Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function.

导出 OA

翻译打印收藏纠错

第一作者： Adam L,Orr

第一单位： Gladstone Institute of Neurological Disease, San Francisco, CA, USA.

作者： Adam L,Orr ^[1] ; Chaeyoung,Kim ^[2] ; David,Jimenez-Morales ^[1] ; Billy W,Newton ^[3] ; Jeffrey R,Johnson ^[4] ; Nevan J,Krogan ^[5] ; Danielle L,Swaney ^[4] ; Robert W,Mahley ^[3]

作者单位： Gladstone Institute of Neurological Disease, San Francisco, CA, USA. ^[1] Present address: Helen & Robert Appel Alzheimer's Disease Research Institute, Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA. ^[2] Gladstone Institute of Data Science and Biotechnology, San Francisco, CA, USA. ^[3] Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA, USA. ^[4] Present address: Department of Medicine, Division of Cardiovascular Medicine, Stanford University, CA, USA. ^[5] Quantitative Biosciences Institute, University of California, San Francisco, CA, USA. ^[6] Department of Pathology and Medicine, University of California, San Francisco, CA, USA. ^[7]

关键词 Alzheimer’s disease apoE4 mitochondrial respiration neurodegeneration neuronal metabolism protein expression