<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Frank M</submitter><funding>NIA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>ar119</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9634964</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(13)</volume><pubmed_abstract>Propofol is a widely used general anesthetic, yet the understanding of its cellular effects is fragmentary. General anesthetics are not as innocuous as once believed and have a wide range of molecular targets that include kinesin motors. Propofol, ketamine, and etomidate reduce the distances that Kinesin-1 KIF5 and Kinesin-2 KIF3 travel along microtubules in vitro. These transport kinesins are highly expressed in the CNS, and their dysfunction leads to a range of human pathologies including neurodevelopmental and neurodegenerative diseases. While in vitro data suggest that general anesthetics may disrupt kinesin transport in neurons, this hypothesis remains untested. Here we find that propofol treatment of hippocampal neurons decreased vesicle transport mediated by Kinesin-1 KIF5 and Kines</pubmed_abstract><journal>Molecular biology of the cell</journal><pubmed_title>Propofol attenuates kinesin-mediated axonal vesicle transport and fusion.</pubmed_title><pmcid>PMC9634964</pmcid><funding_grant_id>T32 AG057464</funding_grant_id><funding_grant_id>R01 MH066179</funding_grant_id><funding_grant_id>R37 GM054141</funding_grant_id><pubmed_authors>Frank M</pubmed_authors><pubmed_authors>Gilbert SP</pubmed_authors><pubmed_authors>Bentley M</pubmed_authors><pubmed_authors>Nabb AT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Propofol attenuates kinesin-mediated axonal vesicle transport and fusion.</name><description>Propofol is a widely used general anesthetic, yet the understanding of its cellular effects is fragmentary. General anesthetics are not as innocuous as once believed and have a wide range of molecular targets that include kinesin motors. Propofol, ketamine, and etomidate reduce the distances that Kinesin-1 KIF5 and Kinesin-2 KIF3 travel along microtubules in vitro. These transport kinesins are highly expressed in the CNS, and their dysfunction leads to a range of human pathologies including neurodevelopmental and neurodegenerative diseases. While in vitro data suggest that general anesthetics may disrupt kinesin transport in neurons, this hypothesis remains untested. Here we find that propofol treatment of hippocampal neurons decreased vesicle transport mediated by Kinesin-1 KIF5 and Kines</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-18T16:13:22.314Z</modification><creation>2025-04-07T03:15:31.446Z</creation></dates><accession>S-EPMC9634964</accession><cross_references><pubmed>36103253</pubmed><doi>10.1091/mbc.E22-07-0276</doi></cross_references></HashMap>