<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rahman MM</submitter><funding>NIDDK NIH HHS</funding><pagination>678-90</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2993798</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2(10)</volume><pubmed_abstract>O-linked-β-N-acetylglucosamine (O-GlcNAc) modification is a regulatory, nuclear and cytoplasmic post-translational glycosylation of proteins associated with age-related diseases such as Alzheimer's, Parkinson's, and type II diabetes. Global elevation of O-GlcNAc levels on intracellular proteins can induce insulin resistance, the hallmark of type II diabetes, in mammalian systems. InC. elegans, attenuation of the insulin-like signal transduction pathway increases adult lifespan of the nematode. We demonstrate that the O-GlcNAc cycling enzymes OGT and OGA, which add and remove O-GlcNAc respectively, modulate lifespan in C. elegans. Median adult lifespan is increased in an oga-1 deletion strain while median adult life span is decreased upon ogt-1 deletion. The O-GlcNAc-mediated effect on nema</pubmed_abstract><journal>Aging</journal><pubmed_title>Intracellular protein glycosylation modulates insulin mediated lifespan in C.elegans.</pubmed_title><pmcid>PMC2993798</pmcid><funding_grant_id>R01DK075069</funding_grant_id><funding_grant_id>R01 DK075069</funding_grant_id><pubmed_authors>Rahman MM</pubmed_authors><pubmed_authors>El-Karim EG</pubmed_authors><pubmed_authors>Stuart R</pubmed_authors><pubmed_authors>Stuchlick O</pubmed_authors><pubmed_authors>Kipreos ET</pubmed_authors><pubmed_authors>Wells L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Intracellular protein glycosylation modulates insulin mediated lifespan in C.elegans.</name><description>O-linked-β-N-acetylglucosamine (O-GlcNAc) modification is a regulatory, nuclear and cytoplasmic post-translational glycosylation of proteins associated with age-related diseases such as Alzheimer's, Parkinson's, and type II diabetes. Global elevation of O-GlcNAc levels on intracellular proteins can induce insulin resistance, the hallmark of type II diabetes, in mammalian systems. InC. elegans, attenuation of the insulin-like signal transduction pathway increases adult lifespan of the nematode. We demonstrate that the O-GlcNAc cycling enzymes OGT and OGA, which add and remove O-GlcNAc respectively, modulate lifespan in C. elegans. Median adult lifespan is increased in an oga-1 deletion strain while median adult life span is decreased upon ogt-1 deletion. The O-GlcNAc-mediated effect on nema</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Oct</publication><modification>2025-04-26T05:23:35.527Z</modification><creation>2019-03-27T00:37:00Z</creation></dates><accession>S-EPMC2993798</accession><cross_references><pubmed>20952811</pubmed><doi>10.18632/aging.100208</doi></cross_references></HashMap>