Autophagic-lysosomal inhibition compromises ubiquitin-proteasome system performance in a p62 dependent manner in cardiomyocytes

Intracellular protein degradation is primarily performed by the ubiquitin-proteasome system (UPS) and the autophagic-lysosomal pathway (ALP). The interplay between these two pathways has been rarely examined in intact animals and the mechanism underlying the interplay remains unclear. Hence, we soug...

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Veröffentlicht in:	PloS one 2014-06, Vol.9 (6), p.e100715-e100715
Hauptverfasser:	Tian, Zongwen, Wang, Changhua, Hu, Chengjun, Tian, Yihao, Liu, Jinbao, Wang, Xuejun
Format:	Artikel
Sprache:	eng
Schlagworte:	Adapter proteins Adenine - analogs & derivatives Adenine - pharmacology Animals Antineoplastic Agents - pharmacology Autophagy Autophagy - drug effects Biodegradation Biology and Life Sciences Boronic Acids - pharmacology Bortezomib Cardiac muscle Cardiomyocytes Fluorescence Genetic engineering Heart Heart cells Heart diseases Heart failure Heat-Shock Proteins - genetics Heat-Shock Proteins - metabolism In vitro methods and tests In vivo methods and tests Inhibition Kidneys Laboratory animals Lysosomes - metabolism Medicine Medicine and Health Sciences Mice Mice, Transgenic mRNA Myocytes Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Neonates Pathogenesis Peptidases Proteases Proteasome Endopeptidase Complex - metabolism Proteasome Inhibitors - pharmacology Proteasomes Proteins Proteolysis Pyrazines - pharmacology Quality control Rats RNA Rodents Sequestosome-1 Protein siRNA Substrates Transgenic mice Ubiquitin Ubiquitin - metabolism Ventricle
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