Lysosomal dysfunction, autophagic defects, and CLN5 accumulation underlie the pathogenesis of KCTD7-mutated neuronal ceroid lipofuscinoses

Author:

Wang Yalan12,Wang Hongyan12ORCID,Wang Chenji3ORCID

Affiliation:

1. Obstetrics and Gynecology Hospital, NHC Key Laboratory of Reproduction Regulation, Shanghai Institute of Planned Parenthood Research, State Key Laboratory of Genetic Engineering, School of Life Sciences, Children’s Hospital, Fudan University, Shanghai, China

2. Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Institute of Reproduction and Development, Fudan University, Shanghai, China

3. Shanghai Stomatological Hospital & School of Stomatology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China

Funder

National Natural Science Foundation of China

National Key R&D Program of China

Commission for Science and Technology of Shanghai Municipality

Natural Science Foundation of Shanghai

Science and Technology Research Program of Shanghai

Publisher

Informa UK Limited

Subject

Cell Biology,Molecular Biology

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