Search results for " Ly"

showing 10 items of 2487 documents

Lawsone derivatives target the Wnt/β-catenin signaling pathway in multidrug-resistant acute lymphoblastic leukemia cells.

2017

Abstract Multidrug resistance (MDR) represents a serious problem in cancer treatment. One strategy to overcome this obstacle is to identify agents that are selectively lethal to MDR cells. The aim of this study was to discover novel compounds against MDR leukemia and to determine the molecular mechanisms behind collateral sensitivity. A library of 1162 compounds was tested against parental, drug-sensitive CCRF-CEM cells using the resazurin assay. A total of 302 compounds showed reasonable activity (less than 50% cell viability). Eleven out of 30 lawsone derivatives revealed considerable collateral sensitivity in MDR P-glycoprotein (Pgp)-overexpressing CEM/ADR5000 cells. They reduced β-caten…

0301 basic medicineFrizzledAntineoplastic AgentsPharmacologyBiologyBiochemistryLawsone03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansViability assaybeta CateninPharmacologyDose-Response Relationship DrugMolecular StructureWnt signaling pathwayResazurinPrecursor Cell Lymphoblastic Leukemia-Lymphomamedicine.diseaseMultiple drug resistanceWnt ProteinsLeukemia030104 developmental biologychemistryCell cultureDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchReactive Oxygen SpeciesNaphthoquinonesSignal TransductionBiochemical pharmacology
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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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Cardiac regenerative capacity is age- and disease-dependent in childhood heart disease

2018

Objective We sought to define the intrinsic stem cell capacity in pediatric heart lesions, and the effects of diagnosis and of age, in order to inform evidence-based use of potential autologous stem cell sources for regenerative medicine therapy. Methods Ventricular explants derived from patients with hypoplastic left heart syndrome (HLHS), tetralogy of Fallot (TF), dilated cardiomyopathy (DCM) and ventricular septal defect (VSD) were analyzed following standard in vitro culture conditions, which yielded cardiospheres (C-spheres), indicative of endogenous stem cell capacity. C-sphere counts generated per 5 mm3 tissue explant and the presence of cardiac progenitor cells were correlated to pa…

0301 basic medicineHeart Septal Defects VentricularAgingHeart diseaseCell TransplantationCardiovascular Proceduresmedicine.medical_treatmentCardiomyopathylcsh:Medicine030204 cardiovascular system & hematologyBiochemistryHypoplastic left heart syndromeTissue Culture TechniquesElectrocardiography0302 clinical medicineAnimal CellsHeart RegenerationHypoplastic Left Heart SyndromeNeurobiology of Disease and RegenerationMedicine and Health SciencesMorphogenesisBlood and Lymphatic System ProceduresMyocytes CardiacChildlcsh:ScienceCells CulturedTetralogy of FallotMultidisciplinaryStem CellsStem Cell TherapyDilated cardiomyopathyHeartStem-cell therapyCardiac Transplantationmedicine.anatomical_structureNeurologyChild PreschoolCardiologyTetralogy of Fallotcardiovascular systemStem cellCellular TypesAnatomyResearch ArticleCardiomyopathy Dilatedmedicine.medical_specialtyAdolescentHeart VentriclesSurgical and Invasive Medical Procedures03 medical and health sciencesInternal medicinemedicineHumansRegenerationVimentincardiovascular diseasesClinical GeneticsTransplantationbusiness.industrylcsh:RInfant NewbornCorrectionInfantBiology and Life SciencesProteinsMesenchymal Stem CellsCell BiologyOrgan Transplantationmedicine.diseaseCytoskeletal Proteins030104 developmental biologyVentricleCardiovascular Anatomylcsh:QbusinessOrganism DevelopmentDevelopmental BiologyStem Cell TransplantationPLoS ONE
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Paroxysmal nocturnal haemoglobinuria: When delay in diagnosis and long therapy occurs

2017

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal disorder characterized by hemolytic anemia, bone marrow failure and thrombosis, caused by a somaticmutation in PIG-A gene that results in theabsence of CD55 and CD59, two important complement regulatory proteins. In thispaper, a case of PNH is retrospectively examined looking for clinical and laboratory features, and the entire course of the disease from the onset of the symptoms isdescribed, together with an adequate follow-up over a 7-years treatment period. Inthis case, the not specificity and the limited clinical relevance of the symptoms led to adelay in diagnosis. After thrombosis, Eculizumab therapy has been shown to be effec…

0301 basic medicineHemolytic anemiaPediatricsmedicine.medical_specialtyrenal failureParoxysmal nocturnal haemoglobinuriaparoxysmal nocturnal hemoglobinuriaCase ReportDiseaseCD5903 medical and health sciencesthrombotic eventshemic and lymphatic diseasesMedicineClinical significancebusiness.industrylcsh:RC633-647.5Bone marrow failureHematologylcsh:Diseases of the blood and blood-forming organsEculizumabEculizumabmedicine.diseaseThrombosisparoxysmal nocturnal hemoglo-binuria thrombotic events renal failure Eculizumab030104 developmental biologyParoxysmal nocturnal hemoglobinuriabusinessmedicine.drug
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Identifying Host Molecular Features Strongly Linked With Responses to Huanglongbing Disease in Citrus Leaves

2018

© 2018 Balan, Ibáñez, Dandekar, Caruso and Martinelli. A bioinformatic analysis of previously published RNA-Seq studies on Huanglongbing (HLB) response and tolerance in leaf tissues was performed. The aim was to identify genes commonly modulated between studies and genes, pathways and gene set categories strongly associated with this devastating Citrus disease. Bioinformatic analysis of expression data of four datasets present in NCBI provided 46–68 million reads with an alignment percentage of 72.95–86.76%. Only 16 HLB-regulated genes were commonly identified between the three leaf datasets. Among them were key genes encoding proteins involved in cell wall modification such as CESA8, pecti…

0301 basic medicineHuanglongbing HLB citrus protein–protein interaction network transcriptomics RNA-SeqPlant BiologyHuanglongbingRNA-SeqPlant Sciencelcsh:Plant cultureBiologycitrusTranscriptometranscriptomics03 medical and health sciencesExpansinSettore AGR/07 - Genetica AgrariaHeat shock proteinGenetics2.1 Biological and endogenous factorslcsh:SB1-1110RNA-SeqAetiologyGeneTranscription factorOriginal Research2. Zero hungerGeneticsHuanglongbing; HLB; citrus; protein–protein interaction network; transcriptomics; RNA-SeqPectinesteraseSettore AGR/03 - Arboricoltura Generale E Coltivazioni ArboreeHLB030104 developmental biologyPectate lyaseprotein–protein interaction networkprotein-protein interaction networkBiotechnologyFrontiers in Plant Science
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Mouse Model of Cytomegalovirus Disease and Immunotherapy in the Immunocompromised Host: Predictions for Medical Translation that Survived the “Test o…

2018

Human Cytomegalovirus (hCMV), which is the prototype member of the β-subfamily of the herpesvirus family, is a pathogen of high clinical relevance in recipients of hematopoietic cell transplantation (HCT). hCMV causes multiple-organ disease and interstitial pneumonia in particular upon infection during the immunocompromised period before hematopoietic reconstitution restores antiviral immunity. Clinical investigation of pathomechanisms and of strategies for an immune intervention aimed at restoring antiviral immunity earlier than by hematopoietic reconstitution are limited in patients to observational studies mainly because of ethical issues including the imperative medical indication …

0301 basic medicineHuman cytomegalovirusmouse modelmedicine.medical_treatmentViral pathogenesislcsh:QR1-502T lymphocytesCytomegalovirusMice TransgenicCD8 T cellsReviewDiseaseCD8-Positive T-Lymphocytesmedicine.disease_causelcsh:MicrobiologyImmunocompromised HostMice03 medical and health sciencesImmune systemVirologymedicineAnimalsHumansadoptive cell transferVirus classificationimmune evasioninterstitial pneumoniaimmune controlviral pathogenesisbusiness.industryHematopoietic Stem Cell Transplantationhematopoietic reconstitutionCytomegalovirusImmunotherapyhematopoietic cell transplantation (HCT)medicine.diseaseAdoptive TransferTransplantationDisease Models Animalhumanized mice030104 developmental biologyInfectious DiseasesCytomegalovirus InfectionsImmunologyimmunotherapybusinessViruses
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Targeting cellular fatty acid synthesis limits T helper and innate lymphoid cell function during intestinal inflammation and infection

2019

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacolog…

0301 basic medicineImmunologyBiologyMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemRAR-related orphan receptor gammamedicineAnimalsImmunology and AllergyFatty acid synthesisBarrier functionLamina propriaEffectorFatty AcidsInnate lymphoid cellT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3ColitisInflammatory Bowel DiseasesImmunity InnateBiosynthetic PathwaysDisease Models Animal030104 developmental biologymedicine.anatomical_structurechemistryImmunologyLipogenesisBiomarkersAcetyl-CoA Carboxylase030215 immunologyMucosal Immunology
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Group 3 Innate Lymphoid Cells Program a Distinct Subset of IL-22BP-Producing Dendritic Cells Demarcating Solitary Intestinal Lymphoid Tissues.

2019

Solitary intestinal lymphoid tissues such as cryptopatches (CPs) and isolated lymphoid follicles (ILFs) constitute steady-state activation hubs containing group 3 innate lymphoid cells (ILC3) that continuously produce interleukin (IL)-22. The outer surface of CPs and ILFs is demarcated by a poorly characterized population of CD11c+ cells. Using genome-wide single-cell transcriptional profiling of intestinal mononuclear phagocytes and multidimensional flow cytometry, we found that CP- and ILF-associated CD11c+ cells were a transcriptionally distinct subset of intestinal cDCs, which we term CIA-DCs. CIA-DCs required programming by CP- and ILF-resident CCR6+ ILC3 via lymphotoxin-β receptor sig…

0301 basic medicineImmunologyPopulationCD11cGene ExpressionMice TransgenicC-C chemokine receptor type 6BiologyFlow cytometryImmunophenotyping03 medical and health sciencesMicePeyer's Patches0302 clinical medicineRNA Small CytoplasmicmedicineImmunology and AllergyAnimalsIntestinal Mucosaeducationeducation.field_of_studymedicine.diagnostic_testGene Expression ProfilingInnate lymphoid cellInterleukinDendritic CellsReceptors InterleukinLipid MetabolismImmunity InnateLymphocyte SubsetsCell biology030104 developmental biologyInfectious DiseasesLymphotoxinGene Expression Regulation030220 oncology & carcinogenesisHomeostasisBiomarkersSignal TransductionImmunity
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HSP110 sustains chronic NF-κB signaling in activated B cell diffuse large B cell lymphoma through MyD88 stabilization

2018

International audience; Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive lymphoproliferative disorder involving chronic NF-κB activation. Several mutations in the BCR and the MyD88 signaling pathway components, such as MyD88 L265P, are implicated in this aberrant activation. Among heat-shock proteins, HSP110 has recently been identified as a pro- survival and/or proliferation factor in many cancers but its role in ABC-DLBCL survival mechanisms remained to be established. We observed that shRNA-mediated HSP110 silencing decreased the survival of several ABC-DLBCL cell lines, decreased IgM-MyD88 co-localization and subsequent NF-κB signaling. Conversely, over-expres…

0301 basic medicineImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies03 medical and health sciencesimmune system diseaseshemic and lymphatic diseasesmedicineTumor Cells CulturedGene silencingHumansHSP110 Heat-Shock ProteinsB cellChemistryProtein StabilityWild typebreakpoint cluster regionNF-kappa BCell BiologyHematologymedicine.disease3. Good healthLymphoma030104 developmental biologymedicine.anatomical_structureCell cultureMyeloid Differentiation Factor 88Cancer researchLymphoma Large B-Cell DiffuseSignal transductionDiffuse large B-cell lymphomaSignal Transduction
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Primary sjogren syndrome: Focus on innate immune cells and inflammation

2020

Primary Sjogren Syndrome (pSS) is a complex, multifactorial rheumatic disease that mainly targets salivary and lacrimal glands, inducing epithelitis. The cause behind the autoimmunity outbreak in pSS is still elusive; however, it seems related to an aberrant reaction to exogenous triggers such as viruses, combined with individual genetic pre-disposition. For a long time, autoantibodies were considered as the hallmarks of this disease; however, more recently the complex interplay between innate and adaptive immunity as well as the consequent inflammatory process have emerged as the main mechanisms of pSS pathogenesis. The present review will focus on innate cells and on the principal mechani…

0301 basic medicineImmunologyinnate lymphoid cellslcsh:MedicineIFN signatureInflammationDiseaseReviewmedicine.disease_causeAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicinestomatognathic systemDrug DiscoverymedicineInnate lymphoid cellPharmacology (medical)Sjogren syndromeCytokine030203 arthritis & rheumatologyPharmacologyInflammationInnate immunityInnate immune systemSjogren syndrome.business.industryInnate lymphoid celllcsh:RAutoantibodyAcquired immune systemcytokinesstomatognathic diseases030104 developmental biologyInfectious DiseasesImmunologymedicine.symptombusiness
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