Titin truncations lead to impaired cardiomyocyte autophagy and mitochondrial function in vivo.
Zhou, Jin
Titin truncations lead to impaired cardiomyocyte autophagy and mitochondrial function in vivo. [electronic resource] - Human molecular genetics 06 2019 - 1971-1981 p. digital
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
1460-2083
10.1093/hmg/ddz033 doi
Acetylation
Animals
Autophagosomes--metabolism
Autophagy--genetics
Cardiomyopathy, Dilated--genetics
Cathepsin B--metabolism
Cells, Cultured
Connectin--genetics
Male
Microtubule-Associated Proteins--metabolism
Mitochondria, Heart--metabolism
Mitochondrial Proteins--metabolism
Myocytes, Cardiac--metabolism
NAD--analogs & derivatives
Rats
Reactive Oxygen Species--metabolism
Sequence Deletion
Sequestosome-1 Protein--metabolism
TOR Serine-Threonine Kinases--metabolism
Ubiquitination
Titin truncations lead to impaired cardiomyocyte autophagy and mitochondrial function in vivo. [electronic resource] - Human molecular genetics 06 2019 - 1971-1981 p. digital
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
1460-2083
10.1093/hmg/ddz033 doi
Acetylation
Animals
Autophagosomes--metabolism
Autophagy--genetics
Cardiomyopathy, Dilated--genetics
Cathepsin B--metabolism
Cells, Cultured
Connectin--genetics
Male
Microtubule-Associated Proteins--metabolism
Mitochondria, Heart--metabolism
Mitochondrial Proteins--metabolism
Myocytes, Cardiac--metabolism
NAD--analogs & derivatives
Rats
Reactive Oxygen Species--metabolism
Sequence Deletion
Sequestosome-1 Protein--metabolism
TOR Serine-Threonine Kinases--metabolism
Ubiquitination