| http://purl.uniprot.org/citations/15623435 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15623435 | http://www.w3.org/2000/01/rdf-schema#comment | "gp130-dependent signaling is known to play a critical role in the onset of heart failure. In that regard, cardiotrophin-1 (CT-1) activates several signaling pathways via gp130, and induces hypertrophy in neonatal rat cardiomyocytes. Among the mediators activated by CT-1, STAT3 is thought to be important for induction of cell hypertrophy, though its precise function in the CT-1 signaling pathway is not fully understood. In the present study, therefore, to better understand the significance of STAT3 activity in CT-1 signaling, we infected cultured cardiomyocytes with adenoviral vectors harboring a dominant-negative STAT3 mutant or one of two endogenous negative regulators of cytokine signaling via the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways [suppressor of cytokine signaling (SOCS) 1 and 3] and then examined their effects on three indexes of CT-1-induced cell hypertrophy: protein synthesis, secretion of brain natriuretic peptide and changes in cell surface area. In control cells, CT-1-induced both STAT3 phosphorylation and cell hypertrophy. Overexpression of dominant-negative STAT3 mutant suppressed CT-1-induced STAT3 phosphorylation, but did not affect cell hypertrophy. On the other hand overexpression of SOCS1 or SOCS3 inhibited both CT-1-induced STAT3 phosphorylation and cell hypertrophy. CT-1 also induced phosphorylations of ERK1/2 and ERK5 in cardiomyocytes, and those, too, were suppressed by overexpression of SOCSs. CT-1-induced cell hypertrophy was suppressed by overexpression of a dominant-negative MEK5 mutant, and not by overexpression of a dominant-negative MEK1 mutant. These findings indicate that the major pathway responsible for the hypertrophic responses to CT-1 is not JAK-STAT3 pathway nor MEK1-ERK1/2 pathway, but MEK5-ERK5 pathway."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yjmcc.2004.10.016"xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Harada M."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Kawakami R."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Nakagawa Y."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Saito Y."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Nakanishi M."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Takahashi N."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Nakao K."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Usami S."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Kuwahara K."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Tanimoto K."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Yoshimura A."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/author | "Yasuno S."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/name | "J Mol Cell Cardiol"xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/pages | "185-192"xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/title | "Hypertrophic responses to cardiotrophin-1 are not mediated by STAT3, but via a MEK5-ERK5 pathway in cultured cardiomyocytes."xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://purl.uniprot.org/core/volume | "38"xsd:string |
| http://purl.uniprot.org/citations/15623435 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15623435 |
| http://purl.uniprot.org/citations/15623435 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15623435 |
| http://purl.uniprot.org/uniprot/Q63086#attribution-098A87024390B065A9F7A2C685DBA354 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/15623435 |
| http://purl.uniprot.org/uniprot/Q62862#attribution-098A87024390B065A9F7A2C685DBA354 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/15623435 |
| http://purl.uniprot.org/uniprot/#_A0A8I5ZZ49-mappedCitation-15623435 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15623435 |