{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:32:18Z","timestamp":1787315538693,"version":"build-2736575974"},"reference-count":43,"publisher":"Elsevier BV","license":[{"start":{"date-parts":[[2017,11,1]],"date-time":"2017-11-01T00:00:00Z","timestamp":1509494400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.elsevier.com\/tdm\/userlicense\/1.0\/"}],"content-domain":{"domain":["jmmc-online.com","clinicalkey.jp","clinicalkey.com","clinicalkey.es","clinicalkey.com.au","clinicalkey.fr","elsevier.com","sciencedirect.com"],"crossmark-restriction":true},"short-container-title":["Journal of Molecular and Cellular Cardiology"],"published-print":{"date-parts":[[2017,11]]},"DOI":"10.1016\/j.yjmcc.2017.09.003","type":"journal-article","created":{"date-parts":[[2017,9,11]],"date-time":"2017-09-11T13:16:41Z","timestamp":1505135801000},"page":"83-90","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":5,"special_numbering":"C","title":["Heterozygous deletion of AKT1 rescues cardiac contractility, but not hypertrophy, in a mouse model of Noonan Syndrome with Multiple Lentigines"],"prefix":"10.1016","volume":"112","author":[{"given":"Rajika","family":"Roy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maike","family":"Krenz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"78","reference":[{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0005","doi-asserted-by":"crossref","first-page":"216","DOI":"10.1161\/CIRCULATIONAHA.105.583500","article-title":"Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy","volume":"114","author":"Harris","year":"2006","journal-title":"Circulation"},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0010","doi-asserted-by":"crossref","first-page":"518","DOI":"10.1172\/JCI24351","article-title":"Genetic causes of human heart failure","volume":"115","author":"Morita","year":"2005","journal-title":"J. Clin. Invest."},{"issue":"1","key":"10.1016\/j.yjmcc.2017.09.003_bb0015","doi-asserted-by":"crossref","first-page":"83","DOI":"10.1016\/j.jacc.2014.05.003","article-title":"Hypertrophic cardiomyopathy: present and future, with translation into contemporary cardiovascular medicine","volume":"64","author":"Maron","year":"2014","journal-title":"J. Am. Coll. Cardiol."},{"issue":"11","key":"10.1016\/j.yjmcc.2017.09.003_bb0020","doi-asserted-by":"crossref","first-page":"803","DOI":"10.1007\/s00431-006-0163-7","article-title":"PTPN11 gene mutations: linking the Gln510Glu mutation to the \u201cLEOPARD syndrome phenotype\u201d","volume":"165","author":"Digilio","year":"2006","journal-title":"Eur. J. Pediatr."},{"issue":"7","key":"10.1016\/j.yjmcc.2017.09.003_bb0025","doi-asserted-by":"crossref","first-page":"1012","DOI":"10.1007\/s00246-009-9473-7","article-title":"PTPN11 gene mutation and severe neonatal hypertrophic cardiomyopathy: what is the link?","volume":"30","author":"Faienza","year":"2009","journal-title":"Pediatr. Cardiol."},{"issue":"1","key":"10.1016\/j.yjmcc.2017.09.003_bb0030","doi-asserted-by":"crossref","first-page":"74","DOI":"10.4103\/0974-2069.79631","article-title":"LEOPARD syndrome in an infant with severe hypertrophic cardiomyopathy and PTPN11 mutation","volume":"4","author":"Ganigara","year":"2011","journal-title":"Ann. Pediatr. Cardiol."},{"issue":"8","key":"10.1016\/j.yjmcc.2017.09.003_bb0035","doi-asserted-by":"crossref","first-page":"497","DOI":"10.1007\/s00431-005-1679-y","article-title":"A novel mutation in the PTPN11 gene in a patient with Noonan syndrome and rapidly progressive hypertrophic cardiomyopathy","volume":"164","author":"Takahashi","year":"2005","journal-title":"Eur. J. Pediatr."},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0040","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1097\/HCO.0b013e3283375698","article-title":"Genetics of hypertrophic cardiomyopathy","volume":"25","author":"Konno","year":"2010","journal-title":"Curr. Opin. Cardiol."},{"issue":"10","key":"10.1016\/j.yjmcc.2017.09.003_bb0045","doi-asserted-by":"crossref","first-page":"2498","DOI":"10.1128\/MCB.00646-09","article-title":"Functional effects of PTPN11 (SHP2) mutations causing LEOPARD syndrome on epidermal growth factor-induced phosphoinositide 3-kinase\/AKT\/glycogen synthase kinase 3beta signaling","volume":"30","author":"Edouard","year":"2010","journal-title":"Mol. Cell. Biol."},{"issue":"4","key":"10.1016\/j.yjmcc.2017.09.003_bb0050","doi-asserted-by":"crossref","first-page":"H1531","DOI":"10.1152\/ajpheart.00216.2011","article-title":"LEOPARD-type SHP2 mutant Gln510Glu attenuates cardiomyocyte differentiation and promotes cardiac hypertrophy via dysregulation of Akt\/GSK-3{beta}\/{beta}-catenin signaling","volume":"301","author":"Ishida","year":"2011","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"issue":"25","key":"10.1016\/j.yjmcc.2017.09.003_bb0055","doi-asserted-by":"crossref","first-page":"18335","DOI":"10.1074\/jbc.M113.483800","article-title":"New approaches to prevent LEOPARD syndrome-associated cardiac hypertrophy by specifically targeting Shp2-dependent signaling","volume":"288","author":"Schramm","year":"2013","journal-title":"J. Biol. Chem."},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0060","doi-asserted-by":"crossref","first-page":"1026","DOI":"10.1172\/JCI44972","article-title":"Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome-associated PTPN11 mutation","volume":"121","author":"Marin","year":"2011","journal-title":"J. Clin. Invest."},{"issue":"1","key":"10.1016\/j.yjmcc.2017.09.003_bb0065","doi-asserted-by":"crossref","first-page":"H231","DOI":"10.1152\/ajpheart.00665.2011","article-title":"The PTPN11 loss-of-function mutation Q510E-Shp2 causes hypertrophic cardiomyopathy by dysregulating mTOR signaling","volume":"302","author":"Schramm","year":"2012","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"issue":"9","key":"10.1016\/j.yjmcc.2017.09.003_bb0070","doi-asserted-by":"crossref","first-page":"658","DOI":"10.1038\/ncb840","article-title":"Akt regulates growth by directly phosphorylating Tsc2","volume":"4","author":"Potter","year":"2002","journal-title":"Nat. Cell Biol."},{"issue":"9","key":"10.1016\/j.yjmcc.2017.09.003_bb0075","doi-asserted-by":"crossref","first-page":"648","DOI":"10.1038\/ncb839","article-title":"TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling","volume":"4","author":"Inoki","year":"2002","journal-title":"Nat. Cell Biol."},{"issue":"11","key":"10.1016\/j.yjmcc.2017.09.003_bb0080","doi-asserted-by":"crossref","first-page":"2477","DOI":"10.1158\/1535-7163.MCT-14-0330","article-title":"Suppression of feedback loops mediated by PI3K\/mTOR induces multiple overactivation of compensatory pathways: an unintended consequence leading to drug resistance","volume":"13","author":"Rozengurt","year":"2014","journal-title":"Mol. Cancer Ther."},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0085","doi-asserted-by":"crossref","first-page":"1023","DOI":"10.1152\/physrev.00024.2010","article-title":"Myocardial AKT: the omnipresent nexus","volume":"91","author":"Sussman","year":"2011","journal-title":"Physiol. Rev."},{"issue":"2","key":"10.1016\/j.yjmcc.2017.09.003_bb0090","doi-asserted-by":"crossref","first-page":"316","DOI":"10.1002\/jcp.21197","article-title":"Activation or inactivation of cardiac Akt\/mTOR signaling diverges physiological from pathological hypertrophy","volume":"214","author":"Kemi","year":"2008","journal-title":"J. Cell. Physiol."},{"issue":"2","key":"10.1016\/j.yjmcc.2017.09.003_bb0095","doi-asserted-by":"crossref","first-page":"160","DOI":"10.1093\/cvr\/cvu243","article-title":"Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy","volume":"105","author":"Moc","year":"2015","journal-title":"Cardiovasc. Res."},{"issue":"12","key":"10.1016\/j.yjmcc.2017.09.003_bb0100","doi-asserted-by":"crossref","first-page":"1332","DOI":"10.1161\/01.RES.0000196568.11624.ae","article-title":"Nuclear targeting of Akt enhances ventricular function and myocyte contractility","volume":"97","author":"Rota","year":"2005","journal-title":"Circ. Res."},{"issue":"32","key":"10.1016\/j.yjmcc.2017.09.003_bb0105","doi-asserted-by":"crossref","first-page":"11946","DOI":"10.1073\/pnas.0510138103","article-title":"Nuclear targeting of Akt antagonizes aspects of cardiomyocyte hypertrophy","volume":"103","author":"Tsujita","year":"2006","journal-title":"Proc. Natl. Acad. Sci. U. S. A."},{"issue":"25","key":"10.1016\/j.yjmcc.2017.09.003_bb0110","doi-asserted-by":"crossref","first-page":"22896","DOI":"10.1074\/jbc.M200347200","article-title":"Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart","volume":"277","author":"Matsui","year":"2002","journal-title":"J. Biol. Chem."},{"issue":"42","key":"10.1016\/j.yjmcc.2017.09.003_bb0115","doi-asserted-by":"crossref","first-page":"38349","DOI":"10.1074\/jbc.C100462200","article-title":"Akt1\/PKBalpha is required for normal growth but dispensable for maintenance of glucose homeostasis in mice","volume":"276","author":"Cho","year":"2001","journal-title":"J. Biol. Chem."},{"issue":"17","key":"10.1016\/j.yjmcc.2017.09.003_bb0120","doi-asserted-by":"crossref","first-page":"2097","DOI":"10.1161\/CIRCULATIONAHA.105.595231","article-title":"Akt1 is required for physiological cardiac growth","volume":"113","author":"DeBosch","year":"2006","journal-title":"Circulation"},{"issue":"9","key":"10.1016\/j.yjmcc.2017.09.003_bb0125","doi-asserted-by":"crossref","first-page":"H1086","DOI":"10.1152\/ajpheart.00501.2014","article-title":"Elevated Ca2+ transients and increased myofibrillar power generation cause cardiac hypercontractility in a model of Noonan syndrome with Multiple Lentigines","volume":"308","author":"Clay","year":"2015","journal-title":"Am. J. Physiol. Heart Circ. Physiol."},{"issue":"8","key":"10.1016\/j.yjmcc.2017.09.003_bb0130","doi-asserted-by":"crossref","first-page":"2123","DOI":"10.1172\/JCI30756","article-title":"Mediating ERK 1\/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome","volume":"117","author":"Nakamura","year":"2007","journal-title":"J. Clin. Invest."},{"issue":"8","key":"10.1016\/j.yjmcc.2017.09.003_bb0135","doi-asserted-by":"crossref","first-page":"2799","DOI":"10.1128\/MCB.22.8.2799-2809.2002","article-title":"Akt\/protein kinase B promotes organ growth in transgenic mice","volume":"22","author":"Shioi","year":"2002","journal-title":"Mol. Cell. Biol."},{"issue":"20","key":"10.1016\/j.yjmcc.2017.09.003_bb0140","doi-asserted-by":"crossref","first-page":"13842","DOI":"10.1074\/jbc.M801510200","article-title":"Cardiac restricted overexpression of kinase-dead mammalian target of rapamycin (mTOR) mutant impairs the mTOR-mediated signaling and cardiac function","volume":"283","author":"Shen","year":"2008","journal-title":"J. Biol. Chem."},{"issue":"13","key":"10.1016\/j.yjmcc.2017.09.003_bb0145","doi-asserted-by":"crossref","first-page":"2943","DOI":"10.1242\/dev.01864","article-title":"Essential role of protein kinase B gamma (PKB gamma\/Akt3) in postnatal brain development but not in glucose homeostasis","volume":"132","author":"Tschopp","year":"2005","journal-title":"Development"},{"issue":"5","key":"10.1016\/j.yjmcc.2017.09.003_bb0150","doi-asserted-by":"crossref","first-page":"1869","DOI":"10.1128\/MCB.25.5.1869-1878.2005","article-title":"Role for Akt3\/protein kinase Bgamma in attainment of normal brain size","volume":"25","author":"Easton","year":"2005","journal-title":"Mol. Cell. Biol."},{"issue":"5522","key":"10.1016\/j.yjmcc.2017.09.003_bb0155","doi-asserted-by":"crossref","first-page":"1728","DOI":"10.1126\/science.292.5522.1728","article-title":"Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta)","volume":"292","author":"Cho","year":"2001","journal-title":"Science"},{"issue":"43","key":"10.1016\/j.yjmcc.2017.09.003_bb0160","doi-asserted-by":"crossref","first-page":"32841","DOI":"10.1074\/jbc.M513087200","article-title":"Akt2 regulates cardiac metabolism and cardiomyocyte survival","volume":"281","author":"DeBosch","year":"2006","journal-title":"J. Biol. Chem."},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0165","doi-asserted-by":"crossref","first-page":"317","DOI":"10.1007\/s00246-010-9879-2","article-title":"Akt2: a critical regulator of cardiomyocyte survival and metabolism","volume":"32","author":"Muslin","year":"2011","journal-title":"Pediatr. Cardiol."},{"issue":"17","key":"10.1016\/j.yjmcc.2017.09.003_bb0170","doi-asserted-by":"crossref","first-page":"2203","DOI":"10.1101\/gad.913901","article-title":"Growth retardation and increased apoptosis in mice with homozygous disruption of the Akt1 gene","volume":"15","author":"Chen","year":"2001","journal-title":"Genes Dev."},{"issue":"19","key":"10.1016\/j.yjmcc.2017.09.003_bb0175","doi-asserted-by":"crossref","first-page":"12333","DOI":"10.1073\/pnas.172376399","article-title":"Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice","volume":"99","author":"Condorelli","year":"2002","journal-title":"Proc. Natl. Acad. Sci. U. S. A."},{"issue":"2","key":"10.1016\/j.yjmcc.2017.09.003_bb0180","doi-asserted-by":"crossref","first-page":"375","DOI":"10.1016\/j.yjmcc.2004.12.002","article-title":"Akt3 overexpression in the heart results in progression from adaptive to maladaptive hypertrophy","volume":"38","author":"Taniyama","year":"2005","journal-title":"J. Mol. Cell. Cardiol."},{"issue":"3","key":"10.1016\/j.yjmcc.2017.09.003_bb0185","doi-asserted-by":"crossref","first-page":"761","DOI":"10.1016\/j.bmcl.2004.11.011","article-title":"Allosteric Akt (PKB) inhibitors: discovery and SAR of isozyme selective inhibitors","volume":"15","author":"Lindsley","year":"2005","journal-title":"Bioorg. Med. Chem. Lett."},{"issue":"13","key":"10.1016\/j.yjmcc.2017.09.003_bb0190","doi-asserted-by":"crossref","first-page":"4803","DOI":"10.1128\/MCB.22.13.4803-4814.2002","article-title":"Myogenic Akt signaling regulates blood vessel recruitment during myofiber growth","volume":"22","author":"Takahashi","year":"2002","journal-title":"Mol. Cell. Biol."},{"issue":"8","key":"10.1016\/j.yjmcc.2017.09.003_bb0195","doi-asserted-by":"crossref","first-page":"2108","DOI":"10.1172\/JCI24682","article-title":"Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure","volume":"115","author":"Shiojima","year":"2005","journal-title":"J. Clin. Invest."},{"issue":"1","key":"10.1016\/j.yjmcc.2017.09.003_bb0200","doi-asserted-by":"crossref","first-page":"128","DOI":"10.1073\/pnas.0403198102","article-title":"Microvascular patterning is controlled by fine-tuning the Akt signal","volume":"102","author":"Sun","year":"2005","journal-title":"Proc. Natl. Acad. Sci. U. S. A."},{"issue":"6","key":"10.1016\/j.yjmcc.2017.09.003_bb0205","article-title":"Multimodal imaging reveals a role for Akt1 in fetal cardiac development","volume":"1","author":"Vandoorne","year":"2013","journal-title":"Phys. Rep."},{"issue":"4","key":"10.1016\/j.yjmcc.2017.09.003_bb0210","doi-asserted-by":"crossref","first-page":"857","DOI":"10.1016\/j.yjmcc.2011.08.028","article-title":"The coronary circulation and blood flow in left ventricular hypertrophy","volume":"52","author":"Camici","year":"2012","journal-title":"J. Mol. Cell. Cardiol."},{"issue":"11","key":"10.1016\/j.yjmcc.2017.09.003_bb0215","doi-asserted-by":"crossref","first-page":"1027","DOI":"10.1056\/NEJMoa025050","article-title":"Coronary microvascular dysfunction and prognosis in hypertrophic cardiomyopathy","volume":"349","author":"Cecchi","year":"2003","journal-title":"N. Engl. J. Med."}],"container-title":["Journal of Molecular and Cellular Cardiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.elsevier.com\/content\/article\/PII:S002228281730305X?httpAccept=text\/xml","content-type":"text\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/api.elsevier.com\/content\/article\/PII:S002228281730305X?httpAccept=text\/plain","content-type":"text\/plain","content-version":"vor","intended-application":"text-mining"}],"deposited":{"date-parts":[[2018,8,27]],"date-time":"2018-08-27T16:08:40Z","timestamp":1535386120000},"score":1,"resource":{"primary":{"URL":"https:\/\/linkinghub.elsevier.com\/retrieve\/pii\/S002228281730305X"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017,11]]},"references-count":43,"alternative-id":["S002228281730305X"],"URL":"https:\/\/doi.org\/10.1016\/j.yjmcc.2017.09.003","relation":{},"ISSN":["0022-2828"],"issn-type":[{"value":"0022-2828","type":"print"}],"subject":[],"published":{"date-parts":[[2017,11]]},"assertion":[{"value":"Elsevier","name":"publisher","label":"This article is maintained by"},{"value":"Heterozygous deletion of AKT1 rescues cardiac contractility, but not hypertrophy, in a mouse model of Noonan Syndrome with Multiple Lentigines","name":"articletitle","label":"Article Title"},{"value":"Journal of Molecular and Cellular Cardiology","name":"journaltitle","label":"Journal Title"},{"value":"https:\/\/doi.org\/10.1016\/j.yjmcc.2017.09.003","name":"articlelink","label":"CrossRef DOI link to publisher maintained version"},{"value":"article","name":"content_type","label":"Content Type"},{"value":"\u00a9 2017 Elsevier Ltd. All rights reserved.","name":"copyright","label":"Copyright"}]}}