RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26486084http://www.w3.org/2000/01/rdf-schema#comment"To study the effect of EGFR activation on the generation of TNF-α and the occurrence of cardiac dysfuncetion during sepsis, PD168393 and erlotinib (both are EGFR inhibitors) were applied to decreased the production of TNF-α and phosphrylation of ERK1/2 and p38 induced by LPS in cardiomyocytes. These results were further proved by specifically knocked down the expression of EGFR in vitro. Both TAPI-1, a TNF-α converting enzyme (TACE) inhibitor, and TGF-α neutralizing antibody could inhibit the activation of EGFR and the generation of TNF-α mRNA after LPS treatment. The increase of TGF-α in response to LPS could also be suppressed by TAPI-1. On the other hand, exogenous TGF-α increased the expression of TNF-α mRNA and partially reversed the inhibitory effect of TAPI-1 on expression of TNF-α mRNA in response to LPS indicating that the transactivation of EGFR by LPS in cardiomyocytes needs the help of TACE and TGF-α. In endotoxemic mice, inhibition the activation of EGFR not only decreased TNF-α production in the myocardium but also improved left ventricular pump function and ameliorated cardiac dysfunction and ultimately improved survival rate. All these results provided a new insight of how EGFR regulation the production of TNF-α in cardiomyocytes and a potential new target for the treatment of cardiac dysfunction in sepsis."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.6071"xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Gu M."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Lu C."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Sun X."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Xu W."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Tang J."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Yao X."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Liang J."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Zhong T."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/author"Hong X."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/name"Oncotarget"xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/pages"35478-35495"xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/title"The activation of EGFR promotes myocardial tumor necrosis factor-alpha production and cardiac failure in endotoxemia."xsd:string
http://purl.uniprot.org/citations/26486084http://purl.uniprot.org/core/volume"6"xsd:string
http://purl.uniprot.org/citations/26486084http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26486084
http://purl.uniprot.org/citations/26486084http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26486084
http://purl.uniprot.org/uniprot/#_Q01279-mappedCitation-26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26486084
http://purl.uniprot.org/uniprot/#_Q3TQS6-mappedCitation-26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26486084
http://purl.uniprot.org/uniprot/#_Q99PK1-mappedCitation-26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26486084
http://purl.uniprot.org/uniprot/#_Q8VHI0-mappedCitation-26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26486084
http://purl.uniprot.org/uniprot/#_Q9ERV6-mappedCitation-26486084http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26486084