| http://purl.uniprot.org/citations/14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/14551246 | http://www.w3.org/2000/01/rdf-schema#comment | "Multiple lines of evidence establish that angiotensin II (Ang II) induces not only hypertension but also directly contributes to cardiac diseases. Apoptosis signal-regulating kinase 1 (ASK1), one of mitogen-activated protein kinase kinase kinases, plays a key role in stress-induced cellular responses. However, nothing is known about the role of ASK1 in cardiac hypertrophy and remodeling in vivo. In this study, by using mice deficient in ASK1 (ASK1-/-mice), we investigated the role of ASK1 in cardiac hypertrophy and remodeling induced by Ang II. Left ventricular (LV) ASK1 was activated by Ang II infusion in wild-type mice, which was mediated by angiotensin II type 1 receptor and superoxide. Although Ang II-induced hypertensive effect was comparable to wild-type and ASK1-/-mice, LV ASK1 activation by Ang II was not detectable in ASK1-/-mice, and p38 and c-Jun N-terminal kinase (JNK) activation was lesser in ASK-/-mice than in wild-type mice. Elevation of blood pressure by continuous Ang II infusion was comparable between ASK1-/- and wild-type mice. However, Ang II-induced cardiac hypertrophy and remodeling, including cardiomyocyte hypertrophy, cardiac hypertrophy-related mRNA upregulation, cardiomyocyte apoptosis, interstitial fibrosis, coronary arterial remodeling, and collagen gene upregulation, was significantly attenuated in ASK1-/-mice compared with wild-type mice. These results provided the first in vivo evidence that ASK1 is the critical signaling molecule for Ang II-induced cardiac hypertrophy and remodeling. Thus, ASK1 is proposed to be a potential therapeutic target for cardiac diseases."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.res.0000100665.67510.f5"xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Izumi Y."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Kim S."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Yoshida K."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Matsuzawa A."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Ichijo H."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Izumiya Y."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Iwao H."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/author | "Yoshiyama M."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/name | "Circ Res"xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/pages | "874-883"xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/title | "Apoptosis signal-regulating kinase 1 plays a pivotal role in angiotensin II-induced cardiac hypertrophy and remodeling."xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://purl.uniprot.org/core/volume | "93"xsd:string |
| http://purl.uniprot.org/citations/14551246 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/14551246 |
| http://purl.uniprot.org/citations/14551246 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/14551246 |
| http://purl.uniprot.org/uniprot/#_A0A1L1ST18-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_D3YVC4-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_D3Z5H1-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_E9PWG9-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_Q14AY4-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_O35099-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |
| http://purl.uniprot.org/uniprot/#_Q8CC79-mappedCitation-14551246 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/14551246 |