Search results for "Biological Phenomena"

showing 10 items of 102 documents

Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
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AURKA (aurora kinase A)

2011

Review on AURKA (aurora kinase A), with data on DNA, on the protein encoded, and where the gene is implicated.

Cancer Researchmacromolecular substancesHematologyBiologyCell biologySettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)chemistry.chemical_compoundOncologychemistryembryonic structuresGeneticsAurora Kinase Abiological phenomena cell phenomena and immunityAURK-AGeneDNAAtlas of Genetics and Cytogenetics in Oncology and Haematology
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Modulation of Cell Cycle Components by Epigenetic and Genetic Events

2005

Cell cycle progression is monitored by surveillance mechanisms, or cell cycle checkpoints, that ensure that initiation of a later event is coupled with the completion of an early cell cycle event. Deregulated proliferation is a characteristic feature of tumor cells. Moreover, defects in many of the molecules that regulate the cell cycle have been implicated in cancer formation and progression. Key among these are p53, the retinoblastoma protein (pRb) and its related proteins, p107 and pRb2/p130, and cdk inhibitors (p15, p16, p18, p19, p21, p27), all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed. The pRb (pRb/p16(INK4a)/cyclin D1) a…

Cell cycle checkpointCyclin ABiologymedicine.disease_causeModels BiologicalRetinoblastoma ProteinEpigenesis GeneticCyclin-dependent kinaseNeoplasmsmedicineAnimalsHumansEpigeneticsCell ProliferationCell growthCell CycleRetinoblastoma proteinHematologyCell cycleCell biologyOncologyDisease Progressionbiology.proteinTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarcinogenesisSignal TransductionSeminars in Oncology
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Symmetric expansion of neural stem cells from the adult olfactory bulb is driven by astrocytes via WNT7A.

2012

Adult neural stem cells (NSCs) located in the subventricular zone (SVZ) persistently produce new neurons destined to the olfactory bulb (OB). Recent research suggests that the OB is also a source of NSCs that remains largely unexplored. Using single/dual-labeling procedures, we address the existence of NSCs in the innermost layers of the OB. In vivo, these cells are more quiescent that their SVZ counterparts, but after in vitro expansion, they behave similarly. Self-renewal and proliferation assays in co-culture with niche astrocytes indicate that OB-glia restricts NSC activity whereas SVZ-glia has the opposite effect. Gene expression profiling identifies WNT7A as a key SVZ-glial factor lac…

Cellular differentiationSubventricular zoneCell Growth ProcessesBiologyMiceNeural Stem CellsIn vivomedicineAnimalsHumansreproductive and urinary physiologyWnt signaling pathwayCell DifferentiationCell BiologyAnatomyOlfactory BulbNeural stem cellnervous system diseasesOlfactory bulbCell biologyGene expression profilingWnt ProteinsWNT7Amedicine.anatomical_structurenervous systemAstrocytesMolecular Medicinebiological phenomena cell phenomena and immunityDevelopmental BiologyStem cells (Dayton, Ohio)
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Comprehensive analysis of expression, subcellular localization, and cognate pairing of SNARE proteins in oligodendrocytes

2009

Oligodendrocytes form the central nervous system myelin sheath by spiral wrapping of their plasma membrane around axons, necessitating a high rate of exocytic membrane addition to the growing myelin membrane. Membrane fusion is mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor proteins (SNAREs), which act by specific pairing of vesicle (R)- and target (Q)-SNAREs. To characterize oligodendroglial SNAREs and their trafficking pathways, we performed a detailed expression analysis of SNAREs in differentiating cultured oligodendrocytes and myelin and determined their subcellular localization. Expression of the plasma membrane Q-SNAREs syntaxin 3, syntaxin 4, SNAP2…

Central Nervous SystemMaleVesicle-Associated Membrane Protein 3SynaptobrevinGolgi ApparatusBiologyMembrane FusionR-SNARE ProteinsMiceCellular and Molecular NeuroscienceSNAP23AnimalsSyntaxinQc-SNARE ProteinsTransport VesiclesCells CulturedMyelin SheathR-SNARE ProteinsQa-SNARE ProteinsVesicleCell MembraneLipid bilayer fusionQb-SNARE ProteinsSyntaxin 3Cell CompartmentationTransport proteinCell biologyOligodendrogliaProtein Transportnervous systemFemalebiological phenomena cell phenomena and immunitySNARE ProteinsDimerizationJournal of Neuroscience Research
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Cyclin-dependent kinase inhibitor p21 controls adult neural stem cell expansion by regulating Sox2 gene expression.

2012

Summary In the adult brain, continual neurogenesis of olfactory neurons is sustained by the existence of neural stem cells (NSCs) in the subependymal niche. Elimination of the cyclin-dependent kinase inhibitor 1A (p21) leads to premature exhaustion of the subependymal NSC pool, suggesting a relationship between cell cycle control and long-term self-renewal, but the molecular mechanisms underlying NSC maintenance by p21 remain unexplored. Here we identify a function of p21 in the direct regulation of the expression of pluripotency factor Sox2, a key regulator of the specification and maintenance of neural progenitors. We observe that p21 directly binds a Sox2 enhancer and negatively regulate…

Cèl·lules mare neuralsCyclin-Dependent Kinase Inhibitor p21Chromatin ImmunoprecipitationImmunoblottingArticle03 medical and health sciencesMice0302 clinical medicineSOX2Neural Stem CellsCyclin-dependent kinaseNeurosphereSubependymal zoneGeneticsExpressió genèticaAnimalsProgenitor cellCells Cultured030304 developmental biology0303 health sciencesbiologyCell growthReverse Transcriptase Polymerase Chain ReactionSOXB1 Transcription FactorsNeurogenesisCell BiologyImmunohistochemistryNeural stem cellMice Mutant Strains3. Good healthAdult Stem Cellsnervous systemCancer researchbiology.proteinMolecular Medicinebiological phenomena cell phenomena and immunity030217 neurology & neurosurgeryProtein BindingCell stem cell
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CD95 death-inducing signaling complex formation and internalization occur in lipid rafts of type I and type II cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

Death Domain Receptor Signaling Adaptor ProteinsEndosomeT-Lymphocytesmedia_common.quotation_subjectImmunologyApoptosisReceptors Tumor Necrosis FactorCell LineMembrane MicrodomainsSettore MED/04 - PATOLOGIA GENERALECell Line TumorReceptorsHumansImmunology and Allergyfas ReceptorFADDInternalizationLipid raftLipid raftsDeath domainmedia_commonTumorbiologyVesicleFas receptorEndocytosisCell biologyProtein TransportCholesterolCD95 death-inducing signaling complexCaspasesCD95biology.proteinlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityCaspase-8Tumor Necrosis FactorCaspase-8; CD95; Lipid rafts; Apoptosis; Caspases; Cell Line Tumor; Cholesterol; Death Domain Receptor Signaling Adaptor Proteins; Humans; Membrane Microdomains; Protein Binding; Protein Transport; Receptors Tumor Necrosis Factor; T-Lymphocytes; fas Receptor; Endocytosis; Signal Transduction; Immunology and Allergy; ImmunologyProtein BindingSignal TransductionEuropean Journal of Immunology
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Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination.

2010

Abstract Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADDODC-KO). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADDODC-KO mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADDODC-KO mice followed an ameliorated clinical di…

Encephalomyelitis Autoimmune ExperimentalMultiple Sclerosisgenetic structuresEncephalomyelitisFas-Associated Death Domain ProteinImmunologyApoptosisurologic and male genital diseasesMiceConditional gene knockoutDemyelinating diseasemedicineImmunology and AllergyAnimalsFADDLymphocytesMyelin SheathDeath domainInflammationMice KnockoutbiologyMultiple sclerosisMacrophagesfungiExperimental autoimmune encephalomyelitismedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureGene Expression RegulationSpinal CordCancer researchbiology.proteinbiological phenomena cell phenomena and immunityGene DeletionJournal of immunology (Baltimore, Md. : 1950)
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Nanog Regulates Primordial Germ Cell Migration Through Cxcr4b

2010

Abstract Gonadal development in vertebrates depends on the early determination of primordial germ cells (PGCs) and their correct migration to the sites where the gonads develop. Several genes have been implicated in PGC specification and migration in vertebrates. Additionally, some of the genes associated with pluripotency, such as Oct4 and Nanog, are expressed in PGCs and gonads, suggesting a role for these genes in maintaining pluripotency of the germ lineage, which may be considered the only cell type that perpetually maintains stemness properties. Here, we report that medaka Nanog (Ol-Nanog) is expressed in the developing PGCs. Depletion of Ol-Nanog protein causes aberrant migration of …

Fish ProteinsHomeobox protein NANOGChromatin ImmunoprecipitationReceptors CXCR4endocrine systemCell typeGenotypeOryziasBiologyNanogCxcr4bOpen Reading FramesCell MovementAnimalsPromoter Regions Genetic3' Untranslated RegionsGeneIn Situ Hybridizationreproductive and urinary physiologyHomeodomain ProteinsRegulation of gene expressionMessenger RNABinding SitesReverse Transcriptase Polymerase Chain Reactionurogenital systemThree prime untranslated regionPGCGene Expression Regulation DevelopmentalCell BiologyImmunohistochemistryPhenotypeMolecular biologyChemokine CXCL12MedakaGerm CellsPhenotypeGene Knockdown Techniquesembryonic structuresMolecular Medicinebiological phenomena cell phenomena and immunityChromatin immunoprecipitationDevelopmental BiologyStem Cells
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