<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Loftus LT</submitter><funding>NINDS NIH HHS</funding><pagination>71-80</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2774733</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>1272</volume><pubmed_abstract>Several recent studies suggest that sumo-2/3 modification of proteins occurs following harmful ischemia, however, sumo-2/3-ylation may also be associated with hibernation-mediated neuroprotection. Here we investigate the sumoylation of proteins following ischemia and ischemic tolerance using our established in vitro model of ischemia (oxygen and glucose deprivation; OGD). Following harmful ischemia (120 min OGD), we observed a significant increase in the sumo-2/3-ylation of high molecular weight proteins (>85 kDa), but not sumo-1-ylation of proteins. Sumo-2/3-ylation following 120 min OGD was reduced when cultures were preconditioned with non-harmful 30 min OGD 24 h earlier (delayed ischemic tolerance). However, we observed no change in sumo-2/3-ylation in a model of rapid ischemic toleran</pubmed_abstract><journal>Brain research</journal><pubmed_title>Sumo-2/3-ylation following in vitro modeled ischemia is reduced in delayed ischemic tolerance.</pubmed_title><pmcid>PMC2774733</pmcid><funding_grant_id>R21 NS054023-02</funding_grant_id><funding_grant_id>R01 NS059588-01A2</funding_grant_id><funding_grant_id>NS024728</funding_grant_id><funding_grant_id>R01 NS059588</funding_grant_id><funding_grant_id>NS059588</funding_grant_id><funding_grant_id>R01 NS024728</funding_grant_id><funding_grant_id>NS054023</funding_grant_id><funding_grant_id>R21 NS050669</funding_grant_id><funding_grant_id>R21 NS054023</funding_grant_id><funding_grant_id>R01 NS024728-22</funding_grant_id><pubmed_authors>Gala R</pubmed_authors><pubmed_authors>Ordonez AN</pubmed_authors><pubmed_authors>Jessick VJ</pubmed_authors><pubmed_authors>Thompson SJ</pubmed_authors><pubmed_authors>Simon RP</pubmed_authors><pubmed_authors>Meller R</pubmed_authors><pubmed_authors>Yang T</pubmed_authors><pubmed_authors>Ashley MD</pubmed_authors><pubmed_authors>Loftus LT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sumo-2/3-ylation following in vitro modeled ischemia is reduced in delayed ischemic tolerance.</name><description>Several recent studies suggest that sumo-2/3 modification of proteins occurs following harmful ischemia, however, sumo-2/3-ylation may also be associated with hibernation-mediated neuroprotection. Here we investigate the sumoylation of proteins following ischemia and ischemic tolerance using our established in vitro model of ischemia (oxygen and glucose deprivation; OGD). Following harmful ischemia (120 min OGD), we observed a significant increase in the sumo-2/3-ylation of high molecular weight proteins (>85 kDa), but not sumo-1-ylation of proteins. Sumo-2/3-ylation following 120 min OGD was reduced when cultures were preconditioned with non-harmful 30 min OGD 24 h earlier (delayed ischemic tolerance). However, we observed no change in sumo-2/3-ylation in a model of rapid ischemic toleran</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 May</publication><modification>2025-04-04T13:38:27.544Z</modification><creation>2019-03-27T00:26:26Z</creation></dates><accession>S-EPMC2774733</accession><cross_references><pubmed>19332039</pubmed><doi>10.1016/j.brainres.2009.03.034</doi></cross_references></HashMap>