{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["57(7)"],"submitter":["Chen Q"],"pubmed_abstract":["Mitochondrial dysfunction is implicated in numerous disorders, including type 2 diabetes, Alzheimer's disease and cancer. Long non-coding RNAs (lncRNAs) are emerging as pivotal regulators of cellular energy metabolism, yet their roles remain largely unclear. In this study, we identify an lncRNA named linc-PMB, which is associated with mTOR and promotes mitochondrial biogenesis, through microarray analysis. We demonstrate that the knockdown of <i>linc-PMB</i> results in significantly impaired mitochondrial respiration and biogenesis, along with altered expressions of related genes. Conversely, overexpression of linc-PMB markedly increases mitochondrial function. We further reveal that linc-PMB interacts with the RNA-binding protein HuR, promoting the stabilization of SIRT1 mRNA and a substa"],"journal":["Acta biochimica et biophysica Sinica"],"pagination":["1057-1067"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12367985"],"repository":["biostudies-literature"],"pubmed_title":["mTOR-related linc-PMB promotes mitochondrial biogenesis via stabilizing SIRT1 mRNA through binding to the HuR protein."],"pmcid":["PMC12367985"],"pubmed_authors":["Liu Y","Chen Q","Yu M","Wang S","Zhang H","Wang D","Liao W","Cai Y"],"additional_accession":[]},"is_claimable":false,"name":"mTOR-related linc-PMB promotes mitochondrial biogenesis via stabilizing SIRT1 mRNA through binding to the HuR protein.","description":"Mitochondrial dysfunction is implicated in numerous disorders, including type 2 diabetes, Alzheimer's disease and cancer. Long non-coding RNAs (lncRNAs) are emerging as pivotal regulators of cellular energy metabolism, yet their roles remain largely unclear. In this study, we identify an lncRNA named linc-PMB, which is associated with mTOR and promotes mitochondrial biogenesis, through microarray analysis. We demonstrate that the knockdown of <i>linc-PMB</i> results in significantly impaired mitochondrial respiration and biogenesis, along with altered expressions of related genes. Conversely, overexpression of linc-PMB markedly increases mitochondrial function. We further reveal that linc-PMB interacts with the RNA-binding protein HuR, promoting the stabilization of SIRT1 mRNA and a substa","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-05-05T19:00:35.539Z","creation":"2026-04-07T21:50:13.886Z"},"accession":"S-EPMC12367985","cross_references":{"pubmed":["39910977"],"doi":["10.3724/abbs.2024236"]}}