Cyclophilin D deficiency attenuates mitochondrial F1Fo ATP synthase dysfunction via OSCP in Alzheimer's disease
Author:
Funder
NIH
Alzheimer's Association
Publisher
Elsevier BV
Subject
Neurology
Reference38 articles.
1. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death;Baines;Nature,2005
2. Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease;Beck;Nat. Commun.,2016
3. Cyclophilin D regulates the dynamic assembly of mitochondrial ATP synthase into synthasomes;Beutner;Sci. Rep.,2017
4. How the N-terminal domain of the OSCP subunit of bovine F1Fo-ATP synthase interacts with the N-terminal region of an alpha subunit;Carbajo;J. Mol. Biol.,2007
5. Modulation of F0F1-ATP synthase activity by cyclophilin D regulates matrix adenine nucleotide levels;Chinopoulos;FEBS J.,2011
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