Search results for "ACTIVATOR"

showing 10 items of 488 documents

Nrf2-interacting nutrients and COVID-19: time for research to develop adaptation strategies

2020

AbstractThere are large between- and within-country variations in COVID-19 death rates. Some very low death rate settings such as Eastern Asia, Central Europe, the Balkans and Africa have a common feature of eating large quantities of fermented foods whose intake is associated with the activation of the Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) anti-oxidant transcription factor. There are many Nrf2-interacting nutrients (berberine, curcumin, epigallocatechin gallate, genistein, quercetin, resveratrol, sulforaphane) that all act similarly to reduce insulin resistance, endothelial damage, lung injury and cytokine storm. They also act on the same mechanisms (mTOR: Mammalian target of …

MAPK/ERK pathwayARIA groupAllergy[SDV]Life Sciences [q-bio]NF-KAPPA-BdebelostReviewPharmacologyResveratrolPROTECTSchemistry.chemical_compound0302 clinical medicineRESPIRATORY SYNDROME CORONAVIRUSENDOPLASMIC-RETICULUM STRESSMedicine and Health SciencesImmunology and AllergyMedicineOXIDATIVE STRESSCOVID-19; Foods; Insulin resistance; Nrf2; Nutrients; Obesity; TRPA12. Zero hunger0303 health sciencesRESPIRATORYINSULIN-RESISTANCEMuscle cell proliferationSULFORAPHANE3. Good health[SDV] Life Sciences [q-bio]Foods030220 oncology & carcinogenesisSIGNALING PATHWAYSignal transductionLife Sciences & BiomedicinePulmonary and Respiratory MedicineNRF2 ACTIVATORSMUSCLE-CELL PROLIFERATIONImmunology610 Medicine & healthLung injurySettore MED/10 - Malattie Dell'Apparato RespiratorioTRPA1Nrf2ACUTE LUNG INJURY03 medical and health sciencesInsulin resistanceCOVID-19 Foods Insulin resistance Nrf2 Nutrients Obesity TRPA1udc:616.9odpornost proti inzulinuSULFORAPHANE PROTECTSObesityTranscription factorPI3K/AKT/mTOR pathway030304 developmental biologyScience & Technologybusiness.industrySARS-CoV-2foodCOVID-19Insulin resistanceNutrientsmedicine.diseasechemistryhranilaSYNDROME CORONAVIRUSbusinesshranaGREEN TEA
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Emerging MEK inhibitors

2010

IMPORTANCE OF THE FIELD: The Ras/Raf/MEK/ERK pathway is often activated by genetic alterations in upstream signaling molecules. Integral components of this pathway such as Ras and B-Raf are also activated by mutation. The Ras/Raf/MEK/ERK pathway has profound effects on proliferative, apoptotic and differentiation pathways. This pathway can often be effectively silenced by MEK inhibitors. AREAS COVERED BY THIS REVIEW: This review will discuss targeting of MEK which could lead to novel methods to control abnormal proliferation which arises in cancer and other proliferative diseases. This review will cover the scientific literature from 1980 to present and is a follow on from a review which fo…

MAPK/ERK pathwayCell signalingAntineoplastic Agentsmedicine.disease_causemekerkEnzyme activatorNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Protein phosphorylationProtein Kinase InhibitorsMEK inhibitorsCell ProliferationCancerPharmacologyapoptosis; cancer; erk; kinases; mek; mek inhibitors; proliferative disorders; protein phosphorylation; signal transductionproliferative disordersMutationKinasebusiness.industryapoptosisApoptosiCancerDrugs InvestigationalMAP Kinase Kinase Kinasesmedicine.diseaseprotein phosphorylationCell biologyEnzyme ActivationTreatment OutcomekinasesChemotherapy AdjuvantRadiotherapy AdjuvantSignal transductionbusinesssignal transductionExpert Opinion on Emerging Drugs
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Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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17β-oestradiol up-regulates longevity-related, antioxidant enzyme expression via the ERK1 and ERK2[MAPK]/NFκB cascade

2005

Females live longer than males. Oestrogens protect females against aging by up-regulating the expression of antioxidant, longevity-related genes such as glutathione peroxidase (GPx) and Mn-superoxide dismutase (Mn-SOD). The mechanism through which oestrogens up-regulate those enzymes remains unidentified, but may have implications for gender differences in lifespan. We show that physiological concentrations of oestradiol act through oestrogen receptors to reduce peroxide levels in MCF-7 cells (a mammary gland tumour cell line). Oestradiol increases MAP kinase (MAPK) activation as indicated by ERK1 and ERK2 phosphorylation in MCF-7 cells, which in turn activates the nuclear factor kappa B (N…

MAPK/ERK pathwaychemistry.chemical_classificationAgingmedicine.medical_specialtyP50Glutathione peroxidaseCell BiologyBiologyEnzyme activatorEndocrinologyDownregulation and upregulationchemistryMitogen-activated protein kinaseInternal medicinemedicinebiology.proteinPhosphorylationskin and connective tissue diseasesReceptorAging Cell
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Reevaluating the function of a transcription factor: MBF-1 as a sea urchin chromatin organizer ?

2014

The Zinc-finger MBF-1 factor is involved in the expression of the early histone genes during devel-opment of the sea urchin embryo (1, 2). In spite of being a transcription activator, the DNA-binding domain of MBF-1 shares high sequence similarity with that of the chromatin organizer CTCF of vertebrates and drosophila (3). On the other hand, extensive in silico analysis failed to identify the sea urchin CTCF ortholog (4). This led us to speculate that MBF-1 somehow could have co-opted the function of CTCF during evolution of the echinoderms. Since in vertebrates CTCF binds Hox chromatin, to support our hypothesis, we first identified high-score putative binding sequences for CTCF/MBF-1 with…

MBF-1 activator; CTCF; Hox genes; chromatin immunoprecipitationSettore BIO/11 - Biologia Molecolarechromatin immunoprecipitationCTCFMBF-1 activatorHox gene
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Agr system of Listeria monocytogenes EGD-e: role in adherence and differential expression pattern.

2007

ABSTRACT In this study, we investigated the agrBDCA operon in the pathogenic bacterium Listeria monocytogenes EGD-e. In-frame deletion of agrA and agrD resulted in an altered adherence and biofilm formation on abiotic surfaces, suggesting the involvement of the agr system of L. monocytogenes during the early stages of biofilm formation. Real-time PCR experiments indicated that the transcript levels of agrBDCA depended on the stage of biofilm development, since the levels were lower after the initial attachment period than during biofilm growth, whereas transcription during planktonic growth was not growth phase dependent. The mRNA quantification data also suggested that the agr system was a…

MESH : RNA MessengerTranscription GeneticOperon[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriologymedicine.disease_causeMESH: Listeria monocytogenesApplied Microbiology and BiotechnologyBacterial AdhesionRapid amplification of cDNA endsTranscription (biology)MESH : Bacterial ProteinsMESH : DNA BacterialMESH: Bacterial Proteins0303 health sciencesMESH : Trans-ActivatorsMESH: Gene Expression Regulation BacterialEcologycell-to-cell communicationMESH : BiofilmsBiotechnologyMESH : Gene Expression Regulation BacterialDNA BacterialMESH : Bacterial AdhesionMESH: Trans-ActivatorsGenetics and Molecular BiologyMESH: BiofilmsBiologyagr systemMicrobiology03 medical and health sciencesListeria monocytogenesBacterial ProteinsmedicineMESH: Bacterial AdhesionRNA MessengerGene030304 developmental biologyMESH: RNA MessengerMessenger RNA030306 microbiologyMESH: Transcription GeneticBiofilmMESH : Transcription GeneticGene Expression Regulation Bacterialbiochemical phenomena metabolism and nutritionbiology.organism_classificationMolecular biologyMESH: DNA Bacterial[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyListeria monocytogenesBiofilmsbiofilm formationTrans-ActivatorsMESH : Listeria monocytogenesBacteriaFood ScienceApplied and environmental microbiology
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Functional Activation of Osteoclast Commitment in Chronic Lymphocytic Leukaemia: A Possible Role for RANK/RANKL Pathway

2017

AbstractSkeletal erosion has been found to represent an independent prognostic indicator in patients with advanced stages of chronic lymphocytic leukaemia (CLL). Whether this phenomenon also occurs in early CLL phases and its underlying mechanisms have yet to be fully elucidated. In this study, we prospectively enrolled 36 consecutive treatment-naïve patients to analyse skeletal structure and bone marrow distribution using a computational approach to PET/CT images. This evaluation was combined with the analysis of RANK/RANKL loop activation in the leukemic clone, given recent reports on its role in CLL progression. Bone erosion was particularly evident in long bone shafts, progressively inc…

Male0301 basic medicineChronic lymphocytic leukaemiaClone (cell biology)Osteoclastslcsh:MedicineMice0302 clinical medicineMice Inbred NODBone MarrowPositron Emission Tomography Computed Tomographyhemic and lymphatic diseases80 and overProspective StudiesChroniclcsh:ScienceAged 80 and overSettore ING-IND/24 - Principi Di Ingegneria ChimicaLeukemiaMultidisciplinaryBone Density Conservation AgentsReceptor Activator of Nuclear Factor-kappa BbiologyMiddle AgedLymphocyticLeukemiamedicine.anatomical_structureDenosumabRANKL030220 oncology & carcinogenesisFemaleDenosumabmedicine.drugAdultStromal cellArticle03 medical and health sciencesOsteoclastmedicineAnimalsHumansAgedRANK/RANKL Pathwaybusiness.industryRANK Ligandlcsh:RB-CellDiagnostic markersRANK LigandAdult; Aged; Aged 80 and over; Animals; Bone Density Conservation Agents; Bone Marrow; Denosumab; Female; Glucose; Humans; Leukemia Lymphocytic Chronic B-Cell; Male; Mice Inbred NOD; Middle Aged; Osteoclasts; Positron Emission Tomography Computed Tomography; Prospective Studies; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Xenograft Model Antitumor Assaysmedicine.diseaseLeukemia Lymphocytic Chronic B-CellXenograft Model Antitumor AssaysGlucose030104 developmental biologyChronic Lymphocytic Leukaemiabiology.proteinCancer researchInbred NODlcsh:QBone marrowbusiness
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Plasminogen activator inhibitor‐1 augments damage by impairing fibrinolysis after traumatic brain injury

2019

Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation b…

Male0301 basic medicineTraumatic brain injurymedicine.medical_treatmentBrain damagePharmacologyLesionMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticSerpin E2FibrinolysisAnimalsMedicineThrombusResearch ArticlesIndoleacetic Acidsbusiness.industryFibrinolysisBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyNeurologychemistryPlasminogen activator inhibitor-1Neurology (clinical)medicine.symptombusinessPlasminogen activator030217 neurology & neurosurgeryIntravital microscopyResearch ArticleAnnals of Neurology
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Deficiency of Plasminogen Activator Inhibitor Type 2 Limits Brain Edema Formation after Traumatic Brain Injury

2019

Plasminogen activator inhibitor-2 (PAI-2/SerpinB2) inhibits extracellular urokinase plasminogen activator (uPA). Under physiological conditions, PAI-2 is expressed at low levels but is rapidly induced by inflammatory triggers. It is a negative regulator of fibrinolysis and serves to stabilize clots. In the present study, PAI-2 expression is upregulated 25-fold in pericontusional brain tissue at 6 h after traumatic brain injury (TBI), with a maximum increase of 87-fold at 12 h. To investigate a potentially detrimental influence of PAI-2 on secondary post-traumatic processes, male PAI-2-deficient (PAI-2-KO) and wild-type mice (WT) were subjected to TBI by controlled cortical impact injury. Br…

Male030506 rehabilitationmedicine.medical_specialtyTraumatic brain injuryBrain EdemaInflammationBlood–brain barrierMice03 medical and health sciences0302 clinical medicineInternal medicineBrain Injuries TraumaticPlasminogen Activator Inhibitor 2medicineExtracellularAnimalsMice KnockoutBrain edemaUrokinase Plasminogen Activatorbusiness.industrymedicine.diseaseMice Inbred C57BLEndocrinologymedicine.anatomical_structureNeurology (clinical)medicine.symptom0305 other medical sciencebusinessPlasminogen activator030217 neurology & neurosurgeryJournal of Neurotrauma
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Prevention of Hereditary Angioedema Attacks with a Subcutaneous C1 Inhibitor

2017

Prevenció; Atac d'angioedema; Inhibidor C1 Prevención; Ataque de angioedema; Inhibidor C1 Prevention; Angioedema attack; C1 inhibitor BACKGROUND: Hereditary angioedema is a disabling, potentially fatal condition caused by deficiency (type I) or dysfunction (type II) of the C1 inhibitor protein. In a phase 2 trial, the use of CSL830, a nanofiltered C1 inhibitor preparation that is suitable for subcutaneous injection, resulted in functional levels of C1 inhibitor activity that would be expected to provide effective prophylaxis of attacks. METHODS: We conducted an international, prospective, multicenter, randomized, double-blind, placebo-controlled, dose-ranging, phase 3 trial to evaluate the …

Male:aminoácidos péptidos y proteínas::péptidos::serpinas::proteínas inactivadoras del complemento C1::proteína inhibidora del complemento C1 [COMPUESTOS QUÍMICOS Y DROGAS]0301 basic medicine:Otros calificadores::Otros calificadores::/prevención & control [Otros calificadores]Enzims proteolítics - InhibidorsSelf AdministrationSeverity of Illness Indexlaw.inventionC1-inhibitorSubcutaneous injection0302 clinical medicineRandomized controlled triallawCross-Over StudiesHereditary Angioedema Types I and IIbiologyEdema - PrevencióGeneral Medicine:Cardiovascular Diseases::Vascular Diseases::Angioedema::Angioedemas Hereditary [DISEASES]AnesthesiaHereditary angioedema:Other subheadings::Other subheadings::/administration & dosage [Other subheadings]Female:Amino Acids Peptides and Proteins::Peptides::Serpins::Complement C1 Inactivator Proteins::Complement C1 Inhibitor Protein [CHEMICALS AND DRUGS]medicine.symptomComplement C1 Inhibitor Protein:enfermedades cardiovasculares::enfermedades vasculares::angioedema::angioedemas hereditarios [ENFERMEDADES]AdultRiskmedicine.medical_specialtyInjections Subcutaneous:Aminoácidos Péptidos y Proteínas::Péptidos::Serpinas::Proteínas Inactivadoras del Complemento 1::Proteína Inhibidora del Complemento C1 [COMPUESTOS QUÍMICOS Y DROGAS]Placebo:Other subheadings::Other subheadings::/prevention & control [Other subheadings]03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineHumans:Therapeutics::Drug Therapy::Drug Administration Routes::Injections::Injections Subcutaneous [ANALYTICAL DIAGNOSTIC AND THERAPEUTIC TECHNIQUES AND EQUIPMENT]:Otros calificadores::Otros calificadores::/administración & dosificación [Otros calificadores]Dose-Response Relationship DrugAngioedemabusiness.industry:Terapéutica::Tratamiento Farmacológico::Vías de Administración de Medicamentos::Inyecciones::Inyecciones Subcutáneas [TÉCNICAS Y EQUIPOS ANALÍTICOS DIAGNÓSTICOS Y TERAPÉUTICOS]Injeccions hipodèrmiquesmedicine.diseaseCrossover studyClinical trial:terapéutica::farmacoterapia::vías de administración de medicamentos::inyecciones::inyecciones subcutáneas [TÉCNICAS Y EQUIPOS ANALÍTICOS DIAGNÓSTICOS Y TERAPÉUTICOS]030104 developmental biology030228 respiratory systembiology.proteinbusinessNew England Journal of Medicine
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