{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yue X"],"funding":["NHLBI NIH HHS"],"pagination":["e1284"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4611712"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5"],"pubmed_abstract":["Rho family guanosine triphosphatase (GTPase) 3 (Rnd3), a member of the small Rho GTPase family, has been suggested to regulate cell actin cytoskeleton dynamics, cell migration, and apoptosis through the Rho kinase-dependent signaling pathway. The biological function of Rnd3 in the heart is unknown. The downregulation of small GTPase Rnd3 transcripts was found in patients with end-stage heart failure. The pathological significance of Rnd3 loss in the transition to heart failure remains unexplored. To investigate the functional consequence of Rnd3 downregulation and the associated molecular mechanism, we generated Rnd3(+/-) haploinsufficient mice to mimic the downregulation of Rnd3 observed in the failing human heart. Rnd3(+/-) mice were viable; however, the mice developed heart failure afte"],"journal":["Cell death & disease"],"pubmed_title":["Rnd3 haploinsufficient mice are predisposed to hemodynamic stress and develop apoptotic cardiomyopathy with heart failure."],"pmcid":["PMC4611712"],"funding_grant_id":["R21 HL094844","R01 HL-087861","K02 HL098956","R21HL094844","R01 HL102314","K02HL098956","R01 HL107537","R01HL102314","R01 HL123953","R01 HL087861"],"pubmed_authors":["Yi X","Lin X","Chen C","Dai Y","Yang X","Guo J","Li T","Fan GC","Yang T","Shi J","Chang J","Yue X","Wei L"],"additional_accession":[]},"is_claimable":false,"name":"Rnd3 haploinsufficient mice are predisposed to hemodynamic stress and develop apoptotic cardiomyopathy with heart failure.","description":"Rho family guanosine triphosphatase (GTPase) 3 (Rnd3), a member of the small Rho GTPase family, has been suggested to regulate cell actin cytoskeleton dynamics, cell migration, and apoptosis through the Rho kinase-dependent signaling pathway. The biological function of Rnd3 in the heart is unknown. The downregulation of small GTPase Rnd3 transcripts was found in patients with end-stage heart failure. The pathological significance of Rnd3 loss in the transition to heart failure remains unexplored. To investigate the functional consequence of Rnd3 downregulation and the associated molecular mechanism, we generated Rnd3(+/-) haploinsufficient mice to mimic the downregulation of Rnd3 observed in the failing human heart. Rnd3(+/-) mice were viable; however, the mice developed heart failure afte","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jun","modification":"2025-04-04T10:50:44.587Z","creation":"2019-03-27T02:00:20Z"},"accession":"S-EPMC4611712","cross_references":{"pubmed":["24901055"],"doi":["10.1038/cddis.2014.235"]}}