Search results for " tyrosine"

showing 10 items of 256 documents

From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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Timely recognition of cardiovascular toxicity by anticancer agents: a common objective of the pharmacologist, oncologist and cardiologist.

2011

Both conventional and new anticancer drugs can frequently cause adverse cardiovascular effects, which can span from subclinical abnormalities to serious life-threatening and sometimes fatal events. This review examines the principal basic and clinical elements that may be of profit to identify, prevent and treat such toxicities. Clearly, the accomplishment of such objectives requires the strong commitment and cooperation of different professional figures including, but not limited to, pharmacologists, oncologists and cardiologists. The aspect of anticancer drug cardiotoxicity seems to be somehow underestimated, mainly due to inadequate reporting of adverse reactions from oncology drugs in t…

Cardiovascular toxicityTime FactorsSettore MED/06 - Oncologia MedicaPharmacology toxicologyCardiologyAntineoplastic AgentsPharmacologyToxicologyMedical OncologyCardiotoxinsCardiovascular SystemProfessional RolePharmacovigilanceMedicineAnimalsHumansPhysician's RoleMolecular BiologyPharmacologyCardiotoxicitybusiness.industryCardiovascular toxicity Anthracyclines Tyrosine kinase inhibitors TrastuzumabSettore MED/11 - Malattie Dell'Apparato CardiovascolareAnticancer drugLaboratory PersonnelCardiovascular DiseasesSettore BIO/14 - FarmacologiaCardiology and Cardiovascular MedicinebusinessOncology drugsCardiovascular toxicology
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Computational Evaluation and In Vitro Validation of New Epidermal Growth Factor Receptor Inhibitors

2020

Background:The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein that acts as a receptor of extracellular protein ligands of the epidermal growth factor (EGF/ErbB) family. It has been shown that EGFR is overexpressed by many tumours and correlates with poor prognosis. Therefore, EGFR can be considered as a very interesting therapeutic target for the treatment of a large variety of cancers such as lung, ovarian, endometrial, gastric, bladder and breast cancers, cervical adenocarcinoma, malignant melanoma and glioblastoma.Methods:We have followed a structure-based virtual screening (SBVS) procedure with a library composed of several commercial collections of chemicals (615,46…

Cell SurvivalDrug Evaluation PreclinicalAntineoplastic Agents01 natural sciencesReceptor tyrosine kinaseStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineErbBEpidermal growth factorCell Line TumorDrug DiscoverymedicineHumansEpidermal growth factor receptorPropidium iodideProtein Kinase InhibitorsCell ProliferationEGFR inhibitorsDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryGeneral Medicine0104 chemical sciencesErbB ReceptorsMolecular Docking Simulation010404 medicinal & biomolecular chemistry030220 oncology & carcinogenesisbiology.proteinCancer researchErlotinibDrug Screening Assays Antitumormedicine.drugCurrent Topics in Medicinal Chemistry
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Activation of α-secretase cleavage

2011

Alpha-secretase-mediated cleavage of the amyloid precursor protein (APP) releases the neuroprotective APP fragment sαAPP and prevents amyloid β peptide (Aβ) generation. Moreover, α-secretase-like cleavage of the Aβ transporter 'receptor for advanced glycation end products' counteracts the import of blood Aβ into the brain. Assuming that Aβ is responsible for the development of Alzheimer's disease (AD), activation of α-secretase should be preventive. α-Secretase-mediated APP cleavage can be activated via several G protein-coupled receptors and receptor tyrosine kinases. Protein kinase C, mitogen-activated protein kinases, phosphatidylinositol 3-kinase, cAMP and calcium are activators of rece…

Cellular and Molecular NeuroscienceRetinoic acid receptorbiologyBiochemistryADAM10Amyloid precursor proteinbiology.proteinP3 peptideSignal transductionBiochemistryAmyloid precursor protein secretaseReceptor tyrosine kinaseG protein-coupled receptorJournal of Neurochemistry
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Control of the mutagenicity of aromatic amines by protein kinases and phosphatases

1997

The role of protein kinase C and protein phosphatases was examined in the control of mutagenic metabolites of aromatic amines. Various metabolic activating systems derived from rat liver were treated with: 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C modulator; okadaic acid (OA), a potent inhibitor of serine/threonine protein phosphatases (PP1 and PP2A); and ortho-vanadate (OV), an inhibitor of tyrosine phosphatases. TPA used over a wide concentration range (10−9–10−6 M) did not affect the bacterial mutagenicity of the aromatic amines and of the aromatic amide investigated, 2-aminoanthracene, 2-aminofluorene and 2-acetylaminofluorene (2AAF). At the molecular level, TPA did…

ChemistryHealth Toxicology and MutagenesisPhosphataseProtein phosphatase 1General MedicineProtein phosphatase 2Protein tyrosine phosphataseOkadaic acidToxicologychemistry.chemical_compoundBiochemistryPhosphorylationProtein Phosphatase InhibitorProtein kinase CArchives of Toxicology
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Preclinical and clinical evidence of activity of pazopanib in solitary fibrous tumour

2014

Abstract Background To explore the activity of pazopanib in solitary fibrous tumour (SFT). Patients and methods In a preclinical study, we compared the activity of pazopanib, sorafenib, sunitinib, regorafenib, axitinib and bevacizumab in a dedifferentiated-SFT (DSFT) xenotransplanted into Severe Combined Immunodeficiency (SCID) mice. Antiangiogenics were administered at their reported optimal doses when mean tumour volume (TV) was 80 mm3. Drug activity was assessed as TV inhibition percentage (TVI%). From May 2012, six consecutive patients with advanced SFT received pazopanib, on a national name-based programme. In one case sunitinib was administered after pazopanib failure. Results In the …

Chemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sulfonamides; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2; Cancer Research; Oncology; Medicine (all)OncologyMaleCancer ResearchIndolesAxitinibPyridinesPyridinemedicine.medical_treatmentSolitary fibrous tumourAdministration OralAngiogenesis InhibitorsMice SCIDPharmacologyPyrroleAntineoplastic Agentchemistry.chemical_compoundMiceSolitary Fibrous TumorChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Cancer Research; Oncology; Medicine (all)Transplantation HeterologouMonoclonalSunitinibHumanizedSulfonamidesHeterologousSunitinibMedicine (all)ImidazolesSarcomaMiddle AgedSorafenibPlatelet-Derived Growth Factor betaAxitinibBevacizumabOncologySolitary Fibrous TumorsAdministrationAngiogenesis InhibitorHumanmedicine.drugReceptorPhenylurea CompoundSorafenibOralAdultNiacinamidemedicine.medical_specialtyIndazolesBevacizumabMAP Kinase Signaling SystemTransplantation HeterologousAntineoplastic AgentsSulfonamideAntibodies Monoclonal HumanizedSCIDAntibodiesReceptor Platelet-Derived Growth Factor betaPazopanibInternal medicineRegorafenibmedicineAnimalsHumansChemotherapyPyrrolesImidazoleTyrosine kinaseAgedChemotherapyTransplantationAnimalbusiness.industryPhenylurea CompoundsPazopanibmedicine.diseaseChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Axitinib; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sorafenib; Sulfonamides; Sunitinib; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-2IndazolePyrimidinesPyrimidinechemistryIndolebusinessProgressive diseaseNeoplasm Transplantation
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Receptor Tyrosine Kinase, an Autapomorphic Character of Metazoa: Identification in Marine Sponges

1999

In the present review we summarize sequence data obtained from cloning of sponge receptor tyrosine kinases [RTK]. The cDNA sequences were mainly obtained from the marine sponge Geodia cydonium. RTKs (i) with immunoglobulin [Ig]-like domains in the extracellular region, (ii) of the type of insulinlike receptors, as well as (iii) RTKs with one extracellular speract domain, have been identified. The analyses revealed that the RTK genes are constructed in blocks [domains], suggesting a blockwise evolution. The phylogenetic relationships of the sequences obtained revealed that all sponge sequences fall into one branch of the evolutionary tree, while related sequences from higher Metazoa, human, …

CloningbiologyPhylogenetic treeEcologyPhylumbiology.organism_classificationGeneral Biochemistry Genetics and Molecular BiologyReceptor tyrosine kinaseSpongeMonophylyNeurologyEvolutionary biologyComplementary DNAbiology.proteinGeneGeneral Environmental ScienceActa Biologica Hungarica
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Genome-Wide Association Study of Diabetic Kidney Disease Highlights Biology Involved in Glomerular Basement Membrane Collagen

2019

BACKGROUND: Although diabetic kidney disease demonstrates both familial clustering and single nucleotide polymorphism heritability, the specific genetic factors influencing risk remain largely unknown.METHODS: To identify genetic variants predisposing to diabetic kidney disease, we performed genome-wide association study (GWAS) analyses. Through collaboration with the Diabetes Nephropathy Collaborative Research Initiative, we assembled a large collection of type 1 diabetes cohorts with harmonized diabetic kidney disease phenotypes. We used a spectrum of ten diabetic kidney disease definitions based on albuminuria and renal function.RESULTS: Our GWAS meta-analysis included association result…

Collagen Type IVMale0301 basic medicineEXPRESSIONNEPHROPATHY030232 urology & nephrologyPROTEINGenome-wide association studyRECEPTOR TYROSINE KINASESBiologySUSCEPTIBILITYBioinformaticsurologic and male genital diseasesAutoantigensNephropathyEnd stage renal diseaseCohort StudiesDiabetic nephropathy03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingDiabetes mellitusGlomerular Basement MembranemedicineHumansDiabetic NephropathiesAlport syndromeLetter to the EditorCOMPLICATIONSNITRIC-OXIDEMUTATIONS1184 Genetics developmental biology physiologyGeneral Medicinemedicine.diseaseGENE3. Good healthDiabetes Mellitus Type 1030104 developmental biologyNephrology3121 General medicine internal medicine and other clinical medicineMutationAlbuminuria/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemale3111 Biomedicinemedicine.symptomCOLLECTIN 11 CL-11Genome-Wide Association StudyKidney disease
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Interaction of Mitogen-activated Protein Kinases with the Kinase Interaction Motif of the Tyrosine Phosphatase PTP-SL Provides Substrate Specificity …

1999

ERK1 and ERK2 associate with the tyrosine phosphatase PTP-SL through a kinase interaction motif (KIM) located in the juxtamembrane region of PTP-SL. A glutathione S-transferase (GST)-PTP-SL fusion protein containing the KIM associated with ERK1 and ERK2 as well as with p38/HOG, but not with the related JNK1 kinase or with protein kinase A or C. Accordingly, ERK2 showed in vitro substrate specificity to phosphorylate GST-PTP-SL in comparison with GST-c-Jun. Furthermore, tyrosine dephosphorylation of ERK2 by the PTP-SLDeltaKIM mutant was impaired. The in vitro association of ERK1/2 with GST-PTP-SL was highly stable; however, low concentrations of nucleotides partially dissociated the ERK1/2.P…

Cytoplasmanimal structuresProtein Kinase C-alphaRecombinant Fusion ProteinsCèl·lulesNerve Tissue ProteinsProtein tyrosine phosphataseMitogen-activated protein kinase kinaseTransfectionenvironment and public healthBiochemistrySH3 domainReceptor tyrosine kinaseMAP2K7Substrate SpecificitySerineAnimalsc-RafAmino Acid SequenceMolecular BiologyProtein Kinase CSequence DeletionMitogen-Activated Protein Kinase 1Binding SitesMitogen-Activated Protein Kinase 3biologyCyclin-dependent kinase 2Intracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyCyclic AMP-Dependent Protein KinasesIsoenzymesenzymes and coenzymes (carbohydrates)KineticsBiochemistryAmino Acid SubstitutionCOS CellsCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMutagenesis Site-DirectedCyclin-dependent kinase 9CattleMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesProteïnes
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A novel regulatory mechanism of MAP kinases activation and nuclear translocation mediated by PKA and the PTP-SL tyrosine phosphatase

1999

Protein tyrosine phosphatase PTP-SL retains mitogen-activated protein (MAP) kinases in the cytoplasm in an inactive form by association through a kinase interaction motif (KIM) and tyrosine dephosphorylation. The related tyrosine phosphatases PTP-SL and STEP were phosphorylated by the cAMP-dependent protein kinase A (PKA). The PKA phosphorylation site on PTP-SL was identified as the Ser231 residue, located within the KIM. Upon phosphorylation of Ser231, PTP-SL binding and tyrosine dephosphorylation of the MAP kinases extracellular signal–regulated kinase (ERK)1/2 and p38α were impaired. Furthermore, treatment of COS-7 cells with PKA activators, or overexpression of the Cα catalytic subunit …

Cytoplasmanimal structuresRecombinant Fusion ProteinsCèl·lulesAmino Acid MotifsNerve Tissue ProteinsProtein tyrosine phosphataseSH2 domainTransfectionenvironment and public healthModels Biologicalp38 Mitogen-Activated Protein KinasesReceptor tyrosine kinaseSH3 domainCell LinePhosphoserinetyrosine phosphatasesAnimalsHumansProtein phosphorylationPKAReceptor-Like Protein Tyrosine Phosphatases Class 7PhosphorylationPTP-SLCell NucleusMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyBrief ReportIntracellular Signaling Peptides and ProteinsBiological TransportCell BiologyProtein Tyrosine Phosphatases Non-ReceptorCyclic AMP-Dependent Protein KinasesEnzyme Activationenzymes and coenzymes (carbohydrates)MAP kinasesBiochemistryMitogen-activated protein kinaseCOS CellsMutationbiology.proteinPhosphorylationMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesEnzimssignal transductionProto-oncogene tyrosine-protein kinase Src
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