respectively, and compared with the length of gross tumor in the resected specimen (Length(gross)). All PET data were reviewed again postoperatively, and the GTV was delineated using various percentages of SUV(max). The optimal-threshold SUV was generated when the length of PET matched the Length(gross).
The mean (+/-SD) Length(gross) was 5.48 +/- 1.98 cm. The mean Length(vis), Length(2.5), and Length(40) were 5.18 +/- 1.93 cm, 5.49 +/- 1.79 cm, and 4.34 +/- 1.54 cm, respectively. The mean Length(vis) (p = 0.123) and Length(2.5) (p = 0.957) were not significantly different from Length(gross), and Length(2.5) seems more approximate to Length(gross.) The mean Length(40) was significantly shorter than Length(gross) (p < 0.001). The mean optimal threshold was 23.81% +/- 11.29% for all tumors, and it was 19.78% +/- 8.59%, 30.92% +/- 12.28% for tumors >/=5 cm, and <5 cm, respectively (p = 0.009). The correlation coefficients of the optimal threshold were -0.802 and -0.561 with SUV(max) and Length(gross), respectively.
The optimal PET method to estimate the length of gross tumor varies with tumor length and SUV(max); an SUV cutoff of 2.5 provided the closest estimation in this study.
International journal of radiation oncology, biology, physics 07/2008; 73(1):136-41. · 4.59 Impact Factor
