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ATP13A2 facilitates HDAC6 recruitment to lysosome to promote autophagosome–lysosome fusion

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成果类型:
期刊论文
作者:
Wang, Ruoxi;Tan, Jieqiong;Chen, Tingting;Han, Hailong;Tian, Runyi;...
通讯作者:
Zhang, Zhuohua
作者机构:
[Tian, Runyi; Lv, Lu; Wu, Yiming; Zhang, Zhuohua; Chen, Tingting; Tan, Ya; Cui, Jingyi; Shang, Shuai; Wang, Ruoxi; Han, Hailong; Chen, Fang; Tan, Jieqiong; Li, Jie; Guan, Xinjie] Cent S Univ, Xiangya Hosp, Inst Mol Precis Med, Changsha, Hunan, Peoples R China.
[Tian, Runyi; Lv, Lu; Wu, Yiming; Zhang, Zhuohua; Chen, Tingting; Tan, Ya; Cui, Jingyi; Shang, Shuai; Wang, Ruoxi; Han, Hailong; Chen, Fang; Tan, Jieqiong; Li, Jie; Guan, Xinjie] Cent S Univ, Ctr Med Genet, Changsha, Hunan, Peoples R China.
[Lu, Jiahong] Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Taipa, Macau, Peoples R China.
[Zhang, Zhuohua] Univ South China, Sch Med, Dept Neurosci, Hengyang, Hunan, Peoples R China.
通讯机构:
[Zhang, Zhuohua] C
[Zhang, Zhuohua] U
Cent S Univ, Xiangya Hosp, Inst Mol Precis Med, Changsha, Hunan, Peoples R China.
Cent S Univ, Ctr Med Genet, Changsha, Hunan, Peoples R China.
Univ South China, Sch Med, Dept Neurosci, Hengyang, Hunan, Peoples R China.
语种:
英文
关键词:
histone deacetylase 6;autophagosomes
期刊:
JOURNAL OF CELL BIOLOGY
ISSN:
0021-9525
年:
2019
卷:
218
期:
1
页码:
267-284
基金类别:
This work was supported by grants from the National Natural Science Foundation of China (31330031, 31730036, 81861138012, 81429002, and 81161120498), the Discipline Innovative Engineering Plan of China (111 Program), a key laboratory grant from Hunan Province (2016TP1006), and a grant from the National Key Plan for Scientific Research and Development of China (2016YFC1306000). The authors declare no competing financial interests.
机构署名:
本校为通讯机构
院系归属:
医学院
摘要:
Mutations in ATP13A2 cause Kufor-Rakeb syndrome, an autosomal recessive form of juvenile-onset atypical Parkinson’s disease (PD). Recent work tied ATP13A2 to autophagy and other cellular features of neurodegeneration, but how ATP13A2 governs numerous cellular functions in PD pathogenesis is not understood. In this study, the ATP13A2-deficient mouse developed into aging-dependent phenotypes resembling those of autophagy impairment. ATP13A2 deficiency impaired autophagosome–lysosome fusion in cultured cells and in in vitro reconstitution assays...

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