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http://purl.uniprot.org/citations/31171760http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31171760http://www.w3.org/2000/01/rdf-schema#comment"Cardiomyocyte apoptosis is a major cause of myocardial ischemia/reperfusion (MI/R) injury, in which the activation of the signal transducer and activator of transcription 1 (STAT1) plays an important role. The E3-ubiquitin ligase TRIM6 has been implicated in regulating STAT1 activity, however, whether it is associated with MI/R injury and the underlying mechanism are not determined. In this study, by investigating a mouse MI/R injury model, we show that TRIM6 expression is induced in mouse heart following MI/R injury. Additionally, TRIM6 depletion reduces and its overexpression increases myocardial infarct size, serum creatine phosphokinase (CPK) level and cardiomyocyte apoptosis in mice subjected to MI/R injury, indicating that TRIM6 functions to aggravate MI/R injury. Mechanistically, TRIM6 promotes IKKε-dependent STAT1 activation, and the inhibition of IKKε or STAT1 with the specific inhibitor, CAY10576 or fludarabine, abolishes TRIM6 effects on cardiomyocyte apoptosis and MI/R injury. Similarly, TRIM6 mutant lacking the ability to ubiquitinate IKKε and induce IKKε/STAT1 activation also fails to promote cardiomyocyte apoptosis and MI/R injury. Thus, these results suggest that TRIM6 aggravates MI/R injury through promoting IKKε/STAT1 activation-dependent cardiomyocyte apoptosis, and that TRIM6 might represent a novel therapeutic target for alleviating MI/R injury."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.org/dc/terms/identifier"doi:10.18632/aging.101995"xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Ren H."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Zheng M."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Yang P."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Zeng G."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/author"Lian C."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/name"Aging (Albany NY)"xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/pages"3536-3550"xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/title"E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis."xsd:string
http://purl.uniprot.org/citations/31171760http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/31171760http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31171760
http://purl.uniprot.org/citations/31171760http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31171760
http://purl.uniprot.org/uniprot/#_Q8BGE7-mappedCitation-31171760http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31171760
http://purl.uniprot.org/uniprot/#_Q8R2Z8-mappedCitation-31171760http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31171760
http://purl.uniprot.org/uniprot/Q8BGE7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31171760
http://purl.uniprot.org/uniprot/Q8R2Z8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31171760