Search results for "Inducible"

showing 10 items of 111 documents

Atrial fibrillation is associated with cardiac hypoxia.

2008

BACKGROUND: Atrial fibrillation (AF), the most common human arrhythmia, is responsible for substantial morbidity and mortality and may be promoted by selective atrial ischemia and atrial fibrosis. Consequently, we investigated markers for hypoxia and angiogenesis in AF. METHODS: Right atrial appendages (n=158) were grouped according to heart rhythm [sinus rhythm (SR) or AF]. The degree of fibrosis and microvessel density of all patients were determined morphometrically using Sirius-Red- and CD34/CD105-stained sections, respectively. Next, sections (n=77) underwent immunostaining to detect hypoxia- and angiogenesis-related proteins [hypoxia-inducible factor (HIF)1 alpha, HIF2 alpha, vascular…

MaleVascular Endothelial Growth Factor Amedicine.medical_specialtyCytoplasmAngiogenesisIschemiaMyocardial IschemiaBiologyPathology and Forensic Medicinechemistry.chemical_compoundFibrosisInternal medicineAtrial FibrillationmedicineBasic Helix-Loop-Helix Transcription FactorsHumansSinus rhythmAtrial AppendageHypoxiaMicrovesselAgedCell NucleusNeovascularization PathologicMicrocirculationMyocardiumAtrial fibrillationGeneral MedicineHypoxia (medical)Middle Agedmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCoronary VesselsFibrosisUp-RegulationVascular endothelial growth factorEndocrinologychemistryCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicineBiomarkersCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Role of reactive oxygen species in the regulation of HIF-1 by prolyl hydroxylase 2 under mild hypoxia

2012

The function and survival of eukaryotic cells depends on a constant and sufficient oxygen supply. Cells recognize and respond to hypoxia by accumulation of the transcription factor hypoxia-inducible factor 1 (HIF-1), composed of an oxygen-sensitive HIF-1α and a constitutive HIF-1β subunit. Besides physiology, HIF-1 induction is involved in major pathological processes such as cardiovascular disease, inflammation and cancer, which are associated with the formation of reactive oxygen species (ROS). ROS have been reported to affect HIF-1 activity but the role for ROS in regulating HIF-1 has not been definitely settled. In order to shed light on the redox-regulation of HIF-1 by ROS, we studied …

Transcriptional ActivationProcollagen-Proline DioxygenaseMedizinBiologyTransfectionBiochemistryHypoxia-Inducible Factor-Proline DioxygenasesTransactivationCell Line TumormedicineHumansRNA Small InterferingTranscription factorchemistry.chemical_classificationRegulation of gene expressionReactive oxygen speciesGene knockdownGeneral MedicineTransfectionHydrogen PeroxideHypoxia (medical)Cell HypoxiaCell biologyHypoxia-inducible factorschemistryBiochemistryHypoxia-Inducible Factor 1medicine.symptomReactive Oxygen SpeciesOxidation-Reduction
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MCC1019, a selective inhibitor of the Polo-box domain of Polo-like kinase 1 as novel, potent anticancer candidate

2019

Polo-like kinase (PLK1) has been identified as a potential target for cancer treatment. Although a number of small molecules have been investigated as PLK1 inhibitors, many of which showed limited selectivity. PLK1 harbors a regulatory domain, the Polo box domain (PBD), which has a key regulatory function for kinase activity and substrate recognition. We report on 3-bromomethyl-benzofuran-2-carboxylic acid ethyl ester (designated: MCC1019) as selective PLK1 inhibitor targeting PLK1 PBD. Cytotoxicity and fluorescence polarization-based screening were applied to a library of 1162 drug-like compounds to identify potential inhibitors of PLK1 PBD. The activity of compound MC1019 against the PLK1…

PBD Polo box domainMTD maximal tolerance doseCDC25 cell division cycle 25HIF-1α hypoxia-inducible factor 1 αMST microscale thermophoresisIC50 50% inhibition concentrationMFP M phase promoting factorPARP-1 poly(ADP-ribose) polymerase-10302 clinical medicineFOXO forkhead box ONec-1 necrostatin 1CDC2 cell division cycle protein 2 homologGeneral Pharmacology Toxicology and PharmaceuticsMitotic catastropheCDK cyclin-dependent kinase0303 health sciencesChemistryPolo-like kinaseMono-targeted therapyCell cycleBUBR1 budding uninhibited by benzimidazole-related 1Polo box domain030220 oncology & carcinogenesisPLK1 Polo-like kinaseNecroptosisSpindle damagePLK1IHC immunohistochemistryOriginal articleNecroptosisCell cyclePLK1APC/C anaphase-promoting complex/cyclosomePLK3ABC avidin-biotin complexPI propidium iodide03 medical and health sciencesFBS fetal bovine serumPDB Protein Data BankKd the dissociation constantKinase activity030304 developmental biologyAkt/PKB signaling pathwayCell growthlcsh:RM1-950LC3 light chain 3lcsh:Therapeutics. PharmacologyCancer researchDAPKs death-associated protein kinase3-MA 3-methyladenineDAPI 4′6-diamidino-2-phenylindoleSAC spindle assembly checkpointActa Pharmaceutica Sinica B
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The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
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Cholesterol Starvation and Hypoxia Activate the FVII Gene via the SREBP1-GILZ Pathway in Ovarian Cancer Cells to Produce Procoagulant Microvesicles

2019

AbstractInteraction between the transcription factors, hypoxia-inducible factor (HIF1α and HIF2α) and Sp1, mediates hypoxia-driven expression of FVII gene encoding coagulation factor VII (fVII) in ovarian clear cell carcinoma (CCC) cells. This mechanism is synergistically enhanced in response to serum starvation, a condition possibly associated with tumor hypoxia. This transcriptional response potentially results in venous thromboembolism, a common complication in cancer patients by producing procoagulant extracellular vesicles (EVs). However, which deficient serum factors are responsible for this characteristic transcriptional mechanism is unknown. Here, we report that cholesterol deficien…

Serum0301 basic medicineLeucine zipper030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCell-Derived MicroparticlesCell Line Tumorhemic and lymphatic diseasesAnimalsHumansHypoxiaTranscription factorOvarian NeoplasmsTumor hypoxiaCoagulantsChemistryHematologyFactor VIIChromatin Assembly and DisassemblyHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysMicrovesiclesChromatinCell biologySterol regulatory element-binding proteinCholesterol030104 developmental biologyFemaleSignal transductionSterol Regulatory Element Binding Protein 1Chromatin immunoprecipitationSignal TransductionTranscription FactorsThrombosis and Haemostasis
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Loss of PHD3 allows tumours to overcome hypoxic growth inhibition and sustain proliferation through EGFR

2014

Solid tumours are exposed to microenvironmental factors such as hypoxia that normally inhibit cell growth. However, tumour cells are capable of counteracting these signals through mechanisms that are largely unknown. Here we show that the prolyl hydroxylase PHD3 restrains tumour growth in response to microenvironmental cues through the control of EGFR. PHD3 silencing in human gliomas or genetic deletion in a murine high-grade astrocytoma model markedly promotes tumour growth and the ability of tumours to continue growing under unfavourable conditions. The growth-suppressive function of PHD3 is independent of the established PHD3 targets HIF and NF-κB and its hydroxylase activity. Instead, l…

MaleColorectal cancerAngiogenesisProcollagen-Proline DioxygenaseGeneral Physics and AstronomyApoptosisGrowth inhibitoryBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyHypoxia-Inducible Factor-Proline DioxygenasesGene Knockout Techniqueschemistry.chemical_compoundCell Line TumormedicineAnimalsHumansEgfr signalingHypoxiaCell ProliferationMice KnockoutMultidisciplinaryCell growthGeneral ChemistryHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseMolecular biologyErbB ReceptorsOxygenchemistryApoptosisCancer researchFemalemedicine.symptomGrowth inhibitionGlioblastomaNature Communications
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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Identification of a novel recurrent 1q42.2-1qter deletion in high risk MYCN single copy 11q deleted neuroblastomas

2012

Neuroblastoma is an aggressive embryonal tumor that accounts for similar to 15% of childhood cancer deaths. Hitherto, despite the availability of comprehensive genomic data on DNA copy number changes in neuroblastoma, relatively little is known about the genes driving neuroblastoma tumorigenesis. In this study, high resolution array comparative genome hybridization (CGH) was performed on 188 primary neuroblastoma tumors and 33 neuroblastoma cell lines to search for previously undetected recurrent DNA copy number gains and losses. A new recurrent distal chromosome 1q deletion (del(1)(q42.2qter)) was detected in seven cases. Further analysis of available array CGH datasets revealed 13 additio…

Neuroblastoma/geneticsCancer ResearchProcollagen-Proline DioxygenaseMedizinGene Dosagecomparative genomic hybridizationBiologymedicine.disease_causeGene dosageN-Myc Proto-Oncogene ProteinFumarate HydrataseHypoxia-Inducible Factor-Proline DioxygenasesNeuroblastomaProcollagen-Proline Dioxygenase/geneticsCell Line TumorNeuroblastomamedicineHumansFumarate Hydratase/geneticsGeneOncogene ProteinsGeneticsN-Myc Proto-Oncogene ProteinChromosomes Human Pair 11BreakpointNuclear ProteinsChromosomemedicine.diseaseOncogene Proteins/geneticsNuclear Proteins/geneticsOncologyChromosome DeletionCarcinogenesisComparative genomic hybridization
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The new HFA/ICOS risk assessment tool to identify patients with chronic myeloid leukaemia at high risk of cardiotoxicity

2022

AimsTyrosine kinase inhibitors (TKIs) used to treat chronic myeloid leukaemia (CML) can cause cardiovascular adverseevents. So far, the Systematic Coronary Risk Evaluation (SCORE) charts of the European Society of Cardiology (ESC) have beenused to identify cancer patients at increased cardiovascular risk. The primary aim of our study was to evaluate the usefulnessof the new cardiovascular risk assessment model proposed by the Cardio-Oncology Study Group of the Heart Failure Associ-ation (HFA) of the ESC in collaboration with the International Cardio-Oncology Society (ICOS) to stratify the cardiovascular riskin CML patients, compared with SCORE risk charts. The secondary aim was to establish…

AdultHeart FailureMaleAspirinMiddle AgedRisk AssessmentCardio-oncology Cardiovascular prevention Chronic myeloid leukaemia Nilotinib Ponatinib Cardiovascular toxicityCardiotoxicityInducible T-Cell Co-Stimulator ProteinLeukemia Myelogenous Chronic BCR-ABL PositiveChronic DiseaseHumansFemaleCardiology and Cardiovascular MedicineAgedRetrospective StudiesESC Heart Failure
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