{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13(10)"],"submitter":["Mateos J"],"pubmed_abstract":["Hutchinson-Gilford progeria syndrome (HGPS) is a very rare fatal disease characterized for accelerated aging. Although the causal agent, a point mutation in LMNA gene, was identified more than a decade ago, the molecular mechanisms underlying HGPS are still not fully understood and, currently, there is no cure for the patients, which die at a mean age of thirteen. With the aim of unraveling non-previously altered molecular pathways in the premature aging process, human cell lines from HGPS patients and from healthy parental controls were studied in parallel using Next-Generation Sequencing (RNAseq) and High-Resolution Quantitative Proteomics (iTRAQ) techniques. After selection of significant proteins and transcripts and crosschecking of the results a small set of protein/transcript pairs w"],"journal":["PloS one"],"pagination":["e0205878"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6209416"],"repository":["biostudies-literature"],"pubmed_title":["Next-Generation Sequencing and Quantitative Proteomics of Hutchinson-Gilford progeria syndrome-derived cells point to a role of nucleotide metabolism in premature aging."],"pmcid":["PMC6209416"],"pubmed_authors":["Lesende-Rodriguez I","Odena MA","de Toro J","Fafian-Labora J","Arufe MC","Morente-Lopez M","Oliveira E","Mateos J","Monserrat L"],"additional_accession":[]},"is_claimable":false,"name":"Next-Generation Sequencing and Quantitative Proteomics of Hutchinson-Gilford progeria syndrome-derived cells point to a role of nucleotide metabolism in premature aging.","description":"Hutchinson-Gilford progeria syndrome (HGPS) is a very rare fatal disease characterized for accelerated aging. Although the causal agent, a point mutation in LMNA gene, was identified more than a decade ago, the molecular mechanisms underlying HGPS are still not fully understood and, currently, there is no cure for the patients, which die at a mean age of thirteen. With the aim of unraveling non-previously altered molecular pathways in the premature aging process, human cell lines from HGPS patients and from healthy parental controls were studied in parallel using Next-Generation Sequencing (RNAseq) and High-Resolution Quantitative Proteomics (iTRAQ) techniques. After selection of significant proteins and transcripts and crosschecking of the results a small set of protein/transcript pairs w","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018","modification":"2026-04-20T03:15:18.368Z","creation":"2019-03-27T00:08:11Z"},"accession":"S-EPMC6209416","cross_references":{"pubmed":["30379953"],"doi":["10.1371/journal.pone.0205878"]}}