Search results for "Reverse transcriptase polymerase chain reaction"

showing 10 items of 591 documents

Tissue- and cell-specific expression of metallothionein genes in cadmium- and copper-exposed mussels analyzed by in situ hybridization and RT–PCR

2007

Abstract Metallothioneins (MTs) are metal-inducible proteins that can be used as biomarkers of metal exposure. In mussels two families of MT isoforms (MT10 and MT20) have been characterized. In this study, mussels (Mytilus galloprovincialis) were exposed to 200 ppb Cd and 40 ppb Cu for 2 and 9 days to characterize the tissue and isoform specificity of metal-induced MT expression. Non-radioactive in situ hybridization demonstrated that both MT isoforms were mainly transcribed in digestive tubule epithelial cells, especially in basophilic cells. Weaker MT expression was detected in non-ciliated duct cells, stomach and gill epithelial cells, haemocytes, adipogranular cells, spermatic follicles…

Gene isoformSilver StainingMytilus edulisCellIn situ hybridizationToxicologyGene expressionImage Processing Computer-AssistedmedicineAnimalsMetallothioneinRNA MessengerIn Situ HybridizationMytilusPharmacologybiologyReverse Transcriptase Polymerase Chain ReactionSpectrophotometry Atomicbiology.organism_classificationMolecular biologyMytilusBasophilsBasophilicReverse transcription polymerase chain reactionmedicine.anatomical_structureGene Expression RegulationOrgan SpecificityMetallothioneinLysosomesCopperCadmiumToxicology and Applied Pharmacology
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Differential Distribution of Harmonin Isoforms and Their Possible Role in Usher-1 Protein Complexes in Mammalian Photoreceptor Cells

2003

PURPOSE. Human Usher syndrome is the most common form of combined deafness and blindness. Usher type I (USH1), the most severe form, is characterized by profound congenital deafness, constant vestibular dysfunction, and prepubertal onset retinitis pigmentosa. Previous studies have shown that the USH1-proteins myosin VIIa, harmonin, and cadherin 23 interact and form a functional network during hair cell differentiation in the inner ear. The purpose of the present study was to analyze the molecular and cellular functions of these USH1 proteins in the mammalian retina. METHODS. Antibodies to USH1 proteins were generated and used in Western blot analysis of subcellular photoreceptor fractions a…

Gene isoformUsher syndromeBlotting WesternSynaptophysinCell Cycle ProteinsMyosinsBiologyPhotoreceptor cellMiceRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsProtein IsoformsRats WistarFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronCytoskeletonGeneticsRetinaHair cell differentiationReverse Transcriptase Polymerase Chain ReactionCadherinDyneinsCadherinsmedicine.diseaseeye diseasesRatsCell biologyMice Inbred C57BLCytoskeletal Proteinsmedicine.anatomical_structureMicroscopy FluorescenceMyosin VIIasense organsCarrier ProteinsPhotoreceptor Cells VertebrateSubcellular FractionsInvestigative Opthalmology & Visual Science
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Mutations in the β-tropomyosin (TPM2) gene – a rare cause of nemaline myopathy

2002

Nemaline myopathy is a clinically and genetically heterogeneous muscle disorder. In the nebulin gene we have detected a number of autosomal recessive mutations. Both autosomal dominant and recessive mutations have been detected in the genes for alpha -actin and alpha -tropomyosin 3. A recessive mutation causing nemaline myopathy among the Old Order Amish has recently been identified in the gene for slow skeletal muscle troponin T. As linkage studies had shown that at least one further gene exists for nemaline myopathy, we investigated another tropomyosin gene expressed in skeletal muscle, the beta -tropomyosin 2 gene. Screening 66 unrelated patients, using single strand conformation polymor…

Genetic MarkersMaleGenetic LinkageProtein ConformationBiopsyMolecular Sequence DataMutation MissenseTropomyosinmacromolecular substancesMuscle disorderMyopathies NemalineTPM203 medical and health sciencesNebulin0302 clinical medicineNemaline myopathymedicineAnimalsHumansAmino Acid SequenceMuscle SkeletalNemaline bodiesPolymorphism Single-Stranded ConformationalGenetics (clinical)DNA Primers030304 developmental biologyGenetics0303 health sciencesSequence Homology Amino AcidbiologyReverse Transcriptase Polymerase Chain Reactionmusculoskeletal systemmedicine.diseaseMolecular biologyTropomyosinCongenital myopathyPedigree3. Good healthHaplotypesNeurologyMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)Sequence Alignment030217 neurology & neurosurgeryCentral core diseaseNeuromuscular Disorders
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Real-Time Quantification in Plasma of Human Telomerase Reverse Transcriptase (hTERT) mRNA: A Simple Blood Test to Monitor Disease in Cancer Patients

2001

Real-Time Quantification in Plasma of Human Telomerase Reverse Transcriptase (hTERT) mRNA: A Simple Blood Test to Monitor Disease in Cancer Patients

Genetic MarkersTelomeraseDiseaseBiologyPathology and Forensic MedicineNeoplasmsBiomarkers TumormedicineHumansBlood testTelomerase reverse transcriptaseRNA MessengerLymphoma FollicularTelomeraseMolecular BiologyMessenger RNAmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionCancerCell BiologyPrognosismedicine.diseaseNucleotidyltransferaseMolecular biologyDNA-Binding ProteinsReverse transcription polymerase chain reactionRNAColorectal NeoplasmsLaboratory Investigation
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Overexpression of bone morphogenetic protein-6 (BMP-6) in murine epidermis suppresses skin tumor formation by induction of apoptosis and downregulati…

2001

Bone morphogenetic protein-6 (BMP-6) is a member of the transforming growth factor-beta superfamily. In murine skin, BMP-6 is highly expressed in postmitotic keratinocytes from day 15.5 p.c. till day 6 p.p. Expression in adult skin remains at very low levels, but pathological conditions such as wounding induce the expression of BMP-6. We demonstrate that tumor promotion by TPA (12-O-tetradecanoylphorbol-13-acetate) also induces expression of BMP-6 in suprabasal keratinocytes. This induction is due to post-transcriptional regulation since the level of BMP-6 mRNA remained unchanged. We performed two-stage skin carcinogenesis experiments with transgenic mice epidermally overexpressing BMP-6. T…

Genetically modified mouseKeratinocytesCancer ResearchSkin NeoplasmsBone Morphogenetic Protein 6Transgene910-Dimethyl-12-benzanthraceneDown-RegulationApoptosisMice TransgenicBiologymedicine.disease_causeMiceDownregulation and upregulationGenes junGeneticsmedicineIn Situ Nick-End LabelingTumor Cells CulturedAnimalsRNA MessengerMolecular BiologyIn Situ Hybridizationintegumentary systemActivator (genetics)Reverse Transcriptase Polymerase Chain ReactionGenes fosImmunohistochemistryCell biologyBone morphogenetic protein 6ApoptosisImmunologyBone Morphogenetic ProteinsMutationTetradecanoylphorbol AcetateTumor promotionEpidermisCarcinogenesisCell DivisionOncogene
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TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
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Mutated cylindromatosis gene affects the functional state of dendritic cells

2010

Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating enzyme, which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling. Here, we report that DC derived from transgenic mice, which solely express a naturally occurring CYLD isoform (CYLD(ex7/8)), display a higher content of nuclear RelB and express elevated levels of NF-κB family members as well as of known NF-κB-target genes comprising costimulatory molecules and pro-inflammatory cytokines, as compared with WT DC. Accordingly, unstimulated CYLD(ex7/8) DC exhibited a significantly higher primary allogenic T-cell stimulatory capacity than WT DC and exerted no tolerogenic activity. Tr…

Genetically modified mouseTransgeneBlotting WesternImmunologyMice TransgenicBiologyDexamethasoneDeubiquitinating enzymeSmall hairpin RNAMiceImmune ToleranceAnimalsImmunology and AllergyGlucocorticoidsMice KnockoutReverse Transcriptase Polymerase Chain ReactionTumor Suppressor ProteinsRELBTranscription Factor RelBNF-kappa BPeripheral toleranceCell DifferentiationDendritic CellsFlow CytometrySpecific Pathogen-Free OrganismsCell biologyIsoenzymesTranscription Factor AP-1MutationKnockout mouseImmunologybiology.proteinRNAFemaleSignal transductionSignal TransductionEuropean Journal of Immunology
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Genomic response programs of Saccharomyces cerevisiae following protoplasting and regeneration.

2007

Abstract Global transcription profiling during regeneration of Saccharomyces cerevisiae protoplasts was explored. DNA microarrays measured the expression of 6388 genes and wall removal resulted initially in over-expression of 861 genes that decayed later on, a behaviour expected from a transient stress response. Kinetics of expression divided the genes into 25 clusters. Transcription of the genes from clusters 14–25 was initially up-regulated, suggesting that the grouped genes permitted cell adaptation to the removal of the wall. Clustering of genes involved in “wall structure and biosynthesis” showed that most of them had initially low levels of expression that increased along the process.…

GeneticsSaccharomyces cerevisiae ProteinsbiologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingProtoplastsSaccharomyces cerevisiaeGenomicsSaccharomyces cerevisiaeProtoplastbiology.organism_classificationMicrobiologyCell biologyGene expression profilingTranscription (biology)Cell WallGene Expression Regulation FungalGene expressionGeneticsDNA microarrayCandida albicansGeneOligonucleotide Array Sequence AnalysisFungal genetics and biology : FGB
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Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype

2007

Abstract Background Genetic instability is a hallmark of tumours and preneoplastic lesions. The predominant form of genome instability in human cancer is chromosome instability (CIN). CIN is characterized by chromosomal aberrations, gains or losses of whole chromosomes (aneuploidy), and it is often associated with centrosome amplification. Centrosomes control cell division by forming a bipolar mitotic spindle and play an essential role in the maintenance of chromosomal stability. However, whether centrosome amplification could directly cause aneuploidy is not fully established. Also, alterations in genes required for mitotic progression could be involved in CIN. A major candidate is represe…

Genome instabilityCancer ResearchCellular differentiationAneuploidyApoptosisCell CommunicationSpindle ApparatusBiologyProtein Serine-Threonine Kinaseslcsh:RC254-282Aurora KinasesChromosome instabilityChromosomal InstabilitymedicineTumor Cells CulturedGeneticsHumansRNA Small InterferingMitosisIn Situ Hybridization FluorescenceAurora Kinase ACentrosomePloidiesReverse Transcriptase Polymerase Chain ReactionAurora-A centrosomes amplification aneuploidyCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAneuploidyCell biologySpindle apparatusUp-RegulationSettore BIO/18 - GeneticaCell Transformation NeoplasticPhenotypeMicroscopy FluorescenceOncologyCentrosomeColonic NeoplasmsEctopic expressionMicrosatellite InstabilityResearch ArticleBMC Cancer
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CENPA overexpression promotes genome instability in pRb-depleted human cells

2009

Abstract Background Aneuploidy is a hallmark of most human cancers that arises as a consequence of chromosomal instability and it is frequently associated with centrosome amplification. Functional inactivation of the Retinoblastoma protein (pRb) has been indicated as a cause promoting chromosomal instability as well centrosome amplification. However, the underlying molecular mechanism still remains to be clarified. Results Here we show that pRb depletion both in wild type and p53 knockout HCT116 cells was associated with the presence of multipolar spindles, anaphase bridges, lagging chromosomes and micronuclei harbouring whole chromosomes. In addition aneuploidy caused by pRb acute loss was…

Genome instabilityCancer ResearchChromosomal Proteins Non-HistoneBlotting WesternBiologyAutoantigensRetinoblastoma Proteinlcsh:RC254-282Genomic InstabilityRNA interferenceChromosome instabilityCentromere Protein ACell Line TumorHumansRNA Processing Post-TranscriptionalDNA PrimersCENPABase SequenceReverse Transcriptase Polymerase Chain ReactionResearchRetinoblastoma proteincentromere protein aneuploidy pRBlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyCell biologySettore BIO/18 - GeneticaSpindle checkpointOncologyMicroscopy FluorescenceCentrosomebiology.proteinMolecular MedicineRNA Interferencebiological phenomena cell phenomena and immunityCentromere Protein AMolecular Cancer
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