<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shao Q</submitter><funding>Intramural NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>National Natural Science Foundation of China (NSFC)</funding><funding>Division of Intramural Research, National Heart, Lung and Blood Institute</funding><funding>China Scholarship Council (CSC)</funding><funding>HHS | NIH | National Institute of Environmental Health Sciences (NIEHS)</funding><funding>HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)</funding><pagination>H505-15</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4796614</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>310(4)</volume><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</pubmed_abstract><journal>American journal of physiology. Heart and circulatory physiology</journal><pubmed_title>Characterization of the sex-dependent myocardial S-nitrosothiol proteome.</pubmed_title><pmcid>PMC4796614</pmcid><funding_grant_id>Z01 HL002065</funding_grant_id><funding_grant_id>ZIA-HL-002065</funding_grant_id><funding_grant_id>R00 HL114721</funding_grant_id><funding_grant_id>R00HL114721</funding_grant_id><funding_grant_id>R01HL039752</funding_grant_id><funding_grant_id>R01 HL039752</funding_grant_id><funding_grant_id>T32ES0741</funding_grant_id><funding_grant_id>T32 ES007141</funding_grant_id><funding_grant_id>R01-HL-039752</funding_grant_id><funding_grant_id>81570390</funding_grant_id><funding_grant_id>T32-ES-0741</funding_grant_id><funding_grant_id>ZIAHL002065</funding_grant_id><funding_grant_id>R00-HL-114721</funding_grant_id><funding_grant_id>81270374</funding_grant_id><pubmed_authors>Steenbergen C</pubmed_authors><pubmed_authors>Kohr MJ</pubmed_authors><pubmed_authors>Casin KM</pubmed_authors><pubmed_authors>Murphy E</pubmed_authors><pubmed_authors>Fallica J</pubmed_authors><pubmed_authors>Shao Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterization of the sex-dependent myocardial S-nitrosothiol proteome.</name><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</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Feb</publication><modification>2026-05-05T06:27:51.851Z</modification><creation>2019-03-27T02:11:22Z</creation></dates><accession>S-EPMC4796614</accession><cross_references><pubmed>26702143</pubmed><doi>10.1152/ajpheart.00681.2015</doi></cross_references></HashMap>