Search results for "KINASE"

showing 10 items of 2635 documents

The Amount of Melanin Influences p16 Loss in Spitzoid Melanocytic Lesions: Correlation With CDKN2A Status by FISH and MLPA.

2019

AIMS The risk assessment of spitzoid lesions is one of the most difficult challenges in dermatopathology practice. In this regard, the loss of p16 expression and the homozygous deletion of CDKN2A, have been pointed in the literature as reliable indicators of high risk. However, these findings are poorly reproducible, and the molecular bases underlying the loss of p16 expression remain unclear. We aimed to identify the underlying events causing loss of CDKN2A/p16 in spitzoid tumors. MATERIALS AND METHODS We evaluated the immunohistochemical expression of p16, and the presence of CDKN2A genetic alterations detected through fluorescence in situ hybridization (FISH) and multiplex ligation-depen…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyHistologySkin NeoplasmsPathology and Forensic MedicineMelanin03 medical and health sciencesYoung Adult0302 clinical medicineCDKN2ANevus Epithelioid and Spindle CellmedicineBiomarkers TumorNevusHumansMultiplex ligation-dependent probe amplificationneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceMelaninsmedicine.diagnostic_testbusiness.industryMelanomamedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMedical Laboratory Technology030104 developmental biology030220 oncology & carcinogenesisMutationImmunohistochemistryMelanocytesFemaleDermatopathologybusinessMultiplex Polymerase Chain ReactionFluorescence in situ hybridizationApplied immunohistochemistrymolecular morphology : AIMM
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The JAK2 pathway is activated in idiopathic pulmonary fibrosis

2018

Background: Idiopathic pulmonary fibrosis (IPF) is the most rapidly progressive and fatal fibrotic disorder, with no curative therapies. The signal transducer and activator of transcription 3 (STAT3) protein is activated in lung fibroblasts and alveolar type II cells (ATII), thereby contributing to lung fibrosis in IPF. Although activation of Janus kinase 2 (JAK2) has been implicated in proliferative disorders, its role in IPF is unknown. The aim of this study was to analyze JAK2 activation in IPF, and to determine whether JAK2/STAT3 inhibition is a potential therapeutic strategy for this disease. Methods and results: JAK2/p-JAK2 and STAT3/pSTAT3 expression was evaluated using quantitative …

0301 basic medicineAdultMaleSTAT3 Transcription FactorIdiopathic pulmonary fibrosisEpithelial cellsLung fibroblastsFibroblast migrationPulmonary fibrosisSTAT303 medical and health sciencesIdiopathic pulmonary fibrosisFibrosishemic and lymphatic diseasesMedicineAnimalsHumansFibroblastAgedlcsh:RC705-779A549 cellCèl·lules epitelialsLungbiologybusiness.industryResearchFibrosi pulmonarlcsh:Diseases of the respiratory systemTransforming growth factor betaFibroblastsJanus Kinase 2Middle Agedrespiratory systemmedicine.diseaseTriterpenesRatsrespiratory tract diseasesEnzyme Activation030104 developmental biologymedicine.anatomical_structureJAK2A549 CellsAlveolar type II epithelial cellsCancer researchbiology.proteinFemalebusinessMyofibroblastSignal Transduction
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SOX2 expression diminishes with ageing in several tissues in mice and humans.

2017

SOX2 (Sex-determining region Y box 2) is a transcription factor expressed in several foetal and adult tissues and its deregulated activity has been linked to chronic diseases associated with ageing. Nevertheless, the level of SOX2 expression in aged individuals at the tissue level has not previously been examined. In this work, we show that SOX2 expression decreases significantly in the brain with ageing, in both humans and rodents. The administration of resveratrol for 6 months in mice partly attenuated this reduction. We also identified an age-related decline in SOX2 mRNA and protein expression in several other organs, namely, the lung, heart, kidney, spleen and liver. Moreover, periphera…

0301 basic medicineAdultMalemedicine.medical_specialtyAgingSOX2SpleenResveratrolBiologyPeripheral blood mononuclear cellGene Expression Regulation Enzymologic03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineSOX2stomatognathic systemInternal medicinemedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Aged 80 and overKidneyMessenger RNASOXB1 Transcription FactorsfungiMiddle AgedAgeing030104 developmental biologymedicine.anatomical_structureEndocrinologychemistryAgeingOrgan Specificityembryonic structuresLeukocytes MononuclearBiomarker (medicine)Femalesense organsbiological phenomena cell phenomena and immunity030217 neurology & neurosurgeryBiomarkersDevelopmental BiologyMechanisms of ageing and development
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Malignant PEComa With Metastatic Disease at Diagnosis and Resistance to Several Chemotherapy Regimens and Targeted Therapy (m-TOR Inhibitor).

2017

Perivascular epithelioid cell tumors (PEComas) are infrequent neoplasms with peculiar myomelanocytic differentiation. The aggressive abdominopelvic variant is rare, with only a small number of published cases. We present an additional case of this unusual variant, which showed an aggressive histologic and clinical behavior with multiple liver metastases and resistance to several therapies. We also discuss the histological and immunohistochemical profiles as well as the differential diagnosis.

0301 basic medicineAdultPathologymedicine.medical_specialtyPerivascular Epithelioid Cell Neoplasmsmedicine.medical_treatmentAntineoplastic AgentsDiseasePathology and Forensic MedicineTargeted therapy03 medical and health sciences0302 clinical medicineMedicineHumansMolecular Targeted TherapyChemotherapybusiness.industryTOR Serine-Threonine Kinasesmedicine.diseasePerivascular Epithelioid Cell Tumors030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisImmunohistochemistrySurgeryFemaleSarcomaAnatomyDifferential diagnosisbusinessInternational journal of surgical pathology
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Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspa…

0301 basic medicineAgingArticle SubjectApoptosis030204 cardiovascular system & hematologyTransfectionBiochemistryUmbilical vein03 medical and health sciences0302 clinical medicineRisk FactorsHuman Umbilical Vein Endothelial CellsHumanslcsh:QH573-671Protein kinase AEndoplasmic Reticulum Chaperone BiPHomocysteinebiologylcsh:CytologyKinaseEndoplasmic reticulumCytochrome cCell BiologyGeneral MedicineEndoplasmic Reticulum StressMitochondriaCell biology030104 developmental biologyApoptosiscardiovascular systemUnfolded protein responsebiology.proteinPhosphorylationResearch ArticleOxidative Medicine and Cellular Longevity
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Overexpression of CYB5R3 and NQO1, two NAD+-producing enzymes, mimics aspects of caloric restriction

2018

© 2018 The Authors.

0301 basic medicineAgingCalorie restrictionInflammationmedicine.disease_cause03 medical and health sciencesDownregulation and upregulationmedicineCytochrome b5 reductaseCalorie restrictionchemistry.chemical_classification030102 biochemistry & molecular biologybiologyCYB5R3Cell BiologyCell biology030104 developmental biologyEnzymechemistrySirtuinbiology.proteinNQO1NAD+ kinasemedicine.symptomCarcinogenesisMetabolic homeostasis
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Adult rat myelin enhances axonal outgrowth from neural stem cells.

2018

Axon regeneration after spinal cord injury (SCI) is attenuated by growth inhibitory molecules associated with myelin. We report that rat myelin stimulated the growth of axons emerging from rat neural progenitor cells (NPCs) transplanted into sites of SCI in adult rat recipients. When plated on a myelin substrate, neurite outgrowth from rat NPCs and from human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) was enhanced threefold. In vivo, rat NPCs and human iPSC-derived NSCs extended greater numbers of axons through adult central nervous system white matter than through gray matter and preferentially associated with rat host myelin. Mechanistic investigations excluded …

0301 basic medicineAgingNeuronalNudeMessengerNeurodegenerativeInbred C57BLRegenerative MedicineMedical and Health SciencesMyelinMiceNeural Stem CellsStem Cell Research - Nonembryonic - HumanCyclic AMPAxonPhosphorylationGray MatterInduced pluripotent stem cellExtracellular Signal-Regulated MAP KinasesSpinal Cord InjuryMyelin SheathInbred F344Neuronal growth regulator 1Stem Cell Research - Induced Pluripotent Stem Cell - HumanChemistryGeneral MedicineBiological SciencesWhite MatterNeural stem cellCell biologymedicine.anatomical_structureSpinal Cord5.1 PharmaceuticalsNeurologicalFemaleStem Cell Research - Nonembryonic - Non-HumanDevelopment of treatments and therapeutic interventionsPhysical Injury - Accidents and Adverse EffectsNeuriteCell Adhesion Molecules NeuronalCentral nervous systemNeuronal OutgrowthArticleWhite matter03 medical and health sciencesRats NudemedicineAnimalsHumansRNA MessengerStem Cell Research - Embryonic - HumanTraumatic Head and Spine InjuryTransplantationStem Cell Research - Induced Pluripotent Stem CellNeurosciencesStem Cell ResearchRats Inbred F344AxonsRatsMice Inbred C57BL030104 developmental biologynervous systemChondroitin Sulfate ProteoglycansRNACell Adhesion Molecules
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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