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• W2029843923 endingPage "865" @default.
• W2029843923 startingPage "861" @default.
• W2029843923 abstract "Mitochondrial uncoupling proteins, which secure physiological uncoupling of oxidative phosphorylation, have been proposed to serve as an oxidative-stress compensatory mechanism. Here, heart-derived H9c2 cells acquired improved resistance to injury upon transfection of the prototypic uncoupling protein UCP1. Following hypoxia/reoxygenation, stable overexpression of UCP1 provided enhanced cardioblast survival with preserved mitochondrial structure and function, while limiting reactive oxygen species formation. Thus, transfection of mitochondrial UCP1 provides a strategy for generation of a stress-resistant cardiac cell phenotype." @default.
• W2029843923 created "2016-06-24" @default.
• W2029843923 creator A5035697355 @default.
• W2029843923 creator A5047902810 @default.
• W2029843923 creator A5076980360 @default.
• W2029843923 date "2003-07-01" @default.
• W2029843923 modified "2023-09-24" @default.
• W2029843923 title "Stable transfection of UCP1 confers resistance to hypoxia/reoxygenation in a heart-derived cell line" @default.
• W2029843923 cites W1529592271 @default.
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• W2029843923 doi "https://doi.org/10.1016/s0022-2828(03)00147-0" @default.
• W2029843923 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12818577" @default.
• W2029843923 hasPublicationYear "2003" @default.
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