Search results for "ADP"

showing 10 items of 423 documents

Identification of the integrin-binding site on coagulation factor VIIa required for proangiogenic PAR2 signaling.

2018

The tissue factor (TF) pathway serves both hemostasis and cell signaling, but how cells control these divergent functions of TF remains incompletely understood. TF is the receptor and scaffold of coagulation proteases cleaving protease-activated receptor 2 (PAR2) that plays pivotal roles in angiogenesis and tumor development. Here we demonstrate that coagulation factor VIIa (FVIIa) elicits TF cytoplasmic domain-dependent proangiogenic cell signaling independent of the alternative PAR2 activator matriptase. We identify a Lys-Gly-Glu (KGE) integrin-binding motif in the FVIIa protease domain that is required for association of the TF-FVIIa complex with the active conformer of integrin β1. A po…

0301 basic medicineCell signalingImmunologyIntegrinNeovascularization PhysiologicFactor VIIa030204 cardiovascular system & hematologyBiochemistryThromboplastinThrombosis and Hemostasis03 medical and health sciencesTissue factorMice0302 clinical medicineAnimalsHumansReceptor PAR-2Protein Interaction Domains and MotifsProtein Interaction MapsProtein kinase ACells CulturedIntegrin bindingBinding SitesbiologyChemistryIntegrin beta1Cell BiologyHematologyCell biologyCrosstalk (biology)030104 developmental biologyADP-Ribosylation Factor 6biology.proteinNIH 3T3 CellsPhosphorylationSignal transductionProtein BindingSignal TransductionBlood
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7-Keto-Cholesterol and Cholestan-3beta, 5alpha, 6beta-Triol Induce Eryptosis through Distinct Pathways Leading to NADPH Oxidase and Nitric Oxide Synt…

2019

Background/aims We showed that patho-physiological concentrations of either 7-keto-cholesterol (7-KC), or cholestane-3beta, 5alpha, 6beta-triol (TRIOL) caused the eryptotic death of human red blood cells (RBC), strictly dependent on the early production of reactive oxygen species (ROS). The goal of the current study was to assess the contribution of the erythrocyte ROS-generating enzymes, NADPH oxidase (RBC-NOX), nitric oxide synthase (RBC-NOS) and xanthine oxido-reductase (XOR) to the oxysterol-dependent eryptosis and pertinent activation pathways. Methods Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, reactive oxygen/nitrogen species (RONS) and nitri…

0301 basic medicineErythrocytesPhysiologyEryptosisNADPH Oxidaselcsh:PhysiologyMethemoglobinHemoglobinsPhosphatidylinositol 3-Kinaseschemistry.chemical_compound0302 clinical medicinelcsh:QD415-436RBC-NOS activationKetocholesterolsHemechemistry.chemical_classificationNADPH oxidaselcsh:QP1-981biologyrac GTP-Binding ProteinsCholestanolErythrocyteNitric oxide synthaseRac GTP-Binding ProteinsRBC-NOX activationToxic oxysterolBiochemistry030220 oncology & carcinogenesisOxidation-ReductionHumanSignal Transductioncirculatory and respiratory physiologyOxidative phosphorylationlcsh:BiochemistryNitrosative stre03 medical and health sciencesHumansHemoglobinReactive oxygen speciesKetocholesterolNADPH Oxidases030104 developmental biologychemistrybiology.proteinTriolPhosphatidylinositol 3-KinaseNitric Oxide SynthaseEryptosiProto-Oncogene Proteins c-aktCholestanolsCellular Physiology and Biochemistry
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Redox signaling in the gastrointestinal tract.

2017

Redox signaling regulates physiological self-renewal, proliferation, migration and differentiation in gastrointestinal epithelium by modulating Wnt/β-catenin and Notch signaling pathways mainly through NADPH oxidases (NOXs). In the intestine, intracellular and extracellular thiol redox status modulates the proliferative potential of epithelial cells. Furthermore, commensal bacteria contribute to intestine epithelial homeostasis through NOX1- and dual oxidase 2-derived reactive oxygen species (ROS). The loss of redox homeostasis is involved in the pathogenesis and development of a wide diversity of gastrointestinal disorders, such as Barrett's esophagus, esophageal adenocarcinoma, peptic ulc…

0301 basic medicineGastrointestinal DiseasesNotch signaling pathwaymedicine.disease_causeBiochemistryGastrointestinal epitheliumSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansSulfhydryl CompoundsIntestinal MucosaWnt Signaling PathwayCell Proliferationchemistry.chemical_classificationReactive oxygen speciesbiologySuperoxideWnt signaling pathwayNADPH OxidasesDual oxidase 2digestive system diseasesGastrointestinal TractIntestinesOxidative Stress030104 developmental biologychemistryImmunologybiology.proteinCancer researchReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree radical biologymedicine
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NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
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Haploinsufficiency of ARFGEF1 is associated with developmental delay, intellectual disability, and epilepsy with variable expressivity

2021

PURPOSE: ADP ribosylation factor guanine nucleotide exchange factors (ARFGEFs) are a family of proteins implicated in cellular trafficking between the Golgi apparatus and the plasma membrane through vesicle formation. Among them is ARFGEF1/BIG1, a protein involved in axon elongation, neurite development, and polarization processes. ARFGEF1 has been previously suggested as a candidate gene for different types of epilepsies, although its implication in human disease has not been well characterized.METHODS: International data sharing, in silico predictions, and in vitro assays with minigene study, western blot analyses, and RNA sequencing.RESULTS: We identified 13 individuals with heterozygous…

0301 basic medicineGeneticsCandidate geneHeterozygoteEpilepsyADP ribosylation factorIn silicoHeterozygote advantageHaploinsufficiency030105 genetics & heredityBiologymedicine.disease03 medical and health sciencesEpilepsy030104 developmental biologyIntellectual DisabilitymedicineGuanine Nucleotide Exchange FactorsHumansGuanine nucleotide exchange factorHaploinsufficiencyGenetics (clinical)MinigeneGenetics in Medicine
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miR-22 suppresses DNA ligase III addiction in multiple myeloma

2019

Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation. We identified miR-22-3p as effective negative regulator of LIG3 in MM. Enforced expression of…

0301 basic medicineGenome instabilityCancer ResearchmiR-22 LIG3DNA repairDNA damageDNA repairApoptosisLIG3ArticleDNA Ligase ATP03 medical and health sciences0302 clinical medicinemicroRNABiomarkers TumorTumor Cells CulturedHumansPoly-ADP-Ribose Binding ProteinsCell ProliferationmiRNAchemistry.chemical_classificationRegulation of gene expressionGene knockdownDNA ligaseLeukemiamicroRNAChemistryHematologyPrognosisXenograft Model Antitumor AssaysGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchpharmacologyDNA DamageLeukemia
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Beta3 adrenergic receptor stimulation in human macrophages inhibits NADPHoxidase activity and induces catalase expression via PPARγ activation

2017

IF 4.521; International audience; The beta3 adrenergic receptor (β3-AR) stimulation plays a protective role against preterm labor by blocking myometrial contraction, cytokine production, remodeling and apoptosis. We previously demonstrated that macrophage-induced ROS production in the myometrium was a key element leading to the induction of all these labor-associated features. We thus aimed to investigate if the β3-AR could be expressed in human macrophages and could trigger its protective role in the myometrium by directly inhibiting ROS production. Using lipopolysaccharide (LPS)-stimulated myometrial samples and cell co-culture experiments, we demonstrated that β3-AR stimulation inhibits …

0301 basic medicineLipopolysaccharidesmedicine.medical_specialtyLipopolysaccharidePPARγPreterm laborMacrophagemedicine.medical_treatmentPeroxisome proliferator-activated receptorStimulationApoptosisAntioxidants03 medical and health scienceschemistry.chemical_compoundTransactivation0302 clinical medicineInternal medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologychemistry.chemical_classificationNADPH oxidasebiologybeta3 adrenergic receptorMacrophagesMyometriumNADPH OxidasesROSCell BiologyCatalaseCoculture Techniques3. Good healthCell biologyPPAR gamma030104 developmental biologyEndocrinologyCytokinechemistryGene Expression RegulationReceptors Adrenergic beta-3biology.proteinMyometriumFemaleSignal transductionReactive Oxygen Species030217 neurology & neurosurgerySignal Transduction
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Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.

2018

The cyclic GMP-AMP synthase/stimulator of IFN genes (cGAS/STING) pathway detects cytosolic DNA to activate innate immune responses. Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively target cancer cells with DNA repair deficiencies such as those caused by BRCA1 mutations or ERCC1 defects. Using isogenic cell lines and patient-derived samples, we showed that ERCC1-defective non-small cell lung cancer (NSCLC) cells exhibit an enhanced type I IFN transcriptomic signature and that low ERCC1 expression correlates with increased lymphocytic infiltration. We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defecti…

0301 basic medicineLung NeoplasmsDNA repairPoly (ADP-Ribose) Polymerase-1Triple Negative Breast NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorB7-H1 AntigenOlaparib03 medical and health scienceschemistry.chemical_compoundInterferon-gamma0302 clinical medicinePARP1Carcinoma Non-Small-Cell LungHumansRucaparibA549 cellChemistryBRCA1 ProteinMembrane ProteinsGeneral MedicineEndonucleasesIsogenic human disease modelsNucleotidyltransferasesDNA-Binding Proteins030104 developmental biologyA549 Cells030220 oncology & carcinogenesisCancer cellCancer researchFemaleResearch ArticleThe Journal of clinical investigation
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Impact of NADPH oxidase functional polymorphisms in acute myeloid leukemia induction chemotherapy.

2016

Efficacy and toxicity of anthracycline treatment in acute myeloid leukemia (AML) is mediated by reactive oxygen species (ROS). NADPH oxidase is the major endogenous source of ROS and a key mediator of oxidative cardiac damage. The impact of NADPH oxidase polymorphisms (CYBA:rs4673, NCF4:rs1883112, RAC2:rs13058338) was evaluated in 225 adult de novo AML patients. Variant alleles of NCF4 and RAC2 were related to higher complete remission (P=0.035, P=0.016), and CYBA homozygous variant showed lower overall survival with recessive model (P=0.045). Anthracycline-induced cardiotoxicity was associated to NCF4 homozygous variant (P=0.012) and CYBA heterozygous genotype (P=0.027). Novel associations…

0301 basic medicineMaleAnthracyclinePharmacologyBiologyPolymorphism Single NucleotideNephrotoxicity03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsGeneticsHumansAgedRetrospective StudiesPharmacologychemistry.chemical_classificationReactive oxygen speciesCardiotoxicityNADPH oxidaseRemission InductionMyeloid leukemiaNADPH OxidasesInduction ChemotherapyMiddle Agedrac GTP-Binding ProteinsRac GTP-Binding ProteinsLeukemia Myeloid Acute030104 developmental biologychemistry030220 oncology & carcinogenesisToxicitybiology.proteinMolecular MedicineFemaleReactive Oxygen SpeciesThe pharmacogenomics journal
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