Intrasarcoplasmic Amyloidosis Impairs Proteolytic Function of Proteasomes in Cardiomyocytes by Compromising Substrate Uptake

The presence of increased ubiquitinated proteins and amyloid oligomers in failing human hearts strikingly resembles the characteristic pathology in the brain of many neurodegenerative diseases. The ubiquitin–proteasome system (UPS) is responsible for degradation of most cellular proteins and plays e...

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Veröffentlicht in:	Circulation research 2005-11, Vol.97 (10), p.1018-1026
Hauptverfasser:	Chen, Quanhai, Liu, Jin-Bao, Horak, Kathleen M, Zheng, Hanqiao, Kumarapeli, Asangi R.K, Li, Jie, Li, Faqian, Gerdes, A Martin, Wawrousek, Eric F, Wang, Xuejun
Format:	Artikel
Sprache:	eng
Schlagworte:	Amyloidosis Amyloidosis - metabolism Animals beta-Crystallin A Chain - genetics Biological and medical sciences Cardiology. Vascular system Cardiomyopathies - etiology Desmin - physiology Endoplasmic Reticulum - metabolism Fundamental and applied biological sciences. Psychology Heart Heart Failure - etiology Medical sciences Metabolic diseases Mice Mice, Transgenic Myocarditis. Cardiomyopathies Myocytes, Cardiac - metabolism Other metabolic disorders Proteasome Endopeptidase Complex - physiology Protein Transport Proteins - metabolism Ubiquitin - metabolism Ventricular Remodeling Vertebrates: cardiovascular system
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