Search results for " tyrosine"

showing 10 items of 256 documents

Differential expression of specific microRNA and their targets in acute myeloid leukemia

2010

Acute myeloid leukemia (AML) the most common acute leukemia in adults is characterized by various cytogenetic and molecular abnormalities. However, the genetic etiology of the disease is not yet fully understood. MicroRNAs (miRNA) are small noncoding RNAs which regulate the expression of target mRNAs both at transcriptional and translational level. In recent years, miRNAs have been identified as a novel mechanism in gene regulation, which show variable expression during myeloid differentiation. We studied miRNA expression of leukemic blasts of 29 cases of newly diagnosed and genetically defined AML using quantitative reverse transcription polymerase chain reaction (RT-PCR) for 365 human miR…

AdultMaleNPM1Down-RegulationBiologySettore MED/15 - Malattie Del SangueYoung Adulthemic and lymphatic diseasesmicroRNAmedicineGene silencingHumansLeukemia microarray data microRNAGranulocyte Precursor CellsAgedCell ProliferationGeneticsRegulation of gene expressionAged 80 and overAcute leukemiaReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCore Binding FactorsMyeloid leukemiaNuclear ProteinsCell DifferentiationHematologyMiddle Agedmedicine.diseaseUp-RegulationGene expression profilingGene Expression Regulation NeoplasticLeukemiaLeukemia Myeloid AcuteMicroRNAsfms-Like Tyrosine Kinase 3Case-Control StudiesMutationFemaleSettore SECS-S/01 - StatisticaNucleophosmin
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The PTPN22gain-of-function+1858T(+) genotypes correlate with low IL-2 expression in thymomas and predispose to myasthenia gravis

2009

Protein tyrosine phosphatase, non-receptor type 22 (PTPN22) inhibits T-cell activation and interleukin-2 (IL-2) production. The PTPN22(gain-of-function)+1858T(+) genotypes predispose to multiple autoimmune diseases, including early-onset (non-thymomatous) myasthenia gravis (MG). The disease association and the requirement of IL-2/IL-2 receptor signaling for intrathymic, negative T-cell selection have suggested that these genotypes may weaken T-cell receptor (TCR) signaling and impair the deletion of autoreactive T cells. Evidence for this hypothesis is missing. Thymoma-associated MG, which depends on intratumorous generation and export of mature autoreactive CD4(+) T cells, is a model of au…

AdultMalemedicine.medical_specialtyThymomaAdolescentGenotypeThymomaImmunologyBiologymedicine.disease_causePolymorphism Single NucleotideWhite PeopleAutoimmunityPTPN22Young AdultAntigens CDInternal medicineMyasthenia GravisCentral tolerance inductionGeneticsmedicineHumansCTLA-4 AntigenGenetic Predisposition to DiseaseReceptorGenetics (clinical)AgedAged 80 and overT-cell receptorProtein Tyrosine Phosphatase Non-Receptor Type 22Thymus NeoplasmsMiddle Agedmedicine.diseaseMyasthenia gravisEndocrinologyImmunologyInterleukin-2FemaleCentral toleranceGenes & Immunity
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Islet autoantibodies in Latvian subjects with non-insulin-dependent diabetes mellitus: slow-onset type 1 diabetes or polyendocrine autoimmunity?

2006

In Latvia diabetes mellitus is diagnosed using the WHO's clinical criteria; assays for the detection of autoantibodies are not available, and hence slowly progressive autoimmune diabetes is likely to be missed. Autoantibodies against glutamic acid decarboxylase (GAD65) and protein tyrosine phosphatase (IA-2) among patients with clinically diagnosed NIDDM identify group of patients with slow-onset type 1 diabetes or LADA. The aim of this study was to estimate the risk of polyendocrine autoimmunity among clinically diagnosed NIDDM patients from Latvia. One hundred NIDDM patients and 100 healthy controls were tested for GAD65 and IA-2 autoantibodies as well as 21-hydroxylase (21-OH) and tissue…

AdultMalemedicine.medical_specialtyendocrine system diseasesAdolescentTissue transglutaminasemedicine.medical_treatmentOverweightmedicine.disease_causeAutoantigensGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityDiagnosis DifferentialHistory and Philosophy of ScienceInternal medicineDiabetes mellitusmedicineHumansReceptor-Like Protein Tyrosine Phosphatases Class 8ChildPolyendocrinopathies AutoimmuneAutoantibodiesProtein Tyrosine Phosphatase Non-Receptor Type 1Type 1 diabetesbiologybusiness.industryGlutamate DecarboxylaseGeneral NeuroscienceInsulinAutoantibodynutritional and metabolic diseasesMembrane Proteinsmedicine.diseaseLatviaIsoenzymesEndocrinologyDiabetes Mellitus Type 1Child Preschoolbiology.proteinFemalemedicine.symptomProtein Tyrosine PhosphatasesbusinessBody mass indexBiomarkersAnnals of the New York Academy of Sciences
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Plasma levels of soluble vascular endothelial growth factor receptor-1 may determine the onset of early and late ovarian hyperstimulation syndrome

2006

BACKGROUND Ovarian hyperstimulation syndrome (OHSS) is a life-threatening condition associated with ovarian stimulation. Its pathophysiology is unknown and its treatment continues to be empirical. Early (E)- and late (L)-OHSS occur in women at risk, though not in all cases. Vascular endothelial growth factor (VEGF) is related to increased vascular permeability in OHSS. We analysed the dynamics of the VEGF system in E- and L-OHSS. METHODS A prospective cohort of women undergoing IVF-ICSI treatment were divided into groups. E-OHSS: Nonpregnant patients classified as women not at risk (group 1) (n = 11) and patients at risk who did not (group 2) (n = 18) and did (group 3) (n = 8) develop sever…

AdultOvulationVascular Endothelial Growth Factor Amedicine.medical_specialtyTime Factorsmedia_common.quotation_subjectOvarian hyperstimulation syndromeVascular permeabilityOvaryFertilization in VitroBiologyCohort StudiesOvarian Hyperstimulation Syndromechemistry.chemical_compoundInternal medicineBlood plasmamedicineHumansalpha-MacroglobulinsSperm Injections IntracytoplasmicProspective cohort studyOvulationmedia_commonVascular Endothelial Growth Factor Receptor-1OvaryRehabilitationObstetrics and Gynecologymedicine.diseaseVascular endothelial growth factorEndocrinologymedicine.anatomical_structureReproductive MedicinechemistryOocytesFemaleSoluble fms-like tyrosine kinase-1Human Reproduction
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Pleural Mesothelial Cells Express Both BLT2 and PPARα and Mount an Integrated Response to Pleural Leukotriene B4

2008

Abstract Leukotriene B4 (LTB4) plays a crucial role in the recruitment of neutrophils into the pleural space. We identified for the first time the mechanisms by which LTB4 interacts with mesothelial cells and recruits neutrophils in the pleural compartment. Primary pleural mesothelial cells express both the proinflammatory receptor for LTB4 BLT2, and the anti-inflammatory receptor for LTB4, PPARα. Parapneumonic pleural effusions highly increase BLT2 expression and, via BLT2 activation, increase the adhesion between mesothelial cells and neutrophils and the expression of ICAM-1 on mesothelial cells. The block of PPARα further increases both cell adhesion and ICAM-1 expression. BLT2 activatio…

Adultmedicine.drug_classLeukotriene B4Blotting WesternImmunologyReceptors Leukotriene B4Protein tyrosine phosphataseBiologyLeukotriene B4EpitheliumTyrosine-kinase inhibitorProinflammatory cytokinechemistry.chemical_compoundCell AdhesionmedicineHumansImmunology and AllergyPPAR alphaCell adhesionCells CulturedAgedInflammationLeukotriene B4 receptorPneumoniaMiddle Agedrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1respiratory tract diseasesPleural EffusionChemotaxis LeukocyteNeutrophil InfiltrationchemistryImmunologyCancer researchPleuraPhosphorylationMesothelial CellThe Journal of Immunology
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Novel 3-Azaindolyl-4-arylmaleimides Exhibiting Potent Antiangiogenic Efficacy, Protein Kinase Inhibition, and Antiproliferative Activity

2012

Tumor growth and metastasis are highly associated with the overexpression of protein kinases (PKs) regulating cell growth, apoptosis resistance, and prolonged cell survival. This study describes novel azaindolyl-maleimides with significant inhibition of PKs, such as VEGFR, FLT-3, and GSK-3β which are related to carcinogenesis. Furthermore, these compounds exhibit high kinase selectivity and potent inhibition of angiogenesis and cell proliferation, offering versatile options in cancer treatment strategies.

AngiogenesisAngiogenesis InhibitorsApoptosisChick EmbryoPharmacologymedicine.disease_causeMetastasisMaleimidesNeovascularizationGlycogen Synthase Kinase 3Structure-Activity RelationshipNeoplasmsDrug DiscoveryHuman Umbilical Vein Endothelial Cellspolycyclic compoundsmedicineAnimalsHumansProtein kinase AProtein Kinase InhibitorsGSK3BCells CulturedCell ProliferationGlycogen Synthase Kinase 3 betaMolecular StructureNeovascularization PathologicKinaseChemistryCell growthCell CycleVascular Endothelial Growth Factor Receptor-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2Growth Inhibitorsfms-Like Tyrosine Kinase 3Molecular Medicinemedicine.symptomCarcinogenesisJournal of Medicinal Chemistry
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A recommended practical approach to the management of target therapy and angiogenesis inhibitors cardiotoxicity: an opinion paper of the working grou…

2016

The US National Cancer Institute estimates that cardiotoxicity (CTX) from target therapy refers mostly to four groups of drugs: epidermal growth factor receptor 2 inhibitors, angiogenic inhibitors, directed Abelson murine leukemia viral oncogene homolog inhibitors, and proteasome inhibitors. The main cardiotoxic side-effects related to antiepidermal growth factor receptor 2 therapy are left ventricular systolic dysfunction and heart failure. Angiogenesis inhibitors are associated with hypertension, left ventricular dysfunction/heart failure, myocardial ischemia, QT prolongation, and thrombosis. Moreover, other agents may be related to CTX induced by treatment. In this study, we review the g…

AngiogenesisLeftAngiogenesis Inhibitors030204 cardiovascular system & hematologyVentricular Dysfunction Left0302 clinical medicinetyrosine kinase inhibitorNeoplasmstyrosine kinase inhibitorsVentricular DysfunctionMolecular Targeted TherapyEpidermal growth factor receptorSocieties Medicalangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitorABLbiologyDisease ManagementGeneral MedicineItalyCardiovascular DiseasesSupplement Submission030220 oncology & carcinogenesisangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Angiogenesis Inhibitors; Antineoplastic Agents; Cardiology; Cardiomyopathies; Cardiotoxicity; Heart Failure; Humans; Italy; Neoplasms; Practice Guidelines as Topic; Societies Medical; Ventricular Dysfunction Left; Disease ManagementPractice Guidelines as TopicCardiologyCardiology and Cardiovascular MedicineCardiomyopathiesmedicine.medical_specialtyCardiologyAntineoplastic AgentsRisk AssessmentQT interval03 medical and health sciencesGrowth factor receptorInternal medicineMedicalmedicineHumansMonitoring PhysiologicHeart FailureCardiotoxicitybusiness.industryCancerHER2/epidermal growth factor receptor 2medicine.diseaseangiogenesis inhibitors; HER2/epidermal growth factor receptor 2; tyrosine kinase inhibitors; Cardiology and Cardiovascular MedicineCardiotoxicityangiogenesis inhibitorHeart failurebiology.proteinbusinessSocietiesJournal of cardiovascular medicine (Hagerstown, Md.)
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Inhibition of tumor angiogenesis by antibodies, synthetic small molecules and natural products.

2011

Cancer remains one of the major causes of death worldwide. The switch to pathological angiogenesis is a key process in the promotion of cancer and consequently provides several new and promising targets to anticancer therapy. Thus, antagonizing angiogenesis cuts off the tumor's oxygen and nutrition supply. This review focuses on angiogenesis inhibitors as option for cancer treatment. Modes of action, adverse effects, mechanisms of resistance as well as new developments are highlighted. One approach in angiogenesis inhibition is intermitting the further VEGF (vascular endothelial growth factor) signal pathway with monoclonal antibodies. Bevacizumab is a highly specific recombinant humanized …

Angiogenesismedicine.drug_classGenisteinAngiogenesis InhibitorsAntineoplastic AgentsBiologyPharmacologyMonoclonal antibodyBiochemistryReceptor tyrosine kinaseNeovascularizationSmall Molecule Librarieschemistry.chemical_compoundGrowth factor receptorNeoplasmsDrug DiscoverymedicineAnimalsHumansPharmacologyBiological ProductsNeovascularization PathologicVascular Endothelial Growth FactorsOrganic ChemistryCancerAntibodies Monoclonalmedicine.diseaseAntineoplastic Agents PhytogenicVascular endothelial growth factorchemistrybiology.proteinMolecular Medicinemedicine.symptomCurrent medicinal chemistry
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S-Nitrosation of Arabidopsis thaliana Protein Tyrosine Phosphatase 1 Prevents Its Irreversible Oxidation by Hydrogen Peroxide

2022

Tyrosine-specific protein tyrosine phosphatases (Tyr-specific PTPases) are key signaling enzymes catalyzing the removal of the phosphate group from phosphorylated tyrosine residues on target proteins. This post-translational modification notably allows the regulation of mitogen-activated protein kinase (MAPK) cascades during defense reactions. Arabidopsis thaliana protein tyrosine phosphatase 1 (AtPTP1), the only Tyr-specific PTPase present in this plant, acts as a repressor of H2O2 production and regulates the activity of MPK3/MPK6 MAPKs by direct dephosphorylation. Here, we report that recombinant histidine (His)-AtPTP1 protein activity is directly inhibited by H2O2 and nitric oxide (NO) …

Arabidopsis thaliananitric oxideoxidationH2O2Plant cultureprotein tyrosine phosphatase 1S-nitrosationSB1-1110Frontiers in Plant Science
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Biphasic Erk1/2 activation sequentially involving Gs and Gi signaling is required in beta3-adrenergic receptor-induced primary smooth muscle cell pro…

2013

Abstract The beta3 adrenergic receptor (B3-AR) reportedly induces cell proliferation, but the signaling pathways that were proposed, involving either Gs or Gi coupling, remain controversial. To further investigate the role of G protein coupling in B3-AR induced proliferation, we stimulated primary human myometrial smooth muscle cells with SAR150640 (B3-AR agonist) in the absence or presence of variable G-protein inhibitors. Specific B3-AR stimulation led to an Erk1/2 induced proliferation. We observed that the proliferative effects of B3-AR require two Erk1/2 activation peaks (the first after 3 min, the second at 8 h). Erk1/2 activation at 3 min was mimicked by forskolin (adenylyl-cyclase a…

Beta-3 adrenergic receptorGs alpha subunitMAP Kinase Signaling SystemMyocytes Smooth MuscleProliferationG protein coupled receptorBiologyGTP-Binding Protein alpha Subunits Gi-GoPertussis toxinchemistry.chemical_compoundErk1/2Protein kinasesCyclinsReceptors Adrenergic betaGTP-Binding Protein alpha Subunits GsHumansMolecular BiologyPI3K/AKT/mTOR pathwayCells CulturedG protein-coupled receptorCell ProliferationForskolinColforsinBeta-3 adrenergic receptorCell BiologyCell biologychemistryGene Expression RegulationPertussis ToxinMyometriumFemaleSignal transductionProto-oncogene tyrosine-protein kinase SrcBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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