Search results for "Rosin"

showing 10 items of 831 documents

A narrative review of MET inhibitors in non-small cell lung cancer with MET exon 14 skipping mutations

2021

Treatment of advanced non-small cell lung cancer (NSCLC) has radically improved in the last years due to development and clinical approval of highly effective agents including immune checkpoint inhibitors (ICIs) and oncogene-directed therapies. Molecular profiling of lung cancer samples for activated oncogenes, including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and BRAF, is routinely performed to select the most appropriate up-front treatment. However, the identification of new therapeutic targets remains a high priority. Recently, MET exon 14 skipping mutations have emerged as novel actionable oncogenic alterations in NSCLC, sensiti…

0301 basic medicineOncologymedicine.medical_specialtybiologybusiness.industryCancernon-small cell lung cancer (NSCLC)medicine.disease03 medical and health sciencesExon030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisInternal medicineROS1biology.proteinMET; MET exon 14 skipping mutations; MET-tyrosine kinase inhibitors (TKIs); Non-small cell lung cancer (NSCLC)MedicineAnaplastic lymphoma kinaseEpidermal growth factor receptorbusinessLung cancerTyrosine kinase
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Target Identification of Active Constituents of Shen Qi Wan to Treat Kidney Yang Deficiency Using Computational Target Fishing and Network Pharmacolo…

2019

Background: Kidney yang deficiency syndrome (KYDS) is one of the most common syndromes treated with traditional Chinese medicine (TCM) among elderly patients. Shen Qi Wan (SQW) has been effectively used in treating various diseases associated with KYDS for hundreds of years. However, due to the complex composition of SQW, the mechanism of action remains unknown. Purpose: To identify the mechanism of the SQW in the treatment of KYDS and determine the molecular targets of SQW. Methods: The potential targets of active ingredients in SQW were predicted using PharmMapper. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out using the …

0301 basic medicinePharmacology03 medical and health scienceschemistry.chemical_compoundtraditional Chinese medicinetranscriptomics0302 clinical medicinemedicinenetwork pharmacologyPharmacology (medical)HRASKEGGBlood urea nitrogenMAPK14Original ResearchPharmacologyCreatinineKidneylcsh:RM1-950phytotherapy030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. PharmacologychemistryMechanism of action030220 oncology & carcinogenesisgene ontologypotential targetsmedicine.symptomProto-oncogene tyrosine-protein kinase SrcFrontiers in Pharmacology
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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Assessing the biological activity of the glucan phosphatase laforin

2016

Glucan phosphatases are a recently discovered family of enzymes that dephosphorylate either starch or glycogen and are essential for proper starch metabolism in plants and glycogen metabolism in humans. Mutations in the gene encoding the only human glucan phosphatase, laforin, result in the fatal, neurodegenerative, epilepsy known as Lafora disease. Here, we describe phosphatase assays to assess both generic laforin phosphatase activity and laforin's unique glycogen phosphatase activity.

0301 basic medicinePhosphataseLafora diseaseArticleSubstrate SpecificityNitrophenols03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsDual-specificity phosphatasemedicineHumansGlucanEnzyme Assayschemistry.chemical_classificationGlycogenbiologyfood and beveragesBiological activitymedicine.diseaseFluoresceinsProtein Tyrosine Phosphatases Non-Receptor030104 developmental biologyEnzymechemistryBiochemistryLafora Diseasebiology.proteinLaforin030217 neurology & neurosurgeryGlycogen
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Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Compar…

2020

Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantifi…

0301 basic medicinePhysiologyClinical BiochemistryDot blotmitochondrial superoxidePronase030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryHigh-performance liquid chromatographyArticleperoxynitritePeroxynitrite03 medical and health sciences0302 clinical medicineProtein-bound 3-nitrotyrosinemedicineoxidative stressBovine serum albuminMolecular Biologychemistry.chemical_classificationDetection limitReactive oxygen speciesChromatographyHPLC with electrochemical detectionbiologylcsh:RM1-950Cell Biology3. Good health030104 developmental biologylcsh:Therapeutics. PharmacologychemistryOxidative stressbiology.proteinprotein-bound 3-nitrotyrosineOxidative stressEx vivoMitochondrial superoxide
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Prognostic use of soluble fms-like tyrosine kinase-1 and placental growth factor in patients with coronary artery disease.

2015

Background: Intention of the study is to assess the cardiovascular mortality of patients with coronary artery disease (CAD) with the biomarkers of angiogenesis PlGF and its endogenous inhibitor sFlt-1. Methods: The cohort included n = 1848 patients with CAD and 282 subjects without CAD. In 85 patients cardiovascular mortality, as combination of fatal myocardial infarction or any cardiac death, during a median follow-up duration of 3.9 years was reported. Results: In Kaplan–Meier curve analysis PlGF in rising thirds was not predictive regarding outcome (p = 0.54), the same was shown for sFlt-1 (p = 0.44). Cox regression for the fully adjusted model provided a hazard ratio (HR) of 0.8 (p = 0…

0301 basic medicinePlacental growth factorMalemedicine.medical_specialtyClinical BiochemistryCoronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyPregnancy ProteinsCoronary artery disease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDrug DiscoveryNatriuretic Peptide BrainmedicineHumansMyocardial infarctionPlacenta Growth FactorVascular Endothelial Growth Factor Receptor-1Proportional hazards modelbusiness.industryBiochemistry (medical)Hazard ratioMiddle Agedmedicine.diseasePrognosisPeptide FragmentsVascular endothelial growth factor030104 developmental biologyEndocrinologychemistryCohortCardiologyFemalebusinessSoluble fms-like tyrosine kinase-1Follow-Up StudiesBiomarkers in medicine
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Fungicide resistance towards fludioxonil conferred by overexpression of the phosphatase gene Mo PTP 2 in Magnaporthe oryzae

2018

The fungicide fludioxonil causes hyperactivation of the Hog1p MAPK within the high-osmolarity glycerol signaling pathway essential for osmoregulation in pathogenic fungi. The molecular regulation of MoHog1p phosphorylation is not completely understood in pathogenic fungi. Thus, we identified and characterized the putative MoHog1p-interacting phosphatase gene MoPTP2 in the filamentous rice pathogen Magnaporthe oryzae. We found overexpression of MoPTP2 conferred fludioxonil resistance in M. oryzae, whereas the 'loss of function' mutant ΔMoptp2 was more susceptible toward the fungicide. Additionally, quantitative phosphoproteome profiling of MoHog1p phosphorylation revealed lower phosphorylati…

0301 basic medicineProteomeMutantPhosphataseGene ExpressionDioxolesBiologyFludioxonilMicrobiologyMicrobiologyFungal Proteins03 medical and health sciencesDrug Resistance FungalGene expressionPyrrolesPhosphorylationMolecular BiologyGenePlant DiseasesOryzaPhosphoproteinsFungicides IndustrialFungicideMagnaporthe030104 developmental biologyPhosphorylationMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesSignal transductionProtein Processing Post-TranslationalGene DeletionMolecular Microbiology
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SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of m…

2018

Background Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, resulting from the t(9;22) chromosomal translocation. Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML. However, even though almost all CML patients respond to treatment with imatinib or third generation inhibitors, these drugs are not curative and need to be taken indefinitely or until patients become resistant. Therefore, to get a definitive eradication of leukemic cells, it is necessary to find novel therapeutic combinations, for achieving greater efficacy and fewer side effec…

0301 basic medicineProteomicsCancer ResearchCurcuminCML cellsCellReceptors Cytoplasmic and NuclearKaryopherinsTransfectionlcsh:RC254-282Mass SpectrometrymiR-22/IPO7/HIF-1α axis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemiR-22/IPO7/HIF-1α axiSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansCML cells; Curcumin; miR-22/IPO7/HIF-1α axis; SWATH-MS; Oncology; Cancer ResearchOncogeneChemistryResearchCML cellImatinibTransfectionmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchCurcuminSWATH-MSK562 CellsTyrosine kinaseK562 cellsChronic myelogenous leukemiamedicine.drug
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TCR signalling network organization at the immunological synapses of murine regulatory T cells.

2017

Regulatory T (Treg) cells require T-cell receptor (TCR) signalling to exert their immunosuppressive activity, but the precise organization of the TCR signalling network compared to conventional T (Tconv) cells remains elusive. By using accurate mass spectrometry and multi-epitope ligand cartography (MELC) we characterized TCR signalling and recruitment of TCR signalling components to the immunological synapse (IS) in Treg cells and Tconv cells. With the exception of Themis which we detected in lower amounts in Treg cells, other major TCR signalling components were found equally abundant, however, their phosphorylation-status notably discriminates Treg cells from Tconv cells. Overall, this s…

0301 basic medicineProteomicsImmunological SynapsesProteomeCD3ImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryArticleImmunological synapse03 medical and health sciencesT-Lymphocyte SubsetsImmunology and AllergyAnimalsPhosphorylationReceptorCells CulturedCD86Mice Inbred BALB CZAP-70 Protein-Tyrosine KinaseZAP70T-cell receptorCD28hemic and immune systemsImmunological SynapsesCell biology030104 developmental biologyMicroscopy Fluorescencebiology.proteinFemaleSignal TransductionEuropean journal of immunology
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Potential treatment strategy for the rare osimertinib resistant mutation EGFR L718Q

2020

Epidermal growth factor receptor (EGFR) L718Q is a rare resistant mutation which independently leads to third-generation tyrosine kinase inhibitor (TKI) resistance. Although a few studies have examined its resistance mechanisms, no effective treatment strategy has yet been proposed for patients with this mutation. Here, we report an effective treatment strategy for the rare EGFR L718Q mutation for the first time. A 44-year-old Chinese male patient initially presented with the sensitizing EGFR L858R mutation, and the progression-free survival (PFS) time after initial icotinib treatment was 9 months. When the progression of the disease (PD) and the EGFR T790M mutation were identified, he did …

0301 basic medicinePulmonary and Respiratory MedicineOncologyiMDT Cornermedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentnon-small cell lung cancer (NSCLC)Tyrosine-kinase inhibitorTargeted therapy03 medical and health sciencesT790M0302 clinical medicineInternal medicinemedicineOsimertinibEpidermal growth factor receptorbiologybusiness.industrymedicine.disease030104 developmental biology030220 oncology & carcinogenesisMutation (genetic algorithm)Icotinibbiology.proteinbusiness
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