2025
Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases
Rubinelli L, Manzo O, Sungho J, Del Gaudio I, Bareja R, Marino A, Palikhe S, Di Mauro V, Bucci M, Falcone D, Elemento O, Ersoy B, Diano S, Sasset L, Di Lorenzo A. Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases. Nature Communications 2025, 16: 1968. PMID: 40000621, PMCID: PMC11862206, DOI: 10.1038/s41467-025-56869-9.Peer-Reviewed Original ResearchConceptsNogo-BEndothelial dysfunctionHFD miceCardiometabolic diseasesSphingolipid signalingDevelopment of therapeutic strategiesBioactive sphingolipidsCeramide degradationSphingosine-1-phosphateHepatic glucose productionIn vivo evidenceEndothelial cellsEndothelial specific deletionCeramideBiosynthesisHigh-fat dietPathological implicationsSphingolipidsGlucose productionHFDIn vivoMale miceMetabolic dysfunctionTherapeutic strategiesMetabolic disorders
2023
Leveraging GWAS data derived from a large cooperative group trial to assess the risk of taxane-induced peripheral neuropathy (TIPN) in patients being treated for breast cancer: Part 2—functional implications of a SNP cluster associated with TIPN risk in patients being treated for breast cancer
Lustberg M, Wu X, Fernández-Martínez J, de Andrés-Galiana E, Philips S, Leibowitz J, Schneider B, Sonis S. Leveraging GWAS data derived from a large cooperative group trial to assess the risk of taxane-induced peripheral neuropathy (TIPN) in patients being treated for breast cancer: Part 2—functional implications of a SNP cluster associated with TIPN risk in patients being treated for breast cancer. Supportive Care In Cancer 2023, 31: 178. PMID: 36809570, PMCID: PMC11344472, DOI: 10.1007/s00520-023-07617-6.Peer-Reviewed Original ResearchConceptsGWAS dataSNP clustersFunctional analysisGO termsNon-protein coding genesGene Ontology termsGene Set Enrichment AnalysisCluster of SNPsNervous system developmentCoding genesRetinoic acid bindingOntology termsProtein kinase C bindingEnrichment analysisMetabolic processesGenesAcid bindingGlycosyltransferase activitySNPsPathological implicationsGWASC bindingGene signaturePhenotypeTransferase activity
1985
Non‐enzymatic modification of proteins by steroids: Pathological implications for autoimmunity and glucocorticoid toxicity
Bucala R, Cerami A. Non‐enzymatic modification of proteins by steroids: Pathological implications for autoimmunity and glucocorticoid toxicity. BioEssays 1985, 3: 55-59. PMID: 3842583, DOI: 10.1002/bies.950030204.Peer-Reviewed Original ResearchConceptsOral contraceptive agentsElevated plasma levelsHigh steroid levelsGlucocorticoid toxicityPlasma levelsCovalent addition productsPathological sequelaeContraceptive agentsSteroid levelsCertain steroidsAddition productsSteroidsPathological implicationsRearrangement productsMicrosomal oxidationNon-enzymatic modification
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