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	1. Parkin RING1 domain mutant impair its mitochondrial translocation and interaction with PINK1
	YANG Hui,YANG Ling,GAO Peiye,ZUO Ji,YE Xiaofei,LIU Wen
	Biology 30 November 2013
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	Abstract:In Mutations in Parkin and PTEN-induced putative kinase 1 (PINK1) could cause autosomal recessive forms of Parkinson's disease (PD), but how these mutations trigger mitochondrial dysfunction and the precise relationship between Parkin and PINK1 are still poorly understood. Recent studies indicate that with the help of PINK1, Parkin can promote the clearance of impaired mitochondria by mitophagy. Especially, it remains to be clarified the role of RING1 domain of Parkin in the interaction with PINK1 and its mitochondrial recruitment. In the present study, we reported that in a non-neuronal human HeLa cell line, the RING1 finger related mutation of Parkin (T240R) affected its ability to interact with full-length PINK1 under normal condition. Furthermore our immunofluorescence results shows that RING1 finger related mutations of Parkin did not affect its subcellular localization, but minimal co-localization of mutant Parkin (T240R and RING1 Del) with mitochondria were observed when cotransfection with PINK1. Our results provide the links between PINK1 and Parkin are important to sustain the mitochondrial integrity and may shed a light on the pathogenesis of PD, especially in the aspect of the PINK1-Parkin pathway.
	TO cite this article:YANG Hui,YANG Ling,GAO Peiye, et al. Parkin RING1 domain mutant impair its mitochondrial translocation and interaction with PINK1[OL].[30 November 2013] http://en.paper.edu.cn/en_releasepaper/content/4571865


	2. Effects of dibutyl phthalate on ovarian active substance of mice
	WANG Yu,WANG Shengqing,YE Wengbin,HE Jiujun
	Biology 15 March 2013
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	Abstract:With superoxide dismutase(SOD), catalase(CAT), alkaline phosphatase(AKP), acid phosphatase(ACP), malondialdehyde(MDA) and Bax protein expression as characteristic indexes, the effects of dibutyl phthalate(DBP) on ovarian active substance of mice were studied, and the toxic mechanisms were discussed. One hundred sixty mice were given intragastric administration of DBP (0, 100, 250, or 500 mg/(kgod)), respectively, for 30 days. At 5, 10, 20, 30 days after DBP exposure, the ovarian examinations were taken. The results revealed that administration of DBP decreased the activities of SOD, CAT, AKP and ACP, while MDA content and Bax protein expression increased. Two-way analysis of variance indicated that dose contributed more to DBP-induced ovarian damage than treatment time. The present study demonstrated that DBP promoted apoptosis and inhibited antioxidant capacity of the ovarian.
	TO cite this article:WANG Yu,WANG Shengqing,YE Wengbin, et al. Effects of dibutyl phthalate on ovarian active substance of mice[OL].[15 March 2013] http://en.paper.edu.cn/en_releasepaper/content/4527462

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