Search results for " tyrosine"

showing 10 items of 256 documents

Cardiotoxic Effects of Anti-VEGFR Tyrosine Kinase Inhibitors

2016

Angiogenesis is a key moment in tumor development and proliferation. Until recently oncologists did not know the mechanisms that were behind this phenomenon, but following the discoveries of Folkman and coworkers, they have gradually created and developed a series of drugs that act against angiogenesis by interacting with molecules belonging to the vascular endothelial growth factor (VEGFs) class and its receptors (VEGFRs) giving rise to anticancer effects. Tyrosine kinase inhibitors (TKIs) are a major class of these new anticancer agents, demonstrating high antitumor activity in a variety of "orphan" neoplasms (such as hepatocellular carcinoma, kidney cancer, sarcomas, etc.). The mechanism…

0301 basic medicineAngiogenesis; Cardio-oncology; Cardiotoxicity; Tyrosine kinase inhibitors; VEGF; VEGF pathway; Medicine (all)Settore MED/06 - Oncologia MedicaAngiogenesisTyrosine kinase inhibitorPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineVEGF pathwaymedicineReceptorCardiotoxicitybusiness.industryMedicine (all)medicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorAngiogenesiCardio-oncology030104 developmental biologyMechanism of actionchemistry030220 oncology & carcinogenesisHepatocellular carcinomamedicine.symptombusinessKidney cancerTyrosine kinase
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Green Tea Catechins Induce Inhibition of PTP1B Phosphatase in Breast Cancer Cells with Potent Anti-Cancer Properties: In Vitro Assay, Molecular Docki…

2020

The catechins derived from green tea possess antioxidant activity and may have a potentially anticancer effect. PTP1B is tyrosine phosphatase that is oxidative stress regulated and is involved with prooncogenic pathways leading to the formation of a.o. breast cancer. Here, we present the effect of selected green tea catechins on enzymatic activity of PTP1B phosphatase and viability of MCF-7 breast cancer cells. We showed also the computational analysis of the most effective catechin binding with a PTP1B molecule. We observed that epigallocatechin, epigallocatechin gallate, epicatechin, and epicatechin gallate may decrease enzymatic activity of PTP1B phosphatase and viability of MCF-7 cells.…

0301 basic medicineAntioxidantPhysiologymedicine.medical_treatmentClinical BiochemistryPhosphataseProtein tyrosine phosphataseEpigallocatechin gallateBiochemistrycomplex mixturesArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicinebreast cancermedicineheterocyclic compoundsViability assayMolecular Biologyepigallocatechinprotein tyrosine phosphatase inhibitorChemistrylcsh:RM1-950food and beveragesPTP1BCell BiologyCatechin bindingIn vitro030104 developmental biologyEpicatechin gallatelcsh:Therapeutics. PharmacologyBiochemistrySettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesissense organshormones hormone substitutes and hormone antagonistsgreen tea catechinsAntioxidants
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Endocytosis of the glutamate transporter 1 is regulated by laforin and malin: Implications in Lafora disease.

2020

Postprint 36 páginas, 7 figuras

0301 basic medicineArrestinsAmino Acid Transport System X-AGPhosphataseProgressive myoclonus epilepsyBiologyEndocytosisLafora diseaseArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineUbiquitinmedicineAnimalsNedd4.2Lafora diseaseGlutamate receptorUbiquitinationTransportermedicine.diseaseProtein Tyrosine Phosphatases Non-ReceptorEndocytosisCell biologyGLT-1030104 developmental biologyNeurologyLafora Diseasebiology.proteinGlutamateLaforin030217 neurology & neurosurgeryGlia
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The cytoprotective protein MANF promotes neuronal survival independently from its role as a GRP78 cofactor

2021

Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER)-stress-regulated protein exhibiting cytoprotective properties through a poorly understood mechanism in various in vitro and in vivo models of neuronal and non-neuronal damage. Although initially characterized as a secreted neurotrophic factor for midbrain dopamine neurons, MANF has recently gained more interest for its intracellular role in regulating the ER homeostasis, including serving as a cofactor of the chaperone glucose-regulated protein 78 (GRP78). We aimed for a better understanding of the neuroprotective mechanisms of MANF. Here we show for the first time that MANF promotes the survival of …

0301 basic medicineBiFC bimolecular fluorescence complementationMST microscale thermophoresisPDIA1 protein disulfide isomerase family A member 1ApoptosisNEUROTROPHIC FACTOR MANFEndoplasmic ReticulumBiochemistryprotein-protein interactionMiceBimolecular fluorescence complementationUPR unfolded protein responseENDOPLASMIC-RETICULUM STRESSMesencephalonNeurotrophic factorsInsulin-Secreting CellsProtein Interaction MappingBINDINGCOMPREHENSIVE RESOURCEATF6unfolded protein response (UPR)PDIA6 protein disulfide isomerase family A member 6PPIs protein-protein interactionsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsNPTN neuroplastinbiologyChemistryapoptosisunfolded protein responsedopamine neurons3. Good healthCell biologyGDNF glial cell line–derived neurotrophic factorIRE1-ALPHASBD substrate-binding domainendoplasmic reticulum stressMANF mesencephalic astrocyte-derived neurotrophic factorTm tunicamycinneuroprotectionResearch ArticleProtein BindingSignal TransductionGRP78Protein Disulfide-Isomerase FamilyCell SurvivalTH tyrosine hydroxylasePrimary Cell CultureSCG superior cervical ganglionProtein Disulfide-IsomerasesIRE1 inositol-requiring enzyme 1ER-STRESSER endoplasmic reticulum03 medical and health sciencesohjelmoitunut solukuolemaC-MANF C-terminal domain of MANFCSPs chemical shift perturbationsAnimalsHumansHSP70 Heat-Shock ProteinsNerve Growth FactorsNBD nucleotide-binding domainNMR nuclear magnetic resonanceMolecular Biology030102 biochemistry & molecular biologyBIPATF6Dopaminergic NeuronsGene Expression ProfilingBinding proteinneuronal cell deathDISSOCIATIONCell BiologyNEI nucleotide exchange inhibitorEmbryo MammalianadenosiinitrifosfaattiATPhermosolutmesencephalic astrocyte-derived neurotrophic factorprotein–protein interactionPERK protein kinase RNA-like ER kinaseHEK293 Cells030104 developmental biologyGene Expression RegulationChaperone (protein)Tg thapsigarginbiology.proteinUnfolded protein responseAP-MS affinity purification mass spectrometry1182 Biochemistry cell and molecular biologyGFP-SH SH-tagged GFPendoplasmic reticulum stress (ER stress)DA dopaminemesencephalic astrocyte-derived neurotrophic factor (MANF)proteiinitNeuroplastin
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The receptor protein tyrosine phosphatase PTPRJ negatively modulates the CD98hc oncoprotein in lung cancer cells.

2018

PTPRJ, a receptor protein tyrosine phosphatase strongly downregulated in human cancer, displays tumor suppressor activity by negatively modulating several proteins involved in proliferating signals. Here, through a proteomic-based approach, we identified a list of potential PTPRJ-interacting proteins and among them we focused on CD98hc, a type II glycosylated integral membrane protein encoded by SLC3A2, corresponding to the heavy chain of a heterodimeric transmembrane amino-acid transporter, including LAT1. CD98hc is widely overexpressed in several types of cancers and contributes to the process of tumorigenesis by interfering with cell proliferation, adhesion, and migration. We first valid…

0301 basic medicineCD98hcChemistryCell growthCellPTPRJProtein tyrosine phosphatasemedicine.disease_causeProtein tyrosine phosphatase03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureProteasomal degradationOncologyMG132Cancer cellCancer researchmedicineProteasome inhibitorGene silencingLung cancerCarcinogenesismedicine.drugResearch Paper
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Frequency and prognostic impact of ALK amplifications and mutations in the European Neuroblastoma Study Group (SIOPEN) high-risk neuroblastoma trial …

2021

Purpose: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Materials and methods: Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Results: Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with …

0301 basic medicineCancer ResearchPrognostic ImpactAnaplastic Lymphoma Kinase/genetics; Child Preschool; Clinical Trials Phase III as Topic; Europe; Female; Follow-Up Studies; Gene Amplification; Humans; Infant; Male; Mutation Rate; N-Myc Proto-Oncogene Protein/genetics; Neuroblastoma/genetics; Prognosis; Randomized Controlled Trials as Topic; Risk Factors; Survival RateEuropean Neuroblastoma Study GroupSIOPENRELAPSE03 medical and health sciencesNeuroblastoma0302 clinical medicineText miningNeuroblastomahemic and lymphatic diseasesREVEALSMedicine and Health SciencesKINASEMedicineHigh risk neuroblastomaHETEROGENEITYCRIZOTINIBSEGMENTAL CHROMOSOMAL ALTERATIONSACTIVATING MUTATIONSPEDIATRIC-PATIENTSbusiness.industryALK receptor tyrosine kinasePoint mutationREARRANGEMENTSCHEMOTHERAPYmedicine.diseaseDoenças Genéticas030104 developmental biologyALKOncology030220 oncology & carcinogenesisCancer researchbusiness
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Molecular Engineering Strategies Tailoring the Apoptotic Response to a MET Therapeutic Antibody

2020

The MET oncogene encodes a tyrosine kinase receptor involved in the control of a complex network of biological responses that include protection from apoptosis and stimulation of cell growth during embryogenesis, tissue regeneration, and cancer progression. We previously developed an antagonist antibody (DN30) inducing the physical removal of the receptor from the cell surface and resulting in suppression of the biological responses to MET. In its bivalent form, the antibody displayed a residual agonist activity, due to dimerization of the lingering receptors, and partial activation of the downstream signaling cascade. The balance between the two opposing activities is variable in different…

0301 basic medicineCancer ResearchProgrammed cell deathlcsh:RC254-282ArticleReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineMET oncogenemedicineantibodiesAntibodies; Apoptosis; MET oncogene; MET targeted therapyReceptorbiologyCell growthChemistryapoptosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmet targeted therapyCell biology030104 developmental biologyOncology<i>met</i> oncogeneApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinHepatocyte growth factorAntibodymedicine.drugCancers
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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PTP1B phosphatase as a novel target of oleuropein activity in MCF-7 breast cancer model.

2019

Phosphatase PTP1B has become a therapeutic target for the treatment of type 2-diabetes, whereas recent studies have revealed that PTP1B plays a pivotal role in pathophysiology and development of breast cancer. Oleuropein is a natural, phenolic compound with anticancer activity. The aim of this study was to address the question whether PTP1B constitutes a target for oleuropein in breast cancer MCF-7 cells. The cellular MCF-7 breast cancer model was used in the study. The experiments were performed using cellular viability tests, Elisa assays, immunoprecipitation, flow cytometry analyses and computer modelling. Herein, we evidenced that the reduced activity of phosphatase PTP1B after treatmen…

0301 basic medicineCell cycle checkpointImmunoprecipitationCell Survivalmedicine.medical_treatmentPhosphataseIridoid GlucosidesAntineoplastic AgentsBreast NeoplasmsAdenocarcinomaMolecular Dynamics SimulationToxicologyFlow cytometry03 medical and health scienceschemistry.chemical_compoundbreast cancer0302 clinical medicineBreast cancerOleuropeinmedicineHumansPTP1B phosphataseIridoidsskin and connective tissue diseasesSettore CHIM/02 - Chimica FisicaCell ProliferationOleuropeinProtein Tyrosine Phosphatase Non-Receptor Type 1MCF-7 cellmedicine.diagnostic_testAnticancer therapyGeneral Medicinemedicine.disease030104 developmental biologychemistryMCF-7Settore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSettore BIO/14 - FarmacologiaCancer researchMCF-7 CellsAdjuvanthormones hormone substitutes and hormone antagonistsToxicology in vitro : an international journal published in association with BIBRA
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