Search results for "Lula"

showing 10 items of 7309 documents

Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming

2016

Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-w…

0301 basic medicineGeneticsProgrammed cell deathCell typeCellular Reprogramming TechniquesMutantCell BiologyBiologyIn vitroCell biology03 medical and health sciencesTransduction (genetics)030104 developmental biologyIn vivoGeneticsMolecular MedicineReprogrammingCell Stem Cell
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The desaturase1 gene affects reproduction before, during and after copulation in Drosophila melanogaster

2019

Desaturase1 (desat1) is one of the few genes known to be involved in the two complementary aspects of sensory communication — signal emission and signal reception — in Drosophila melanogaster. In p...

0301 basic medicineGenetics[SDV.GEN]Life Sciences [q-bio]/Geneticsbiologymedia_common.quotation_subject[SDV]Life Sciences [q-bio]MARCMSensory systembiology.organism_classification03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biology0302 clinical medicineGeneticsDrosophila melanogasterReproductionGene[SDV.BDD]Life Sciences [q-bio]/Development Biology030217 neurology & neurosurgeryComputingMilieux_MISCELLANEOUSmedia_common
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The dark side of centromeres: types, causes and consequences of structural abnormalities implicating centromeric DNA

2018

Centromeres are the chromosomal domains required to ensure faithful transmission of the genome during cell division. They have a central role in preventing aneuploidy, by orchestrating the assembly of several components required for chromosome separation. However, centromeres also adopt a complex structure that makes them susceptible to being sites of chromosome rearrangements. Therefore, preservation of centromere integrity is a difficult, but important task for the cell. In this review, we discuss how centromeres could potentially be a source of genome instability and how centromere aberrations and rearrangements are linked with human diseases such as cancer.

0301 basic medicineGenome instabilityCell division[SDV]Life Sciences [q-bio]ScienceCentromereGeneral Physics and AstronomyAneuploidy[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReview ArticleBiologyChromosomeModels BiologicalGenomeChromosomesGenomic InstabilityGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundCentromeremedicineHumansDiseaselcsh:ScienceChromosome separationComputingMilieux_MISCELLANEOUSGeneticsMultidisciplinaryQChromosomeDNAGeneral Chemistrymedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologychemistrylcsh:QDNANature Communications
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Causes and consequences of DNA damage-induced autophagy.

2021

Abstract Autophagy is a quality control pathway that maintains cellular homeostasis by recycling surplus and dysregulated cell organelles. Identification of selective autophagy receptors demonstrated the existence of pathways that selectively degrade organelles, protein aggregates or pathogens. Interestingly, different types of DNA damage can induce autophagy and autophagy-deficiency leads to genomic instability. Recent studies provided first insights into the pathways that connect autophagy with the DNA damage response. However, the physiological role of autophagy and the identity of its targets after DNA damage remain enigmatic. In this review, we summarize recent literature on the target…

0301 basic medicineGenome instabilityDNA RepairDNA damageAutophagyCellular homeostasisProtein aggregationBiologyGenomic InstabilityCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistry030220 oncology & carcinogenesisOrganelleAutophagyHumansReceptorMolecular BiologyDNADNA DamageMatrix biology : journal of the International Society for Matrix Biology
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro

2017

Giardia intestinalis (G.I), is an anaerobic protozoan and the aetiological agent of giardiasis, a diarrhoea present worldwide and associated with poverty. G.I has a simple life cycle alternating between cyst and trophozoite. Cysts are transmitted orally to the stomach and transform to trophozoites in the intestine by a multifactorial process. Recently, microvesicles (MVs) have been found to be released from a wide range of eukaryotic cells. We have observed a release of MVs during the life cycle of G.I., identifying MVs from active trophozoites and from trophozoites differentiating to the cyst form. The aim of the current work was to investigate the role of MVs from G.I in the pathogenesis …

0301 basic medicineGiardiasisHistologydewey610Biologymedicine.disease_causePathology and Forensic MedicineMicrobiologyPathogenesis03 medical and health sciencesExtracellular VesiclesCell-Derived MicroparticlesmedicineGiardia lambliaAnimalsHumansPathogenLipid raftdewey570Innate immunityInnate immune systemParasite-host cell interactionsCell BiologyGeneral Medicine030108 mycology & parasitologyGiardia intestinalisExtracellular vesiclesIn vitroMicrovesiclesImmunity InnateDiarrhoea030104 developmental biologyHost-Pathogen InteractionsCaco-2 CellsGiardia lambliaBiogenesisMicrovesicles
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Diabetic microangiopathy: Pathogenetic insights and novel therapeutic approaches.

2017

Diabetic microangiopathy, including retinopathy, is characterized by abnormal growth and leakage of small blood vessels, resulting in local edema and functional impairment of the depending tissues. Mechanisms leading to the impairment of microcirculation in diabetes are multiple and still largely unclear. However, a dysregulated vascular regeneration appears to play a key role. In addition, oxidative and hyperosmolar stress, as well as the activation of inflammatory pathways triggered by advanced glycation end-products and toll-like receptors, have been recognized as key underlying events. Here, we review recent knowledge on cellular and molecular pathways of microvascular disease in diabet…

0301 basic medicineGlycation End Products AdvancedPhysiologyDiabetes retinopathyGlycation End ProductsDiseaseFibroblast growth factorHMGB1DiabeteMicrocirculationCapillary Permeability03 medical and health sciencesGlycationDiabetes mellitusmedicineSettore MED/05 - Patologia ClinicaAnimalsHumansCellular and molecular pathways; Diabetes; Diabetes retinopathy; Microangiopathy; Physiology; Molecular Medicine; PharmacologyNeovascularizationPharmacologyPathologicbiologyNeovascularization Pathologicbusiness.industryMicrocirculationMicroangiopathyDiabetesToll-Like Receptorsmedicine.diseasePrognosisCellular and molecular pathways; Diabetes; Diabetes retinopathy; Microangiopathy; Animals; Capillary Permeability; Diabetic Angiopathies; Glycation End Products Advanced; Humans; Inflammation Mediators; Microcirculation; Microvessels; Neovascularization Pathologic; Oxidative Stress; Prognosis; Signal Transduction; Toll-Like ReceptorsOxidative Stress030104 developmental biologyCellular and molecular pathwaysMicroangiopathyImmunologyMicrovesselsbiology.proteinMolecular MedicineAdvancedCellular and molecular pathwayInflammation MediatorsbusinessDiabetic AngiopathiesRetinopathySignal TransductionVascular pharmacology
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Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation

2016

While the role of both elevated levels of circulating bacterial cell wall components and adipose tissue in hepatic fat accumulation has been recognized, it has not been considered that the bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content. In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms of these associations, human HepG2 he…

0301 basic medicineGlycerollcsh:MedicineAdipose tissueWhite adipose tissueflagellinBiochemistryImmune ReceptorsFatsEndocrinologyAnimal CellsAdipocytesMedicine and Health SciencesInsulinlcsh:ScienceToll-like ReceptorsConnective Tissue CellsMultidisciplinaryImmune System ProteinsbiologyLiver DiseasesFatty liverin kaltaiset reseptorit [toll]Lipidsadipose tissuePhysical sciencesChemistryMitochondrial respiratory chainAdipose TissueConnective Tissuebacterial componentsCellular TypesAnatomyinsuline sensitivityResearch ArticleSignal Transductionmedicine.medical_specialtyadipocytesImmunologyMonomers (Chemistry)Gastroenterology and Hepatologyta311103 medical and health sciencesInsulin resistanceInternal medicinemedicinePolymer chemistryDiabetic Endocrinologylcsh:Rta1183ta1182Biology and Life SciencesProteinsCell Biologyliver fatmedicine.diseasehepatic fatfat accumulationHormonesIRS1Fatty LiverInsulin receptor030104 developmental biologyEndocrinologyBiological TissueTLR5biology.proteinlcsh:QPLoS ONE
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GH57 amylopullulanase from Desulfurococcus amylolyticus JCM 9188 can make highly branched cyclodextrin via its transglycosylation activity.

2018

Abstract Desulfurococcus amylolyticus is an anaerobic and hyperthermophilic crenarchaeon that can use various carbohydrates as energy sources. We found a gene encoding a glycoside hydrolase family 57 amylolytic enzymes (DApu) in a putative carbohydrate utilization gene cluster in the genome of D. amylolyticus . This gene has an open reading frame of 1,878 bp and consists of 626 amino acids with a molecular mass of 71 kDa. Recombinant DApu (rDApu) completely hydrolyzed pullulan to maltotriose by attacking α-1,6-glycosidic linkages, and was able to produce glucose and maltose from soluble starch and amylopectin. Although rDApu showed no activity toward α-cyclodextrin (CD) and β-CD, maltooctao…

0301 basic medicineGlycosylationGlycoside HydrolasesArchaeal ProteinsBioengineeringApplied Microbiology and BiotechnologyBiochemistrySubstrate Specificity03 medical and health scienceschemistry.chemical_compoundHydrolysisOpen Reading FramesGene clusterEnzyme StabilityMaltotrioseGlycoside hydrolaseCloning MolecularMaltoseGlucansCyclodextrins030102 biochemistry & molecular biologyDesulfurococcaceaePullulanMaltoseMolecular Weight030104 developmental biologychemistryBiochemistryAmylopectinEnergy sourceTrisaccharidesBiotechnologyEnzyme and microbial technology
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