COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.

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作者： Daniel C,Maddison ^[1] ; Bilal,Malik ^[2] ; Leonardo,Amadio ^[3] ; Dana M,Bis-Brewer ^[4] ; Stephan,Züchner ^[4] ; Owen M,Peters ^[2] ; Gaynor A,Smith ^[5]

作者单位： UK Dementia Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, UK. ^[1] UK Dementia Research Institute, School of Biosciences, Cardiff University, Cardiff CF24 4HQ, UK. ^[2] UK Dementia Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, UK; UK Dementia Research Institute, School of Biosciences, Cardiff University, Cardiff CF24 4HQ, UK. ^[3] John P. Hussman Institute for Human Genomics, University of Miami, Miami, FL, USA; Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miami, FL, USA. ^[4] UK Dementia Research Institute, School of Medicine, Cardiff University, Cardiff CF24 4HQ, UK. Electronic address: smithga@cf.ac.uk. ^[5]

关键词 Axon transport COPI CP: Cell biology Calcium homeostasis Endoplasmic reticulum Golgi Mitochondria Neuronal cell biology Vesicle trafficking

主题词人类(Humans);内质网(Endoplasmic Reticulum);外壳蛋白质复合物Ⅰ(Coat Protein Complex I);高尔基体(Golgi Apparatus);线粒体(Mitochondria);轴突(Axons)

DOI 10.1016/j.celrep.2023.112883

PMID 37498742

发布时间 2024-10-26

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