<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Doulias PT</submitter><funding>NIDA NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><pagination>367-378</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8477648</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(3)</volume><pubmed_abstract>In the brain, both HIV-1 and methamphetamine (meth) use result in increases in oxidative and nitrosative stress. This redox stress is thought to contribute to the pathogenesis of HIV-associated neurocognitive disorder (HAND) and further worsening cognitive activity in the setting of drug abuse. One consequence of such redox stress is aberrant protein S-nitrosylation, derived from nitric oxide, which may disrupt normal protein activity. Here, we report an improved, mass spectrometry-based technique to assess S-nitrosylated protein in human postmortem brains using selective enrichment of S-nitrosocysteine residues with an organomercury resin. The data show increasing S-nitrosylation of tricarboxylic acid (TCA) enzymes in the setting of HAND and HAND/meth use compared with HIV+ control brains</pubmed_abstract><journal>Journal of neurovirology</journal><pubmed_title>TCA cycle metabolic compromise due to an aberrant S-nitrosoproteome in HIV-associated neurocognitive disorder with methamphetamine use.</pubmed_title><pmcid>PMC8477648</pmcid><funding_grant_id>R01 AG056259</funding_grant_id><funding_grant_id>U24 MH100928</funding_grant_id><funding_grant_id>RF1 AG057409</funding_grant_id><funding_grant_id>R01 AG061845</funding_grant_id><funding_grant_id>DP1 DA041722</funding_grant_id><funding_grant_id>R01 NS086890</funding_grant_id><pubmed_authors>Scott H</pubmed_authors><pubmed_authors>Ischiropoulos H</pubmed_authors><pubmed_authors>McKercher SR</pubmed_authors><pubmed_authors>Albertolle M</pubmed_authors><pubmed_authors>Lipton SA</pubmed_authors><pubmed_authors>Doulias PT</pubmed_authors><pubmed_authors>Nakamura T</pubmed_authors><pubmed_authors>Deal A</pubmed_authors><pubmed_authors>Sultan A</pubmed_authors></additional><is_claimable>false</is_claimable><name>TCA cycle metabolic compromise due to an aberrant S-nitrosoproteome in HIV-associated neurocognitive disorder with methamphetamine use.</name><description>In the brain, both HIV-1 and methamphetamine (meth) use result in increases in oxidative and nitrosative stress. This redox stress is thought to contribute to the pathogenesis of HIV-associated neurocognitive disorder (HAND) and further worsening cognitive activity in the setting of drug abuse. One consequence of such redox stress is aberrant protein S-nitrosylation, derived from nitric oxide, which may disrupt normal protein activity. Here, we report an improved, mass spectrometry-based technique to assess S-nitrosylated protein in human postmortem brains using selective enrichment of S-nitrosocysteine residues with an organomercury resin. The data show increasing S-nitrosylation of tricarboxylic acid (TCA) enzymes in the setting of HAND and HAND/meth use compared with HIV+ control brains</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2025-04-19T18:16:57.651Z</modification><creation>2025-02-18T23:35:48.12Z</creation></dates><accession>S-EPMC8477648</accession><cross_references><pubmed>33876414</pubmed><doi>10.1007/s13365-021-00970-4</doi></cross_references></HashMap>