Search results for "Cyclin D2"

showing 7 items of 7 documents

Macrophage migration inhibitory factor is critically involved in basal and fluoxetine-stimulated adult hippocampal cell proliferation and in anxiety,…

2011

Intensive research is devoted to unravel the neurobiological mechanisms mediating adult hippocampal neurogenesis, its regulation by antidepressants, and its behavioral consequences. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that is expressed in the CNS, where its function is unknown. Here, we show, for the first time, the relevance of MIF expression for adult hippocampal neurogenesis. We identify MIF expression in neurogenic cells (in stem cells, cells undergoing proliferation, and in newly proliferated cells undergoing maturation) in the subgranular zone of the rodent dentate gyrus. A causal function for MIF in cell proliferation was shown using genetic (M…

Receptors SteroidStem-Cellsanimal diseasesmedicine.medical_treatmentHippocampusExpressionHippocampal formationHippocampusSubgranular zonememoryMice0302 clinical medicineConditioning PsychologicalCyclin D2Rat Dentate GyrusMice KnockoutNeurons0303 health sciencesMicroscopy ConfocalChronic StressMifNeurogenesisBrainFearrespiratory systemanxietyPsychiatry and Mental healthC-Reactive ProteinCytokinemedicine.anatomical_structuredepressionAntidepressive Agents Second-GenerationStem cellPsychologyAnimal-ModelNeurogenesisSpatial BehaviorNerve Tissue Proteinschemical and pharmacologic phenomena03 medical and health sciencesCellular and Molecular Neurosciencemedicineotorhinolaryngologic diseasesAnimalsRats WistarMaze LearningMacrophage Migration-Inhibitory FactorsMolecular BiologyCell Proliferation030304 developmental biologyMemory DisordersDentate gyrusfluoxetineFactor Mifbiological factorsRatsDisease Models AnimalAcoustic StimulationBromodeoxyuridineMacrophage migration inhibitory factorCorticosteroneNeuroscience030217 neurology & neurosurgery
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2,3,7,8-Tetrachlorodibenzo-p-dioxin-Dependent Release from Contact Inhibition in WB-F344 Cells: Involvement of Cyclin A

2002

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent tumor promoter ever tested in rodents. Although it is known that most of TCDD actions are mediated by binding to the aryl hydrocarbon receptor (AhR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact inhibition is one characteristic hallmark in tumorigenesis. In rat liver epithelial WB-F344 cells, TCDD induces a release from contact inhibition, which is manifested by a twofold increase in cell number when TCDD (1 nM for 48 h) is added to confluent cells in the presence of serum, but not when given to exponentially growing or subconfluent, serum-deprived WB-F344 cells. Loss of G1 arrest was a…

Pharmacologyendocrine systemmedicine.medical_specialtybiologyCyclin DCyclin-dependent kinase 2Cyclin ARetinoblastoma proteinContact inhibitionToxicologyMolecular biologystomatognathic diseasesEndocrinologyCyclin D2Cyclin-dependent kinaseInternal medicinebiology.proteinmedicineheterocyclic compoundsCyclinToxicology and Applied Pharmacology
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Modeling human osteosarcoma in mice through 3AB‐OS cancer stem cell xenografts

2012

Osteosarcoma is the second leading cause of cancer-related death for children and young adults. In this study, we have subcutaneously injected—with and without matrigel—athymic mice (Fox1nu/nu) with human osteosarcoma 3AB-OS pluripotent cancer stem cells (CSCs), which we previously isolated from human osteosarcoma MG63 cells. Engrafted 3AB-OS cells were highly tumorigenic and matrigel greatly accelerated both tumor engraftment and growth rate. 3AB-OS CSC xenografts lacked crucial regulators of beta-catenin levels (E-cadherin, APC, and GSK-3beta), and crucial factors to restrain proliferation, resulting therefore in a strong proliferation potential. During the first weeks of engraftment 3AB-…

MaleIntegrin beta ChainsXENOGRAFTNudeAnimals; Bone Neoplasms; Collagen; Drug Combinations; Focal Adhesion Kinase 1; Gene Expression Regulation Neoplastic; Humans; Injections Subcutaneous; Integrin beta Chains; Laminin; Male; Mice; Mice Nude; Neoplasm Transplantation; Neoplastic Stem Cells; Osteosarcoma; Pluripotent Stem Cells; Proteoglycans; Proto-Oncogene Proteins c-akt; Signal Transduction; Transplantation Heterologous; Tumor Markers Biological3AB-OS CSCSBiochemistryMiceInduced pluripotent stem cellTumor MarkersOsteosarcomaHeterologousSubcutaneousXIAPGene Expression Regulation NeoplasticDrug CombinationsANIMAL MODELSNeoplastic Stem CellsOsteosarcomaProteoglycansCollagenMATRIGELSignal TransductionPluripotent Stem CellsInjections SubcutaneousTransplantation HeterologousMice NudeBone NeoplasmsBiologyInjectionsCyclin D2Cancer stem cellBiomarkers TumormedicineAnimalsHumansMolecular BiologyProtein kinase BNeoplasticTransplantationMatrigelMesenchymal stem cellCell BiologyBiologicalmedicine.disease3AB-OS CSCS; OSTEOSARCOMA; XENOGRAFT; MATRIGEL; ANIMAL MODELSGene Expression RegulationFocal Adhesion Kinase 1ImmunologyCancer researchLamininProto-Oncogene Proteins c-aktNeoplasm TransplantationJournal of Cellular Biochemistry
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De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome

2014

Activating mutations in genes encoding phosphatidylinositol 3-kinase (PI3K)-AKT pathway components cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH, OMIM 603387)(1-3). Here we report that individuals with MPPH lacking upstream PI3K-AKT pathway mutations carry de novo mutations in CCND2 (encoding cyclin D2) that are clustered around a residue that can be phosphorylated by glycogen synthase kinase 313 (GSK-3 beta)(4). Mutant CCND2 was resistant to proteasomal degradation in vitro compared to wild-type CCND2. The PI3K-AKT pathway modulates GSK-3 beta activity(4), and cells from individuals with PIK3CA, PIK3R2 or AKT3 mutations showed similar CCND2 accumulation. CCND…

endocrine systemBlotting WesternMolecular Sequence DataMutantMedizinBiologymedicine.disease_causeArticleAKT3Mice03 medical and health sciences0302 clinical medicineCyclin D2GSK-3GeneticsmedicineAnimalsCyclin D2HumansAbnormalities MultipleExomeMegalencephalyPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesMutationBase SequenceSequence Analysis DNASyndromeCell cyclemedicine.diseaseImmunohistochemistryMolecular biologyMegalencephalyMalformations of Cortical DevelopmentPolydactylyElectroporationHEK293 CellsBromodeoxyuridineMicroscopy FluorescenceMutagenesis Site-DirectedFemale030217 neurology & neurosurgeryHydrocephalusNature Genetics
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The IgG1 B-cell receptor provides survival and proliferative signals analogue to the Igα but not the Igβ co-receptor.

2016

The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Igα and Igβ, both of which contain a cytoplasmic tail bearing an immunoreceptor tyrosine-based activation motif. We have previously demonstrated that the cytoplasmic tail of the IgG1 BCR can partially compensate for the loss of the signaling moiety of Igα. Here, we show that unlike Igα, Igβ signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Igβ compromised the survival and proliferation not only of IgM(+) B cells but also of IgG1-expressing B cells. In the absence of the signaling tail of Igβ, the transcription …

0301 basic medicineCo-receptorImmunologyB-cell receptorbcl-X ProteinReceptors Antigen B-CellBiologyCell Line03 medical and health sciencesTransduction (genetics)Mice0302 clinical medicineTranscription (biology)Immunology and AllergyAnimalsCyclin D2TyrosineReceptorCell ProliferationB-Lymphocytesbreakpoint cluster regionFlow CytometryCell biology030104 developmental biologyImmunoglobulin MCytoplasmImmunoglobulin GCancer researchCD79 Antigens030215 immunologySignal TransductionEuropean journal of immunology
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Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload

2017

Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2-expressing mice. On the other hand, cardiac structure and function were compr…

0301 basic medicineCardiac function curvemedicine.medical_specialtyAortic DiseasesVolume overloadCardiomegalyMice TransgenicConstriction Pathologic030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCyclin D2FibrosisInternal medicinemedicineAnimalsCyclin D2Myocytes CardiacCell ProliferationCyclinHeart FailurePressure overloadbusiness.industryGeneral MedicineCell cyclemedicine.disease030104 developmental biologyEndocrinologyHeart failurebusinessResearch ArticleJournal of Clinical Investigation
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A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
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