{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li R"],"funding":["The Veterans Administration","NHLBI NIH HHS","NIH"],"pagination":["952-962"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3349893"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["180(3)"],"pubmed_abstract":["How mechanical signals are transmitted in the cardiac myocyte is poorly understood. In this study, we produced a tamoxifen-inducible mouse model in which β1 integrin could be reduced specifically in the adult cardiomyocyte, so that the function of this integrin could be assessed in the postnatal and mechanically stressed heart. The expression of β1 integrin was reduced to 35% of control levels, but function remained normal at baseline. With aortic constriction, the knockout mice survived but had a blunted hypertrophic response. Integrin knockout myocytes, in contrast to controls, showed reduced integrin-linked kinase expression both at baseline and after hemodynamic stress; focal adhesion kinase expression was reduced after stress. Alterations in multiple signaling pathways were detected i"],"journal":["The American journal of pathology"],"pubmed_title":["β1 integrin gene excision in the adult murine cardiac myocyte causes defective mechanical and signaling responses."],"pmcid":["PMC3349893"],"funding_grant_id":["R01 HL092116","T32 HL007444","R01 HL092116-01A2","R01 HL092116-03","R01 HL092116-02"],"pubmed_authors":["Dalton ND","Manso AM","Gu Y","Israeli S","Nguyen U","Ross RS","Peterson KL","Huang MS","Li R","Wu Y","Liao P","Yajima T"],"additional_accession":[]},"is_claimable":false,"name":"β1 integrin gene excision in the adult murine cardiac myocyte causes defective mechanical and signaling responses.","description":"How mechanical signals are transmitted in the cardiac myocyte is poorly understood. In this study, we produced a tamoxifen-inducible mouse model in which β1 integrin could be reduced specifically in the adult cardiomyocyte, so that the function of this integrin could be assessed in the postnatal and mechanically stressed heart. The expression of β1 integrin was reduced to 35% of control levels, but function remained normal at baseline. With aortic constriction, the knockout mice survived but had a blunted hypertrophic response. Integrin knockout myocytes, in contrast to controls, showed reduced integrin-linked kinase expression both at baseline and after hemodynamic stress; focal adhesion kinase expression was reduced after stress. Alterations in multiple signaling pathways were detected i","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Mar","modification":"2025-04-05T15:40:15.354Z","creation":"2019-03-27T00:53:23Z"},"accession":"S-EPMC3349893","cross_references":{"pubmed":["22248583"],"doi":["10.1016/j.ajpath.2011.12.007"]}}