0000000000493959

AUTHOR

Ornella Moltedo

showing 5 related works from this author

Endoplasmic Reticulum stress reduces COPII vesicle formation and modifies Sec23a cycling at ERESs

2013

AbstractExit from the Endoplasmic Reticulum (ER) of newly synthesized proteins is mediated by COPII vesicles that bud from the ER at the ER Exit Sites (ERESs). Disruption of ER homeostasis causes accumulation of unfolded and misfolded proteins in the ER. This condition is referred to as ER stress. Previously, we demonstrated that ER stress rapidly impairs the formation of COPII vesicles. Here, we show that membrane association of COPII components, and in particular of Sec23a, is impaired by ER stress-inducing agents suggesting the existence of a dynamic interplay between protein folding and COPII assembly at the ER.

Vesicular Transport ProteinsBiophysicsEndoplasmic ReticulumBiochemistryCell LineVesicular Transport ProteinGeneticStructural BiologyERESGeneticsVesicular Transport ProteinsHumansCOPIIEndoplasmic Reticulum StreMolecular BiologyCOPIIChemistryVesicleEndoplasmic reticulumSec23Cell BiologyCOP-Coated VesiclesSEC23AEndoplasmic Reticulum StressCell biologyBiophysicUnfolded protein responseER streProtein foldingCOP-Coated VesiclesER stressCOP-Coated VesicleHumanProtein BindingFEBS Letters
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miR-128 Is Implicated in Stress Responses by Targeting MAFG in Skeletal Muscle Cells.

2017

MAFG (v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog G) is a bZIP-type transcriptional regulator that belongs to the small MAF (sMAFs) protein family. By interacting with other bZIP transcription factors, sMAFs can form homo- and heterodimers governing either repressive or activating transcriptional functions. As heterodimeric partner of Nrf2, MAFG positively influences the ARE-dependent antioxidant/xenobiotic pathways, at least in condition of a correct MAFG:Nrf2 balance. MicroRNAs (miRs) participate to different regulatory networks being involved as fine-tuning regulators of gene expression. However, the connections between cellular surveillance to stresses mediated by MAFG:…

0301 basic medicineMafG Transcription FactorMaleAgingProtein familyArticle SubjectNF-E2-Related Factor 2Muscle Fibers SkeletalBiologyTransfectionBiochemistryAntioxidants03 medical and health sciencesMiceGene expressionmicroRNATranscriptional regulationAnimalsHumanslcsh:QH573-671Gene3' Untranslated RegionsGeneticsBinding SitesOncogeneThree prime untranslated regionlcsh:CytologyHEK 293 cellsMembrane ProteinsCell BiologyGeneral MedicineMice Inbred C57BLRepressor ProteinsMicroRNAsOxidative Stress030104 developmental biologyHEK293 CellsHeme Oxygenase-1Research ArticleOxidative medicine and cellular longevity
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Synthesis and preliminary biological evaluation of a new pyridocarbazole derivative covalently linked to a thymidine nucleoside as a potential target…

2003

The therapy of human cancer is one of the more pursued goals by medicinal chemistry research. Most of the compounds clinically used as a treatment owe their efficacy to their cytotoxic interaction (direct or indirect) with nuclear DNA. This interaction results in the inhibition of DNA synthesis and the degradation of nucleic strands. Ellipticine is a naturally occurring 6H-pyrido[4,3-b]carbazole alkaloid endowed with antitumor activity, and several ellipticine derivatives have been used in clinical trials. We previously reported some 1,4-dimethyl-9H-carbazole derivatives structurally related to ellipticine. The purpose of our research was to transform the pyridocarbazole in a prodrug so tha…

PyridonesCarbazolesDrug Evaluation PreclinicalAntineoplastic Agentschemistry.chemical_compoundDrug Delivery SystemsCell Line TumorDrug DiscoveryHumansCytotoxicitynucleoside analogueDNA synthesisBiological activityGeneral ChemistryGeneral MedicineProdrugorganic synthesisPyrimidine NucleosidesBiochemistrychemistryNucleic acidantitumour activityThymidineNucleosideDNAThymidineChemicalpharmaceutical bulletin
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Identification of Cysteine Ubiquitylation Sites on the Sec23A Protein of the COPII Complex Required for Vesicle Formation from the ER

2017

Background COPII is a multiprotein complex that surrounds carrier vesicles budding from the Endoplasmic Reticulum and allows the recruitment of secretory proteins. The Sec23a protein plays a crucial role in the regulation of the dynamics of COPII formation ensuring the proper function of the secretory pathway. Objective Since few evidences suggest that ubiquitylation could have a role in the COPII regulation, the present study was aimed to establish whether the Sec23a component of the vesicular envelope COPII could be ubiquitylated. Method Sec23a ubiquitylation was revealed by co-immunoprecipitation experiments. Recombinant Sec23a was gel-purified and analyzed by mass spectrometry subjected…

0301 basic medicineMultiprotein complexUbiquitylationbiologyVescicular transportEndoplasmic reticulumVesicleSEC23AArticleSec23aGeneral Biochemistry Genetics and Molecular BiologyCell biology03 medical and health sciences030104 developmental biologySecretory proteinUbiquitinERESbiology.proteinCOPIICOPIISecretory pathwayThe Open Biochemistry Journal
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Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction

2017

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the U…

0301 basic medicineAgingProgrammed cell deathendocrine systemOxidative phosphorylationReview Articlemedicine.disease_causeEndoplasmic ReticulumBiochemistryINITIATION-FACTOR 2-ALPHA03 medical and health sciencesProgrammed cell-deathSELECTIVE-INHIBITIONProgrammed cell-death;TXNIP/NLRP3 INFLAMMASOME ACTIVATION; MITOCHONDRIAL ELECTRON-TRANSPORT; SPONTANEOUSLY HYPERTENSIVE-RATS; INITIATION-FACTOR 2-ALPHA; CORONARY-ARTERY FUNCTION; ER STRESS; SELECTIVE-INHIBITION; MESSENGER-RNA; TRANSMEMBRANE PROTEINmedicineHumansEndothelial dysfunctionlcsh:QH573-671TXNIP/NLRP3 INFLAMMASOME ACTIVATIONSPONTANEOUSLY HYPERTENSIVE-RATSEndothelial Cellbusiness.industrylcsh:CytologyEndoplasmic reticulumfungiEndothelial CellsOxidative StreCell BiologyGeneral MedicineAdaptive responseMITOCHONDRIAL ELECTRON-TRANSPORTER STRESSmedicine.diseaseCell biologyOxidative Stress030104 developmental biologyProteostasisTRANSMEMBRANE PROTEINUnfolded protein responseUnfolded Protein ResponsebusinessMESSENGER-RNAOxidative stressCORONARY-ARTERY FUNCTIONHumanOxidative Medicine and Cellular Longevity
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