{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cooley N"],"funding":["NHLBI NIH HHS"],"pagination":["318-25"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4028972"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(2)"],"pubmed_abstract":["<h4>Background</h4>We investigated the contribution of inositol(1,4,5)-trisphosphate (Ins(1,4,5)P3 [IP3]) receptors (IP3-R) to disease progression in mouse models of dilated cardiomyopathy (DCM) and pressure overload hypertrophy. Mice expressing mammalian sterile 20-like kinase and dominant-negative phosphatidylinositol-3-kinase in heart (Mst1×dn-PI3K-2Tg; DCM-2Tg) develop severe DCM and conduction block, associated with increased expression of type 2 IP3-R (IP3-R(2)) and heightened generation of Ins(1,4,5)P3. Similar increases in Ins(1,4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.<h4>Methods and results</h4>To evaluate the contribution of IP3-R(2) to disease progression, the DCM-2Tg mice were further crossed with mice in which the type 2 IP3-R (IP3-R(2)-/-) had been de"],"journal":["Circulation. Heart failure"],"pubmed_title":["No contribution of IP3-R(2) to disease phenotype in models of dilated cardiomyopathy or pressure overload hypertrophy."],"pmcid":["PMC4028972"],"funding_grant_id":["P01 HL080101","T32 HL007444","R01 HL095780"],"pubmed_authors":["Sheikh F","Du XJ","Woodcock EA","Mu Y","Chen J","Cooley N","Ouyang K","Kiriazis H","McMullen JR","Wu W"],"additional_accession":[]},"is_claimable":false,"name":"No contribution of IP3-R(2) to disease phenotype in models of dilated cardiomyopathy or pressure overload hypertrophy.","description":"<h4>Background</h4>We investigated the contribution of inositol(1,4,5)-trisphosphate (Ins(1,4,5)P3 [IP3]) receptors (IP3-R) to disease progression in mouse models of dilated cardiomyopathy (DCM) and pressure overload hypertrophy. Mice expressing mammalian sterile 20-like kinase and dominant-negative phosphatidylinositol-3-kinase in heart (Mst1×dn-PI3K-2Tg; DCM-2Tg) develop severe DCM and conduction block, associated with increased expression of type 2 IP3-R (IP3-R(2)) and heightened generation of Ins(1,4,5)P3. Similar increases in Ins(1,4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.<h4>Methods and results</h4>To evaluate the contribution of IP3-R(2) to disease progression, the DCM-2Tg mice were further crossed with mice in which the type 2 IP3-R (IP3-R(2)-/-) had been de","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Mar","modification":"2025-04-19T07:50:51.191Z","creation":"2019-03-26T23:49:30Z"},"accession":"S-EPMC4028972","cross_references":{"pubmed":["23258573"],"doi":["10.1161/circheartfailure.112.972158","10.1161/CIRCHEARTFAILURE.112.972158"]}}