Search results for "Tyro"

showing 10 items of 816 documents

Molecular markers for germ cell differentiation in the demosponge Suberites domuncula

2004

Sponges (phylum Porifera) are simple metazoans for which no molecular information on gametogenesis and larval development is available. To support the current study, it was confirmed by histology that oocytes and larvae were produced by the demosponge Suberites domuncula. Three genes/expressed products from S. domuncula whose expression correlated with sexual reproduction were identified and characterized (they are used here as marker genes): i) a receptor tyrosine kinase (RTK) with sequence similarity in the tyrosine kinase domain to fibroblast growth factor receptors; ii) the sex-determining protein FEM1 and iii) the sperm associated antigen (SAA) of triploblasts. Antibodies against the e…

MaleEmbryologyMolecular Sequence DataReceptor tyrosine kinaseDemospongemedicineAnimalsAmino Acid SequenceAntigensPhylogenyGametogenesisCaenorhabditis elegansGeneticsBase SequenceSequence Homology Amino AcidbiologyfungiGene Expression Regulation DevelopmentalReceptor Protein-Tyrosine KinasesCell DifferentiationDNASex Determination Processesbiology.organism_classificationSpermatozoaCell biologySuberites domunculamedicine.anatomical_structureFibroblast growth factor receptorOocytesbiology.proteinFemaleSeasonsSuberitesTyrosine kinaseBiomarkersGerm cellDevelopmental Biology
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The molecular evolution of sperm zonadhesin.

2008

Based on pioneering work of Hardy and Garbers, zonadhesin has become one of the best studied sperm ligands in boreoeutherian mammals, both from a biochemical and evolutionary perspective. Zonadhesin is a mosaic-type protein that localizes to the apical head of spermatozoa. In pig, cattle, rabbit and primates, zonadhesin precursor essentially consists of two or three MAM (meprin/A5 antigen/mu receptor tyrosine phosphatase) domains, one mucin-like domain, one incomplete and four complete D domains (homologous to vWFD). Mouse zonadhesin is distinguished from this general pattern by 20 extra partial D3 domains. While concerted evolution drives the divergence of the mucin-like domain in the orth…

MaleEmbryologySwineMolecular Sequence DataProtein tyrosine phosphataseBiologyModels BiologicalEvolution MolecularNegative selectionMiceTandem repeatSpecies SpecificityMolecular evolutionTestisvon Willebrand FactorAnimalsAmino Acid SequencePeptide sequenceSperm competitionZona PellucidaGeneticsConcerted evolutionSequence Homology Amino AcidMembrane ProteinsSpermatozoaSexual dimorphismFemaleDevelopmental BiologyThe International journal of developmental biology
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Phospholipase D in rat myocardium: formation of lipid messengers and synergistic activation by G-protein and protein kinase C.

1998

Activation of phospholipase D (PLD) and phosphoinositide-specific phospholipase C (PI-PLC) by fluoride, to stimulate heterotrimeric G-proteins, and by phorbol esters, to stimulate protein kinase C (PKC), was studied in rat atria. Fluoride and 4beta-phorbol-12beta,13alpha-dibutyrate (PDB), in contrast to 4beta-phorbol-13alpha-acetate (PAc), activated PLD, catalyzing the formation of [3H]-phosphatidylethanol ([3H]-PETH), [3H]-phosphatidic acid ([3H]-PA), choline and sn-1,2-diacylglycerol (DAG). Basal PLD activity was resistant to drastic changes in Ca2+ and to Ro 31-8220, a PKC inhibitor, but was decreased by genistein, an inhibitor of tyrosine kinase, and increased by vanadate, a tyrosine ph…

MaleG proteinProtein tyrosine phosphataseBiologyBiochemistrySecond Messenger Systemschemistry.chemical_compoundPhosphoinositide Phospholipase CGTP-Binding ProteinsPhorbol EstersPhospholipase DAnimalsRats WistarProtein kinase CPhorbol 1213-DibutyrateProtein Kinase CDiacylglycerol kinasePharmacologyPhospholipase CPhospholipase DMyocardiumPhosphatidylinositol Diacylglycerol-LyaseTyrosine phosphorylationDrug SynergismLipid MetabolismLipidsRatsEnzyme ActivationBiochemistrychemistryType C PhospholipasesSecond messenger systemlipids (amino acids peptides and proteins)Biochemical pharmacology
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Mechanisms of Ca2+ liberation at fertilization

2005

The mechanisms underlying the Ca2+ release at fertilization of several animal organisms are reported. Four main classical theories are described, i.e., that of Ca2+ release following simple sperm contact and a G protein stimulation; that of simple sperm contact followed by a tyrosine kinase receptor activation; that of the necessity of introduction by sperm into the egg of molecules for Ca2+ release; and that the molecule introduced into the marine eggs for Ca2+ release is the same Ca2+. Two other mechanisms for Ca2+ release are also illustrated: that of ryanodine receptor stimulation and that of NAADP formation.

MaleG proteinXenopusBiophysicsStimulationChick EmbryoFERTILIZATION CALCIUM RELEASEBiologyModels BiologicalBiochemistryReceptor tyrosine kinaseMiceHuman fertilizationGTP-Binding ProteinsAnimalsMolecular BiologySperm-Ovum InteractionsAdenine NucleotidesRyanodine receptorCell BiologySpermatozoaSpermCell biologyBiochemistryFertilizationbiology.proteinLiberationCalciumBiochemical and Biophysical Research Communications
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Effect of soluble guanylyl cyclase activator and stimulator therapy on nitroglycerin-induced nitrate tolerance in rats

2015

Chronic nitroglycerin (GTN) anti-ischemic therapy induces side effects such as nitrate tolerance and endothelial dysfunction. Both phenomena could be based on a desensitization/oxidation of the soluble guanylyl cyclase (sGC). Therefore, the present study aims at investigating the effects of the therapy with the sGC activator BAY 60-2770 and the sGC stimulator BAY 41-8543 on side effects induced by chronic nitroglycerin treatment. Male Wistar rats were treated with nitroglycerin (100mg/kg/d for 3.5days, s.c. in ethanol) and BAY 60-2770 (0.5 or 2.5mg/kg/d) or BAY 41-8543 (1 and 5mg/kg/d) for 6days. Therapy with BAY 60-2770 but not with BAY 41-8543 improved nitroglycerin-triggered endothelial …

MaleHydrocarbons FluorinatedPhysiologyMorpholinesReceptors Cytoplasmic and NuclearVasodilationStimulationPharmacologymedicine.disease_causeBenzoatesNitric oxideNitroglycerinchemistry.chemical_compoundOrgan Culture TechniquesSoluble Guanylyl CyclasemedicineAnimalsPharmacology (medical)Rats WistarEndothelial dysfunctionAortaWhole bloodPharmacologyNitratesActivator (genetics)business.industryNitrotyrosineBiphenyl Compoundsmedicine.diseaseRatsBiphenyl compoundEnzyme ActivationOxidative StressPyrimidineschemistryGuanylate CyclaseMeeting Abstractcardiovascular systemMolecular MedicineSoluble guanylyl cyclasebusinessOxidative stressBMC Pharmacology and Toxicology
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Observational study of chronic myeloid leukemia Italian patients who discontinued tyrosine kinase inhibitors in clinical practice.

2018

It is judged safe to discontinue treatment with tyrosine kinase inhibitors (TKI) for chronic myeloid leukemia (CML) in experimental trials on treatment-free remission (TFR). We collected a total of 293 Italian patients with chronic phase CML who discontinued TKI in deep molecular response. Seventy-two percent of patients were on treatment with imatinib, and 28% with second generation TKI at the time of discontinuation. Median duration of treatment with the last TKI was 77 months [Interquartile Range (IQR) 54;111], median duration of deep molecular response was 46 months (IQR 31;74). Duration of treatment with TKI and duration of deep molecular response were shorter with second generation TK…

MaleImatinib mesylate discontinuation; chronic myelogenous leukemia; treatment-free remission; long-term outcomes; molecular response; cml patients; recommendations; management; dasatinib; cessationchemistry.chemical_compound0302 clinical medicineTreatment Free RemissionPregnancyMED/15 - MALATTIE DEL SANGUEInterquartile rangeingleseMedicinedasatinibChronic Myelogenous Leukemiatreatment-free remissionPonatinibmolecular responseHematologyMiddle AgedProtein-Tyrosine Kinasescml patientsDasatinibTreatment OutcomeLeukemia Myeloid Chronic-PhaseDisease ProgressionImatinib MesylateFemaleChronic Myelogenous Leukemia; Discontinuation; Treatment Free Remissionlong-term outcomesmanagementmedicine.drugAdultmedicine.medical_specialtyChronic Myeloid LeukemiaSocio-culturaleDiscontinuationArticletyrosine kinase inhibitors discontinued treatment chronic myeloid leukemia treatment-free remission (TFR)Safety-Based Drug Withdrawals03 medical and health scienceschronic myeloid leukemia tyrosine kinase inhibitors discontinuationMedian follow-upLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicineImatinib mesylate discontinuationHumansProtein Kinase InhibitorsRetrospective Studiesbusiness.industryImatinibmedicine.diseaseDiscontinuationrespiratory tract diseasesSettore MED/15 - MALATTIE DEL SANGUEcessationNilotinibchemistryrecommendationsbusiness030215 immunologyChronic myelogenous leukemia
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Increased Circulating Levels of 3-Nitrotyrosine Autoantibodies

2012

3-nitrotyrosine formation is an oxidative protein modification that was first discovered in vivo in the early 1990s by Beckman and colleagues.1,2 The biological relevance of this process was extensively investigated in the subsequent years and further facilitated by the development of 3-nitrotyrosine–specific antibodies.3 Protein tyrosine nitration is mainly mediated by 3 biochemical processes (Figure): (1) by peroxynitrite (ONOO−) formation,4–6 the reaction product of nitric oxide (•NO) and superoxide (•O2−); (2) by a (myelo)peroxidase-catalyzed nitrogen dioxide radical (•NO2) formation from hydrogen peroxide and nitrite;7,8 and (3) by a nonspecific formation of the nitrogen dioxide radica…

MaleImmunoglobulinsProstacyclinCoronary Artery DiseasePharmacologyArticleProstacyclin synthaseNitric oxideEpitopeschemistry.chemical_compoundPhysiology (medical)medicineHumansbiologySuperoxidebusiness.industryNitric Oxide Synthase Type IIIPeroxynitrous acidchemistryBiochemistryMyeloperoxidasebiology.proteinTyrosineFemaleCardiology and Cardiovascular MedicinebusinessPeroxynitritemedicine.drugCirculation
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Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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Detection of increased tyrosine phosphorylation in murine Langerhans cells after stimulation with contact sensitizers.

1999

The signalling pathways in epidermal Langerhans cells (LC) during activation by contact sensitizers are poorly understood. Recently, we have described an increased phosphorylation of tyrosine residues in human MHC class II-positive cells in vitro following stimulation with contact sensitizers. In the study reported here the formation of phosphotyrosine (p-tyr) in murine epidermal LC upon stimulation with contact sensitizers was examined. By the use of a flow cytometric technique a significant increase in p-tyr was demonstrated in LC stimulated in vitro with the strong contact sensitizers TNCB (2,4,6-trinitro-chlorobenzene) and MCI/MI (5-chloro-2-methylisothiazolinone plus 2-methylisothiazol…

MaleLangerhans cellBlotting WesternDermatologyPicryl ChlorideBiologyCell Linechemistry.chemical_compoundMicemedicineAnimalsTyrosinePhosphorylationPhosphotyrosineMice Inbred BALB CTyrosine phosphorylationGeneral MedicineDendritic cellFlow CytometryMolecular biologyIn vitromedicine.anatomical_structureBiochemistrychemistryLangerhans CellsPhosphorylationTyrosineFemaleTyrphostin A9Signal transductionSignal TransductionArchives of dermatological research
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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