{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361418520740938112.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/j.1749-6632.2009.05088.x"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1749-6632.2009.05088.x"}},{"identifier":{"@type":"URI","@value":"https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2009.05088.x"}}],"dc:title":[{"@value":"Extracellular signal‐regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Cardiac hypertrophy results from increased mechanical load on the heart and through the action of neurohumoral mediators. ERK1/2 are known to be activated in response to almost every stress‐ and agonist‐induced hypertrophic stimulus examined to date, suggesting the straightforward hypothesis that these kinases are required for promoting the cardiac growth response. However, recent data from genetically modified mouse models suggest a more complicated picture. For example, inducible expression of dual‐specificity phosphatase 6, an ERK1/2‐inactivating phosphatase, eliminated ERK1/2 phosphorylation in transgenic mice, but it did not diminish the hypertrophic response to pressure overload. Similarly, <jats:italic>Erk1</jats:italic><jats:sup>−/−</jats:sup> and <jats:italic>Erk2</jats:italic><jats:sup>+/−</jats:sup> mice showed no reduction in stimulus‐induced cardiac growth <jats:italic>in vivo</jats:italic>. However, blockade or deletion of cardiac ERK1/2 did predispose the heart to decompensation and failure after long‐term pressure overload. Thus, ERK1/2 signaling is not to be absolutely necessary for mediating cardiac hypertrophy, although it does appear to provide critical protective effects/signals during stress‐stimulation.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381418520740938112","@type":"Researcher","foaf:name":[{"@value":"Izhak Kehat"}]},{"@id":"https://cir.nii.ac.jp/crid/1381418520740938113","@type":"Researcher","foaf:name":[{"@value":"Jeffery D. Molkentin"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00778923"},{"@type":"EISSN","@value":"17496632"}],"prism:publicationName":[{"@value":"Annals of the New York Academy of Sciences"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2010-02","prism:volume":"1188","prism:number":"1","prism:startingPage":"96","prism:endingPage":"102"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1749-6632.2009.05088.x"},{"@id":"https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2009.05088.x"}],"createdAt":"2010-02-23","modifiedAt":"2023-09-25","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360004232000898688","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Midkine exacerbates pressure overload-induced cardiac remodeling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285705138142464","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Disruption of Tumor Necrosis Factor Receptor Associated Factor 5 Exacerbates Pressure Overload Cardiac Hypertrophy and Fibrosis"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567182514365056","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Targeted deletion of ERK2 in cardiomyocytes attenuates hypertrophic response but provokes pathological stress induced cardiac dysfunction"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848658890404096","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"MURC/Cavin-4 facilitates recruitment of ERK to caveolae and concentric cardiac hypertrophy induced by α1-adrenergic receptors"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848661361220352","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Crucial Role of Rho-Kinase in Pressure Overload–Induced Right Ventricular Hypertrophy and Dysfunction in Mice"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1111/j.1749-6632.2009.05088.x"},{"@type":"CROSSREF","@value":"10.1016/j.bbrc.2013.11.083_references_DOI_8MVbkLjMt9lpdjbJ9Yair7IjzR5"},{"@type":"CROSSREF","@value":"10.1002/jcb.24669_references_DOI_8MVbkLjMt9lpdjbJ9Yair7IjzR5"},{"@type":"CROSSREF","@value":"10.1016/j.yjmcc.2014.03.002_references_DOI_8MVbkLjMt9lpdjbJ9Yair7IjzR5"},{"@type":"CROSSREF","@value":"10.1073/pnas.1315359111_references_DOI_8MVbkLjMt9lpdjbJ9Yair7IjzR5"},{"@type":"CROSSREF","@value":"10.1161/atvbaha.114.303320_references_DOI_8MVbkLjMt9lpdjbJ9Yair7IjzR5"}]}