Search results for "Transduction"

showing 10 items of 2149 documents

Insights into apoptotic proteins in chemotherapy: quantification techniques and informing therapy choice.

2018

Cancer is one of the leading causes of morbidity and mortality worldwide. A hallmark of cancer is evasion of apoptosis leading to tumor progression and drug resistance. Biomarker research has become a sign of the times, and proteins involved in apoptosis may be used for clinical diagnostic or prognostic purposes in cancer treatment. The recent progress in proteomic technology has triggered an emerging number of researchers to study the molecular mechanisms that regulate the apoptotic signal transduction pathways in cancer. Areas covered: A PubMed search for 'Proteomics' and 'cancer' and 'chemotherapy' and 'apoptosis' has been conducted for literature until December 2017.The study of apoptot…

0301 basic medicineProteomicsmedicine.medical_treatmentAntineoplastic AgentsApoptosisDrug resistanceProteomicsBioinformaticsBiochemistry03 medical and health sciencesMedicineAnimalsHumansPrecision MedicineMolecular BiologyChemotherapybusiness.industryCancerProteinsPrecision medicinemedicine.diseaseBiomarker (cell)030104 developmental biologyTumor progressionDrug Resistance NeoplasmSignal transductionbusinessExpert review of proteomics
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JAK2 mediates lung fibrosis, pulmonary vascular remodelling and hypertension in idiopathic pulmonary fibrosis: an experimental study

2018

BackgroundPulmonary hypertension (PH) is a common disorder in patients with idiopathic pulmonary fibrosis (IPF) and portends a poor prognosis. Recent studies using vasodilators approved for PH have failed in improving IPF mainly due to ventilation (V)/perfusion (Q) mismatching and oxygen desaturation. Janus kinase type 2 (JAK2) is a non-receptor tyrosine kinase activated by a broad spectrum of profibrotic and vasoactive mediators, but its role in PH associated to PH is unknown.ObjectiveThe study of JAK2 as potential target to treat PH in IPF.Methods and resultsJAK2 expression was increased in pulmonary arteries (PAs) from IPF (n=10; 1.93-fold; P=0.0011) and IPF+PH (n=9; 2.65-fold; P<0.00…

0301 basic medicinePulmonary and Respiratory Medicinemedicine.medical_specialtyHypertension PulmonaryBlotting WesternMyocytes Smooth MuscleFluorescent Antibody TechniqueVasodilationVascular RemodelingReal-Time Polymerase Chain ReactionVascular remodelling in the embryo03 medical and health sciencesIdiopathic pulmonary fibrosisTransforming Growth Factor betaRight ventricular hypertrophyInternal medicinepulmonary hypertensionAnimalsHumansMedicineRNA Small InterferingRats WistarCells CulturedCell ProliferationBKCaJanus kinase 2biologybusiness.industryEndothelial CellsJanus Kinase 2idiopathic pulmonary fibrosismedicine.diseaseImmunohistochemistryPulmonary hypertensionIdiopathic Pulmonary FibrosisTriterpenesRatsPhenotype030104 developmental biologyJAK2biology.proteinCardiologyAnimal studiesJanus kinasebusinessSignal TransductionPulmonary artery smooth muscle cells Pulmonary artery endothelial cells.Thorax
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Mechanical ventilation alters the development of staphylococcus aureus pneumonia in rabbit

2016

Ventilator-associated pneumonia (VAP) is common during mechanical ventilation (MV). Beside obvious deleterious effects on muco-ciliary clearance, MV could adversely shift the host immune response towards a pro-inflammatory pattern through toll-like receptor (TLRs) up-regulation. We tested this hypothesis in a rabbit model of Staphylococcus aureus VAP. Pneumonia was caused by airway challenge with S. aureus, in either spontaneously breathing (SB) or MV rabbits (n = 13 and 17, respectively). Pneumonia assessment regarding pulmonary and systemic bacterial burden, as well as inflammatory response was done 8 and 24 hours after S. aureus challenge. In addition, ex vivo stimulations of whole blood…

0301 basic medicinePulmonologyPhysiologyStaphylococcusmedicine.medical_treatment[SDV]Life Sciences [q-bio]lcsh:MedicinePharmacologyPathology and Laboratory Medicinemedicine.disease_causeStaphylococcal/immunology/pathologyImmune ReceptorsBiochemistry0302 clinical medicineImmune PhysiologyPneumonia StaphylococcalMedicine and Health SciencesMedicineStaphylococcus Aureuslcsh:ScienceImmune ResponseToll-like ReceptorsMammalsddc:616Innate Immune SystemImmune System ProteinsMultidisciplinaryddc:617RespirationPneumonia Ventilator-AssociatedInterleukinAnimal ModelsHematologyBacterial PathogensBody Fluids3. Good healthBloodmedicine.anatomical_structureMedical MicrobiologyStaphylococcus aureusVertebratesArtificialCytokinesRabbitsPathogensAnatomymedicine.symptomStaphylococcus aureus/immunologyResearch ArticleSignal TransductionToll-Like Receptor 2/immunologyImmunologyInflammationLung injuryResearch and Analysis MethodsMicrobiology03 medical and health sciencesModel OrganismsSigns and SymptomsDiagnostic MedicineAnimalsMicrobial PathogensInflammationMechanical ventilationInterleukin-8/immunologyLung[ SDV ] Life Sciences [q-bio]BacteriaTumor Necrosis Factor-alphabusiness.industrylcsh:RInterleukin-8OrganismsBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyPneumoniaMolecular Developmentmedicine.diseaseTumor Necrosis Factor-alpha/immunologyRespiration ArtificialToll-Like Receptor 2Pneumonia030104 developmental biologyVentilator-Associated/immunology/microbiology/pathologyImmune SystemAmniotesImmunologylcsh:QbusinessSpleenEx vivoDevelopmental Biology
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Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells

2020

Tumor-associated macrophages facilitate tumor progression and resistance to therapy. Their capacity for metabolic and inflammatory reprogramming represents an attractive therapeutic target. ONC201/TIC10 is an anticancer molecule that antagonizes the dopamine receptor D2 and affects mitochondria integrity in tumor cells. We examined whether ONC201 induces a metabolic and pro-inflammatory switch in primary human monocyte-derived macrophages that reactivates their antitumor activities, thus enhancing the onco-toxicity of ONC201. Contrary to glioblastoma cells, macrophages exhibited a low ratio of dopamine receptors D2/D5 gene expression and were resistant to ONC201 cytotoxicity. Macrophages re…

0301 basic medicinePyridinesImmunology610 MedizinGlutamic AcidAntineoplastic AgentsMitochondrionBiology570 Life sciences03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorDopamine receptor D2610 Medical sciencesTumor MicroenvironmentHumansImmunology and AllergyMacrophageReceptors Dopamine D5Tumor microenvironmentReceptors Dopamine D2MacrophagesImidazolesMitochondriaCell biologyGene Expression Regulation NeoplasticPyrimidines030104 developmental biologyDrug Resistance NeoplasmTumor progressionDopamine receptorEnergy MetabolismGlioblastomaReprogrammingTranscription Factor CHOPSignal Transduction030215 immunology570 Biowissenschaften
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Noncoding RNAs in Critical Limb Ischemia

2020

Peripheral artery disease, caused by chronic arterial occlusion of the lower extremities, affects over 200 million people worldwide. Peripheral artery disease can progress into critical limb ischemia (CLI), its more severe manifestation, which is associated with higher risk of limb amputation and cardiovascular death. Aiming to improve tissue perfusion, therapeutic angiogenesis held promise to improve ischemic limbs using delivery of growth factors but has not successfully translated into benefits for patients. Moreover, accumulating studies suggest that impaired downstream signaling of these growth factors (or angiogenic resistance) may significantly contribute to CLI, particularly under h…

0301 basic medicineRNA UntranslatedAngiogenesisCritical IllnessNeovascularization PhysiologicDisease030204 cardiovascular system & hematologyBioinformaticsArticlePeripheral Arterial Disease03 medical and health sciences0302 clinical medicineIschemiaRisk FactorsmicroRNADiabetes MellitusAnimalsHumansMedicineTherapeutic angiogenesisProgenitor cellHypoxiaInflammationbusiness.industryStem CellsHemodynamicsCritical limb ischemiaHypoxia (medical)Prognosisbody regions030104 developmental biologyGene Expression RegulationRegional Blood FlowArteriogenesismedicine.symptomCardiology and Cardiovascular MedicinebusinessSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Hypoxia‐induced non‐coding rnas controlling cell viability in cancer

2021

Hypoxia, a characteristic of the tumour microenvironment, plays a crucial role in cancer progression and therapeutic response. The hypoxia-inducible factors (HIF-1α, HIF-2α, and HIF-3α), are the master regulators in response to low oxygen partial pressure, modulating hypoxic gene expression and signalling transduction pathways. HIFs’ activation is sufficient to change the cell phenotype at multiple levels, by modulating several biological activities from metabolism to the cell cycle and providing the cell with new characteristics that make it more aggressive. In the past few decades, growing numbers of studies have revealed the importance of non-coding RNAs (ncRNAs) as molecular mediators i…

0301 basic medicineRNA UntranslatedCellProliferationReviewlcsh:ChemistryTransduction (genetics)0302 clinical medicineNeoplasmsGene expressionBasic Helix-Loop-Helix Transcription FactorsTumor MicroenvironmentRNA NeoplasmHypoxialcsh:QH301-705.5SpectroscopyCancerGeneral MedicineCell cycleCell HypoxiaComputer Science ApplicationsCell biologyNeoplasm Proteinsmedicine.anatomical_structure030220 oncology & carcinogenesismiRNAscell cyclemedicine.symptomMiRNASignal TransductionCell SurvivallncRNAsBiologyCatalysisInorganic Chemistry03 medical and health sciencesmicroRNAmedicineHumansHIFViability assayPhysical and Theoretical ChemistryMolecular BiologyOrganic ChemistryCancerHypoxia (medical)medicine.diseaseLncRNA030104 developmental biologylcsh:Biology (General)lcsh:QD1-999
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The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development

2018

Cofilin is an essential actin remodeling protein promoting depolymerization and severing of actin filaments. To address the relevance of cofilin for the development and function of T cells in vivo, we generated knock-in mice in which T-cell–specific nonfunctional (nf) cofilin was expressed instead of wild-type (WT) cofilin. Nf cofilin mice lacked peripheral αβ T cells and showed a severe thymus atrophy. This was caused by an early developmental arrest of thymocytes at the double negative (DN) stage. Importantly, even though DN thymocytes expressed the TCRβ chain intracellularly, they completely lacked TCRβ surface expression. In contrast, nf cofilin mice possessed normal numbers of γδ T cel…

0301 basic medicineReceptors Antigen T-Cell alpha-betaT-LymphocytesJurkat cellsenvironment and public healthImmune ReceptorsBiochemistryWhite Blood CellsJurkat CellsMice0302 clinical medicineContractile ProteinsSpectrum Analysis TechniquesShort ReportsAnimal CellsCell MovementT-Lymphocyte SubsetsMedicine and Health SciencesGene Knock-In TechniquesBiology (General)Post-Translational ModificationPhosphorylationThymocytesImmune System ProteinsT CellsGeneral NeuroscienceStem CellsReceptors Antigen T-Cell gamma-deltaTransfectionAnimal ModelsCofilinFlow CytometryCell biologyThymusmedicine.anatomical_structureExperimental Organism SystemsActin Depolymerizing FactorsSpectrophotometry030220 oncology & carcinogenesisPhosphorylationCytophotometryCellular TypesGeneral Agricultural and Biological SciencesSignal TransductionHematopoietic Progenitor CellsProlineQH301-705.5T cellImmune CellsImmunologyDouble negativeMouse Modelsmacromolecular substancesThymus GlandBiologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesModel OrganismsmedicineAnimalsHumansActinBlood CellsGeneral Immunology and MicrobiologyActin remodelingBiology and Life SciencesProteinsCell BiologyActinsT Cell ReceptorsCytoskeletal Proteins030104 developmental biologyImmune SystemMutationPLoS Biology
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CXCL10 and CCL21 Promote Migration of Pancreatic Cancer Cells Toward Sensory Neurons and Neural Remodeling in Tumors in Mice, Associated With Pain in…

2018

Background & Aims Pancreatic ductal adenocarcinoma (PDAC) is frequently accompanied by excruciating pain, which has been associated with attraction of cancer cells and their invasion of intrapancreatic sensory nerves. Neutralization of the chemokine CCL2 reduced cancer-associated pain in a clinical trial, but there have been no systematic analyses of the highly diverse chemokine families and their receptors in PDAC. Methods We performed an open, unbiased RNA-interference screen of mammalian chemokines in co-cultures of mouse PDAC cells (K8484) and mouse peripheral sensory neurons, and confirmed findings in studies of DT8082 PDAC cells. We studied the effects of chemokines on migration of PD…

0301 basic medicineReceptors CCR7ChemokineReceptors CXCR3Sensory Receptor Cellsendocrine system diseasesC-C chemokine receptor type 7CXCR303 medical and health sciencesChemokine receptor0302 clinical medicineCell MovementCell Line TumorGanglia SpinalPancreatic cancermedicineAnimalsHumansCXCL10AnalgesicsChemokine CCL21Hepatologybiologybusiness.industryGastroenterologyCancer Painmedicine.diseaseAntibodies NeutralizingCoculture Techniquesdigestive system diseasesChemokine CXCL10Mice Inbred C57BLPancreatic Neoplasms030104 developmental biologyCancer cellCancer researchbiology.protein030211 gastroenterology & hepatologybusinessCarcinoma Pancreatic DuctalSignal TransductionCCL21Gastroenterology
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The RAB GTPase RAB18 modulates macroautophagy and proteostasis

2017

Macroautophagy is a conserved degradative pathway and its deterioration is linked to disturbances in cellular proteostasis and multiple diseases. Here, we show that the RAB GTPase RAB18 modulates autophagy in primary human fibroblasts. The knockdown of RAB18 results in a decreased autophagic activity, while its overexpression enhances the degradative pathway. Importantly, this function of RAB18 is dependent on RAB3GAP1 and RAB3GAP2, which might act as RAB GEFs and stimulate the activity of the RAB GTPase. Moreover, the knockdown of RAB18 deteriorates proteostasis and results in the intracellular accumulation of ubiquitinated degradation-prone proteins. Thus, the RAB GTPase RAB18 is a positi…

0301 basic medicineRecombinant Fusion Proteinsrab3 GTP-Binding ProteinsPrimary Cell CultureBiophysicsGTPaseBiochemistry03 medical and health sciencesUbiquitinGenes ReporterAutophagyHumansRNA Small InterferingMolecular BiologyGene knockdownbiologyProtein StabilityChemistryfungiAutophagyCell BiologyFibroblastsCell biologyLuminescent Proteins030104 developmental biologyProteostasisGene Expression Regulationrab GTP-Binding ProteinsProteolysisbiology.proteinCancer researchRabSignal transductionRAB18Signal TransductionBiochemical and Biophysical Research Communications
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Nuclear Factor Kappa B Signaling Complexes in Acute Inflammation.

2020

[Significance]: Nuclear factor kappa B (NF-κB) is a master regulator of the inflammatory response and represents a key regulatory node in the complex inflammatory signaling network. In addition, selective NF-κB transcriptional activity on specific target genes occurs through the control of redox-sensitive NF-κB interactions.

0301 basic medicineRedox signalingPhysiologyClinical BiochemistryRepressorCREBInteractomeBiochemistry03 medical and health sciencesCoactivatorHumansSTAT3Transcription factorMolecular BiologyGeneral Environmental ScienceInflammation030102 biochemistry & molecular biologybiologyChemistryActivator (genetics)NF-kappa BCell Biology3. Good healthCell biology030104 developmental biologyGene Expression RegulationMultiprotein ComplexesAcute DiseaseSTAT proteinbiology.proteinGeneral Earth and Planetary SciencesDisease SusceptibilitySignaling complexesCarrier ProteinsBiomarkersProtein BindingSignal TransductionAntioxidantsredox signaling
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