{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shao Q"],"funding":["Intramural NIH HHS","NIEHS NIH HHS","NHLBI NIH HHS","National Natural Science Foundation of China (NSFC)","Division of Intramural Research, National Heart, Lung and Blood Institute","China Scholarship Council (CSC)","HHS | NIH | National Institute of Environmental Health Sciences (NIEHS)","HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)"],"pagination":["H505-15"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4796614"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["310(4)"],"pubmed_abstract":["Premenopausal women exhibit endogenous cardioprotective signaling mechanisms that are thought to result from the beneficial effects of estrogen, which we have shown to increase protein S-nitrosylation in the heart. S-nitrosylation is a labile protein modification that increases with a number of different forms of cardioprotection, including ischemic preconditioning. Herein, we sought to identify a potential role for protein S-nitrosylation in sex-dependent cardioprotection. We utilized a Langendorff-perfused mouse heart model of ischemia-reperfusion injury with male and female hearts, and S-nitrosylation-resin-assisted capture with liquid chromatography tandem mass spectrometry to identify S-nitrosylated proteins and modification sites. Consistent with previous studies, female hearts exhib"],"journal":["American journal of physiology. Heart and circulatory physiology"],"pubmed_title":["Characterization of the sex-dependent myocardial S-nitrosothiol proteome."],"pmcid":["PMC4796614"],"funding_grant_id":["Z01 HL002065","ZIA-HL-002065","R00 HL114721","R00HL114721","R01HL039752","R01 HL039752","T32ES0741","T32 ES007141","R01-HL-039752","81570390","T32-ES-0741","ZIAHL002065","R00-HL-114721","81270374"],"pubmed_authors":["Steenbergen C","Kohr MJ","Casin KM","Murphy E","Fallica J","Shao Q"],"additional_accession":[]},"is_claimable":false,"name":"Characterization of the sex-dependent myocardial S-nitrosothiol proteome.","description":"Premenopausal women exhibit endogenous cardioprotective signaling mechanisms that are thought to result from the beneficial effects of estrogen, which we have shown to increase protein S-nitrosylation in the heart. S-nitrosylation is a labile protein modification that increases with a number of different forms of cardioprotection, including ischemic preconditioning. Herein, we sought to identify a potential role for protein S-nitrosylation in sex-dependent cardioprotection. We utilized a Langendorff-perfused mouse heart model of ischemia-reperfusion injury with male and female hearts, and S-nitrosylation-resin-assisted capture with liquid chromatography tandem mass spectrometry to identify S-nitrosylated proteins and modification sites. Consistent with previous studies, female hearts exhib","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Feb","modification":"2026-05-05T06:27:51.851Z","creation":"2019-03-27T02:11:22Z"},"accession":"S-EPMC4796614","cross_references":{"pubmed":["26702143"],"doi":["10.1152/ajpheart.00681.2015"]}}