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http://purl.uniprot.org/citations/32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32424140http://www.w3.org/2000/01/rdf-schema#comment"Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment. REGγ is emerging as 11S proteasome activator of 20S proteasome to promote the degradation of cellular proteins in a ubiquitin- and ATP-independent manner. Here, we found that REGγ was significantly upregulated in the transverse aortic constriction (TAC)-induced hypertrophic hearts and angiotensin II (Ang II)-treated cardiomyocytes. REGγ deficiency ameliorated pressure overload-induced cardiac hypertrophy were associated with inhibition of cardiac reactive oxygen species (ROS) accumulation and suppression of protein phosphatase 2A catalytic subunit α (PP2Acα) decay. Mechanistically, REGγ interacted with and targeted PP2Acα for degradation directly, thereby leading to increase of phosphorylation levels and nuclear export of Forkhead box protein O (FoxO) 3a and subsequent of SOD2 decline, ROS accumulation, and cardiac hypertrophy. Introducing exogenous PP2Acα or SOD2 to human cardiomyocytes significantly rescued the REGγ-mediated ROS accumulation of Ang II stimulation in vitro. Furthermore, treatment with superoxide dismutase mimetic, MnTBAP prevented cardiac ROS production and hypertrophy features that REGγ caused in vivo, thereby establishing a REGγ-PP2Acα-FoxO3a-SOD2 pathway in cardiac oxidative stress and hypertrophy, indicates modulating the REGγ-proteasome activity may be a potential therapeutic approach in cardiac hypertrophy-associated disorders."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.org/dc/terms/identifier"doi:10.1038/s41418-020-0554-8"xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Dong Z."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Gao R."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Gao Y."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Ge J."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Xie Y."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Yang W."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Moses R.E."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/author"Sun A."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/name"Cell Death Differ"xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/pages"2952-2972"xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/title"The proteasome activator REGgamma accelerates cardiac hypertrophy by declining PP2Acalpha-SOD2 pathway."xsd:string
http://purl.uniprot.org/citations/32424140http://purl.uniprot.org/core/volume"27"xsd:string
http://purl.uniprot.org/citations/32424140http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32424140
http://purl.uniprot.org/citations/32424140http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32424140
http://purl.uniprot.org/uniprot/#_B7Z8D3-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140
http://purl.uniprot.org/uniprot/#_B3KQ25-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140
http://purl.uniprot.org/uniprot/#_J7FRP4-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140
http://purl.uniprot.org/uniprot/#_K9J957-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140
http://purl.uniprot.org/uniprot/#_O43524-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140
http://purl.uniprot.org/uniprot/#_P61289-mappedCitation-32424140http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32424140