<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang W</submitter><funding>NIA NIH HHS</funding><funding>BrightFocus Foundation</funding><funding>NCI NIH HHS</funding><funding>National Institute on Aging</funding><pagination>353-361</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8900146</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(4)</volume><pubmed_abstract>The AMP-activated protein kinase (AMPK) is a molecular sensor to help maintain cellular energy homeostasis. AMPK is a heterotrimeric complex and its enzymatic catalytic subunit includes two isoforms: α1 and α2. Dysregulation of AMPK signaling is linked to neuronal diseases characterized with cognitive impairments. Emerging evidence also suggest isoform-specific roles of AMPK in the brain. AMPK regulates protein synthesis, which is critical for memory formation and neuronal plasticity. However, the consequence of altering AMPK activity on the translation of specific proteins in the brain is unknown. Here, we use unbiased mass spectrometry-based proteomics approach to analyze protein profile alterations in hippocampus and prefrontal cortex of transgenic mice in which the genes for the two AM</pubmed_abstract><journal>Hippocampus</journal><pubmed_title>Protein expression alteration in hippocampus upon genetic repression of AMPKα isoforms.</pubmed_title><pmcid>PMC8900146</pmcid><funding_grant_id>R01 AG056622</funding_grant_id><funding_grant_id>R01 CA172115</funding_grant_id><funding_grant_id>A2017457S</funding_grant_id><funding_grant_id>P30 CA012197</funding_grant_id><funding_grant_id>R01 CA131231</funding_grant_id><funding_grant_id>R01 AG055581</funding_grant_id><pubmed_authors>Yang W</pubmed_authors><pubmed_authors>Sun P</pubmed_authors><pubmed_authors>Lee J</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Wu D</pubmed_authors><pubmed_authors>Ma T</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Furdui CM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Protein expression alteration in hippocampus upon genetic repression of AMPKα isoforms.</name><description>The AMP-activated protein kinase (AMPK) is a molecular sensor to help maintain cellular energy homeostasis. AMPK is a heterotrimeric complex and its enzymatic catalytic subunit includes two isoforms: α1 and α2. Dysregulation of AMPK signaling is linked to neuronal diseases characterized with cognitive impairments. Emerging evidence also suggest isoform-specific roles of AMPK in the brain. AMPK regulates protein synthesis, which is critical for memory formation and neuronal plasticity. However, the consequence of altering AMPK activity on the translation of specific proteins in the brain is unknown. Here, we use unbiased mass spectrometry-based proteomics approach to analyze protein profile alterations in hippocampus and prefrontal cortex of transgenic mice in which the genes for the two AM</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2026-06-01T02:32:41.008Z</modification><creation>2024-10-16T14:57:01.04Z</creation></dates><accession>S-EPMC8900146</accession><cross_references><pubmed>33492732</pubmed><doi>10.1002/hipo.23305</doi></cross_references></HashMap>