Search results for "RIP"

showing 10 items of 9780 documents

Pathological modelling of pigmentation disorders associated with Hutchinson-Gilford Progeria Syndrome (HGPS) revealed an impaired melanogenesis pathw…

2018

AbstractHutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic disorder that leads to premature aging. In this study, we used induced pluripotent stem cells to investigate the hypopigmentation phenotypes observed in patients with progeria. Accordingly, two iPS cell lines were derived from cells from HGPS patients and differentiated into melanocytes. Measurements of melanin content revealed a lower synthesis of melanin in HGPS melanocytes as compared to non-pathologic cells. Analysis of the melanosome maturation process by electron microscopy revealed a lower percentage of mature, fully pigmented melanosomes. Finally, a functional rescue experiment revealed the direct role of progerin…

0301 basic medicinePremature agingcongenital hereditary and neonatal diseases and abnormalitiesInduced Pluripotent Stem Cellslcsh:MedicineBiologyModels BiologicalArticleMelanin03 medical and health sciencesProgeriamedicineHumansInduced pluripotent stem celllcsh:SciencePigmentation disorderMelanosomeHypopigmentationProgeriaMelanosomesMultidisciplinaryintegumentary systemlcsh:Rnutritional and metabolic diseasesmedicine.diseaseProgerinCell biology030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMelanocyteslcsh:Qmedicine.symptomPigmentation Disorders
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De la querelle du quinquina à la querelle de l’hydroxychloroquine, ou comment notre système de protection du médicament est mis à l’épreuve : une ana…

2020

Resume La querelle actuelle sur l’utilisation de l’hydroxychloroquine, dans le cadre de la coronavirus disease 2019 (covid-19), trouve un echo dans une autre querelle, celle du quinquina, qui prit place au XVIIe siecle. Cet aparte historique est de nature a nous rappeler que les disputes scientifiques ont toujours existe, et il n’est donc pas etonnant que les proprietes de l’hydroxychloroquine soient sujettes a polemique. Cependant, les faits sont les faits : son efficacite est douteuse, alors que les risques sont certains. C’est pourquoi en France le Premier ministre a fait le choix d’encadrer sa prescription par un decret. Mais ce decret, bien que surement la seule option possible, soulev…

0301 basic medicinePrescription (drugs)Prescription (réglementation)Covid-19 (médicaments)Médicaments (réglementation)General Medicine030204 cardiovascular system & hematologyPharmacist (liability)ArticleTemporary recommendation for use (drugs)3. Good health[SHS]Humanities and Social Sciences03 medical and health sciences030104 developmental biology0302 clinical medicineCovid-19 (drugs)Pharmacien (responsabilité)Recommandation temporaire d’utilisationLaw
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A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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The anti-oxidative role of cytoglobin in podocytes: implications for a role in chronic kidney disease

2020

Abstract: Aims: Cytoglobin (CYGB) is a member of the mammalian globin family of respiratory proteins. Despite extensive research efforts, its physiological role remains largely unknown, but potential functions include reactive oxygen species (ROS) detoxification and signaling. Accumulating evidence suggests that ROS play a crucial role in podocyte detachment and apoptosis during diabetic kidney disease. This study aimed to explore the potential antioxidative renal role of CYGB both in vivo and in vitro. Results: Using a Cygb-deficient mouse model, we demonstrate a Cygb-dependent reduction in renal function, coinciding with a reduced number of podocytes. To specifically assess the putative a…

0301 basic medicineProgrammed cell death1303 BiochemistryCell SurvivalPhysiologyClinical Biochemistry610 Medicine & healthBiology1308 Clinical Biochemistrymedicine.disease_causeBiochemistryAntioxidantsPodocyteNephropathy10052 Institute of PhysiologyTranscriptomeDiabetic nephropathy1307 Cell Biology03 medical and health sciencesMicemedicine1312 Molecular BiologyAnimalsHumansRenal Insufficiency ChronicBiologyMolecular BiologyCells CulturedGeneral Environmental ScienceMice KnockoutGene knockdown030102 biochemistry & molecular biologyPodocytesCytoglobinCytoglobin1314 PhysiologyCell Biologymedicine.diseaseCell biologyMice Inbred C57BLChemistryDisease Models Animal030104 developmental biologymedicine.anatomical_structureGeneral Earth and Planetary Sciences570 Life sciences; biologyHuman medicineOxidative stress
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Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
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Metabolic Imaging in Multicellular Spheroids of Oncogene-transfected Fibroblasts

2000

Four rat embryo fibroblast (REF) cell lines with defined oncogenic transformation were used to study the relationship between tumorigenic conversion, metabolism, and development of cell death in a 3D spheroid system. Rat1 (spontaneously immortalized) and M1 ( myc-transfected) fibroblasts represent early nontumorigenic transformation stages, whereas Rat1-T1 (T24Ha- ras-transfected Rat1) and MR1 ( myc/T24Ha- ras-co-transfected REF) cells express a highly tumorigenic phenotype. Localized ATP, glucose, and lactate concentrations in spheroid median sections were determined by imaging bioluminescence. ATP concentrations were low in the nonproliferating Rat1 aggregates despite sufficient oxygen an…

0301 basic medicineProgrammed cell deathHistologyGenes mycApoptosisBiology030218 nuclear medicine & medical imaging03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSpheroids CellularImage Processing Computer-AssistedmedicineAnimalsFrozen SectionsLactic AcidFibroblastCell Line Transformed030102 biochemistry & molecular biologyOncogeneSpheroidEmbryoTransfectionMetabolismMolecular biologyRats Inbred F344RatsCell biologyGenes rasGlucosemedicine.anatomical_structureCell cultureLuminescent Measurementsembryonic structuresAnatomyCell DivisionJournal of Histochemistry & Cytochemistry
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation

2017

IF 3.226; International audience; Ubiquitination is a post-translational modification that defines the cellular fate of intracellular proteins. It can modify their stability, their activity, their subcellular location, and even their interacting pattern. This modification is a reversible event whose implementation is easy and fast. It contributes to the rapid adaptation of the cells to physiological intracellular variations and to intracellular or environmental stresses. E2F1 (E2 promoter binding factor 1) transcription factor is a potent cell cycle regulator. It displays contradictory functions able to regulate both cell proliferation and cell death. Its expression and activity are tightly…

0301 basic medicineProgrammed cell deathReviewubiquitinationCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciencesUbiquitinAnimalsHumansE2F1Physical and Theoretical Chemistry[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologylcsh:QH301-705.5Molecular BiologyTranscription factorSpectroscopybiologyCell growthOrganic ChemistryE2F1 Transcription FactorGeneral MedicineCell cycleComputer Science ApplicationsCell biology030104 developmental biologyE2F1lcsh:Biology (General)lcsh:QD1-999biology.proteinDNA damagecell cycleE2F1 Transcription FactorIntracellularInternational Journal of Molecular Sciences
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SERCA and P-glycoprotein inhibition and ATP depletion are necessary for celastrol-induced autophagic cell death and collateral sensitivity in multidr…

2019

Multidrug resistance (MDR) represents an obstacle in anti-cancer therapy. MDR is caused by multiple mechanisms, involving ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp), which reduces intracellular drug levels to sub-therapeutic concentrations. Therefore, sensitizing agents retaining effectiveness against apoptosis- or drug-resistant cancers are desired for the treatment of MDR cancers. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump is an emerging target to overcome MDR, because of its continuous expression and because the calcium transport function is crucial to the survival of tumor cells. Previous studies showed that SERCA inhibitors exhibit anti-c…

0301 basic medicineProgrammed cell deathSERCALung NeoplasmsCell SurvivalAntineoplastic AgentsAutophagy-Related Protein 7Sarcoplasmic Reticulum Calcium-Transporting ATPases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell Line TumorAutophagyAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinPharmacologybiologyDose-Response Relationship DrugChemistryAutophagyXenograft Model Antitumor AssaysDrug Resistance MultipleTriterpenesMultiple drug resistanceMice Inbred C57BL030104 developmental biologyCelastrolApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchHepatocytesPentacyclic TriterpenesPharmacological research
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E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death

2018

International audience; E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.

0301 basic medicineProgrammed cell deathTranscription Geneticbcl-X ProteinRegulatorBcl-xL[SDV.CAN]Life Sciences [q-bio]/CancerBCL-xL mobilityMitochondrionBiochemistrylaw.invention[ SDV.CAN ] Life Sciences [q-bio]/CancerE2F1 Subject Category Autophagy & Cell Death03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerlawBCL-2 familyCell Line TumorGeneticsJournal ArticleHumansE2F1Molecular BiologyCell DeathbiologyManchester Cancer Research CentreEffectorChemistryResearchInstitutes_Networks_Beacons/mcrcScientific ReportsapoptosisSubcellular localizationMitochondriaCell biologyProtein Transportbcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyGene Expression RegulationProto-Oncogene Proteins c-bcl-2biology.proteinSuppressorbiological phenomena cell phenomena and immunityExtracellular SpaceE2F1 Transcription FactorProtein Binding
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