http://purl.uniprot.org/citations/26486084 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26486084 | http://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/26486084 | http://purl.org/dc/terms/identifier | "doi:10.18632/oncotarget.6071"xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Gu M."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Lu C."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Sun X."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Xu W."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Tang J."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Yao X."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Liang J."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Zhong T."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/author | "Hong X."xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/name | "Oncotarget"xsd:string |
http://purl.uniprot.org/citations/26486084 | http://purl.uniprot.org/core/pages | "35478-35495"xsd:string |
http://purl.uniprot.org/citations/26486084 | http://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/26486084 | http://purl.uniprot.org/core/volume | "6"xsd:string |
http://purl.uniprot.org/citations/26486084 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26486084 |
http://purl.uniprot.org/citations/26486084 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26486084 |
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