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- W2969836417 endingPage "e201900348" @default.
- W2969836417 startingPage "e201900348" @default.
- W2969836417 abstract "Lipid homeostasis is crucial in human health. Barth syndrome (BTHS), a life-threatening disease typically diagnosed with cardiomyopathy and neutropenia, is caused by mutations in the mitochondrial transacylase tafazzin. By high-resolution 31 P nuclear magnetic resonance (NMR) with cryoprobe technology, recently we found a dramatic loss of choline plasmalogen in the tafazzin-knockdown (TAZ-KD) mouse heart, besides observing characteristic cardiolipin (CL) alterations in BTHS. In inner mitochondrial membrane where tafazzin locates, CL and diacyl phosphatidylethanolamine are known to be essential via lipid–protein interactions reflecting their cone shape for integrity of respiratory chain supercomplexes and cristae ultrastructure. Here, we investigate the TAZ-KD brain, liver, kidney, and lymphoblast from patients compared with controls. We identified common yet markedly cell type–dependent losses of ethanolamine plasmalogen as the dominant plasmalogen class therein. Tafazzin function thus critically relates to homeostasis of plasmalogen, which in the ethanolamine class has conceivably analogous and more potent molecular functions in mitochondria than diacyl phosphatidylethanolamine. The present discussion of a loss of plasmalogen–protein interaction applies to other diseases with mitochondrial plasmalogen loss and aberrant forms of this organelle, including Alzheimer's disease." @default.
- W2969836417 created "2019-08-29" @default.
- W2969836417 creator A5017442405 @default.
- W2969836417 creator A5030953137 @default.
- W2969836417 creator A5032304374 @default.
- W2969836417 creator A5045709526 @default.
- W2969836417 creator A5057880834 @default.
- W2969836417 creator A5076057133 @default.
- W2969836417 creator A5078221622 @default.
- W2969836417 creator A5086027794 @default.
- W2969836417 date "2019-08-01" @default.
- W2969836417 modified "2023-10-02" @default.
- W2969836417 title "Plasmalogen loss caused by remodeling deficiency in mitochondria" @default.
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