Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Plasmonic Nanosensors for the Label-Free Imaging of Dynamic Protein Patterns.

2020

We introduce a new approach to monitor the dynamics and spatial patterns of biological molecular assemblies. Our molecular imaging method relies on plasmonic gold nanoparticles as point-like detectors and requires no labeling of the molecules. We show spatial resolution of up to 5 μm and 30 ms temporal resolution, which is comparable to wide-field fluorescence microscopy, while requiring only readily available gold nanoparticles and a dark-field optical microscope. We demonstrate the method on MinDE proteins attaching to and detaching from lipid membranes of different composition for 24 h. We foresee our new imaging method as an indispensable tool in advanced molecular biology and biophysic…

Materials scienceCardiolipinsLipid BilayersMetal NanoparticlesNanotechnologyCell Cycle Proteins02 engineering and technology010402 general chemistry01 natural sciencesNanosensorFluorescence microscopeEscherichia coliGeneral Materials SciencePhysical and Theoretical ChemistryImage resolutionPlasmonAdenosine TriphosphatasesMicroscopyNanotubesEscherichia coli ProteinsPhosphatidylglycerols021001 nanoscience & nanotechnology0104 chemical sciencesMembraneColloidal goldTemporal resolutionPhosphatidylcholinesGoldMolecular imaging0210 nano-technologyThe journal of physical chemistry letters
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Nitric oxide inhibits the ATPase activity of the chaperone-like AAA+ ATPase CDC48, a target for S-nitrosylation in cryptogein signalling in tobacco c…

2012

NO has important physiological functions in plants, including the adaptative response to pathogen attack. We previously demonstrated that cryptogein, an elicitor of defence reaction produced by the oomycete Phytophthora cryptogea , triggers NO synthesis in tobacco. To decipher the role of NO in tobacco cells elicited by cryptogein, in the present study we performed a proteomic approach in order to identify proteins undergoing S-nitrosylation. We provided evidence that cryptogein induced the S-nitrosylation of several proteins and identified 11 candidates, including CDC48 (cell division cycle 48), a member of the AAA+ ATPase (ATPase associated with various cellular activities) family. In vit…

Models Molecular0106 biological sciencesProtein Conformation[SDV]Life Sciences [q-bio]Nicotiana tabacumATPaseMolecular Sequence DataCell Cycle ProteinsNitric Oxide01 natural sciencesBiochemistrycryptogeinFungal Proteins03 medical and health sciencesValosin Containing ProteinTobaccoAmino Acid Sequencenitric oxide (no)Molecular BiologyPlant Proteins030304 developmental biologyAdenosine Triphosphatases0303 health sciencesbiologyWalker motifsCell BiologyS-Nitrosylationcell division cycle 48 (cdc48)Biotic stressbiology.organism_classificationAAA proteinsProtein Structure TertiaryElicitorBiochemistryChaperone (protein)[SDE]Environmental Sciencesbiology.proteins-nitrosylationplant defence responses010606 plant biology & botanyBiochemical Journal
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Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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germline mutations in women with familial breast cancer and a relative with haematological malignancy

2009

Biallelic inactivation of the ATM gene causes ataxia-telangiectasia (A-T), a complex neurological disease associated with a high risk of leukaemias and lymphomas. Mothers of A-T children, obligate ATM heterozygote mutation carriers, have a breast cancer (BC) relative risk of about 3. The frequency of ATM carriers in BC women with a BC family history has been estimated to be 2.70%. To further our clinical understanding of familial BC and examine whether haematological malignancies are predictive of ATM germline mutation, we estimated the frequency of heterozygote mutation carriers in a series of 122 BC women with a family history of both BC and haematological malignancy and without BRCA1/2 m…

OncologyCancer ResearchLymphomaDNA Mutational AnalysisCell Cycle ProteinsAtaxia Telangiectasia Mutated Proteins0302 clinical medicineBreast cancerGene FrequencyRisk FactorsMissense mutationGenetics0303 health scienceseducation.field_of_studyLeukemiafamilial breast cancerAtaxia–telangiectasiaPedigreeDNA-Binding ProteinsOncology030220 oncology & carcinogenesisMutation (genetic algorithm)EMMAFemaleAdultHeterozygotemedicine.medical_specialtyMolecular Sequence DataPopulationBreast NeoplasmsProtein Serine-Threonine KinasesBiologyRisk Assessment03 medical and health sciencesGermline mutationBreast cancerPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic TestingeducationAllele frequencyGerm-Line Mutation030304 developmental biologyBase SequenceTumor Suppressor ProteinsHeterozygote advantagemedicine.diseaseAtaxia-telangiectasia
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Molecular and immunohistochemical analysis of the prognostic value of cell-cycle regulators in urothelial neoplasms of the bladder.

2006

Abstract Objective To evaluate the prognostic and predictive value of molecular and immunohistochemical markers related to cell-cycle control in terms of recurrence, progression, and survival in urothelial neoplasms of the bladder (UNB). Patients and Methods Clinical and pathological findings of 84 patients with UNB were assessed. Homozygous deletion (HD) and promoter methylation of p14 ARF , p15 INK4B , p16 INK4A , loss of heterozygosity of the locus 9p21, p53 mutations, and immunohistochemical expression of p53, p16, p14, p21, p27, pRb, Ki67, MDM2, and cyclin D1 proteins were evaluated in relation to overall survival (OS), recurrence-free survival (RFS), and progression-free survival (PFS…

OncologyMalemedicine.medical_specialtyUrologyCell Cycle ProteinsLoss of heterozygosityCyclin D1p14arfPredictive Value of TestsInternal medicineTumor Suppressor Protein p14ARFmedicineBiomarkers TumorHumansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Univariate analysisBladder cancerbusiness.industryCarcinomaRetinoblastomaAnatomical pathologyProto-Oncogene Proteins c-mdm2Cell cyclemedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisKi-67 AntigenMolecular Diagnostic TechniquesUrinary Bladder NeoplasmsCancer researchDisease ProgressionImmunohistochemistryFemaleNeoplasm Recurrence LocalTumor Suppressor Protein p53UrotheliumbusinessCyclin-Dependent Kinase Inhibitor p27European urology
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The giant spectrin βV couples the molecular motors to phototransduction and Usher syndrome type I proteins along their trafficking route.

2013

International audience; Mutations in the myosin VIIa gene cause Usher syndrome type IB (USH1B), characterized by deaf-blindness. A delay of opsin trafficking has been observed in the retinal photoreceptor cells of myosin VIIa-deficient mice. We identified spectrin bV, the mammalian b-heavy spectrin, as a myosin VIIa-and rhodopsin-interacting partner in photoreceptor cells. Spectrin bV displays a polarized distribution from the Golgi apparatus to the base of the outer segment, which, unlike that of other b spectrins, matches the trafficking route of opsin and other phototransduction proteins. Formation of spectrin bV-rhodopsin complex could be detected in the differentiating photoreceptors a…

OpsinRhodopsinLight Signal Transductiongenetic structures[SDV]Life Sciences [q-bio]Cell Cycle Proteinsmacromolecular substancesBiologyMyosinsOpsin transportRetinaMotor protein03 medical and health sciencesMice0302 clinical medicineMyosinotorhinolaryngologic diseasesGeneticsAnimalsHumansSpectrinMolecular BiologyGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal Transducing0303 health sciencesEPB41SpectrinGeneral Medicineeye diseasesCell biologyCytoskeletal ProteinsRhodopsinMyosin VIIabiology.proteinMicrotubule Proteinssense organsUsher Syndromes030217 neurology & neurosurgeryVisual phototransductionHeLa CellsPhotoreceptor Cells VertebrateHuman molecular genetics
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Gadd45α modulates aversive learning through post‐transcriptional regulation of memory‐related mRNA s

2018

Abstract Learning is essential for survival and is controlled by complex molecular mechanisms including regulation of newly synthesized mRNAs that are required to modify synaptic functions. Despite the well‐known role of RNA‐binding proteins (RBPs) in mRNA functionality, their detailed regulation during memory consolidation is poorly understood. This study focuses on the brain function of the RBP Gadd45α (growth arrest and DNA damage‐inducible protein 45 alpha, encoded by the Gadd45a gene). Here, we find that hippocampal memory and long‐term potentiation are strongly impaired in Gadd45a‐deficient mice, a phenotype accompanied by reduced levels of memory‐related mRNAs. The majority of the Ga…

Pain ThresholdUntranslated regionRegulatorGene ExpressionCell Cycle ProteinsHippocampusBiochemistryArticlememoryMice03 medical and health sciences0302 clinical medicineGeneticsAnimalsLearningRNA MessengerMolecular BiologyPost-transcriptional regulationGrin2a030304 developmental biologyMice Knockout0303 health sciencesMessenger RNANeuronal PlasticityBehavior AnimalbiologyLong-term potentiationArticlesRNA stabilityAmygdalaRNA BiologyCell biologyGene Expression Regulationbiology.proteinGRIN2ARNA InterferenceMemory consolidationGADD45A030217 neurology & neurosurgeryGadd45aNeuroscienceEMBO reports
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Beneficial Read-Through of aUSH1CNonsense Mutation by Designed Aminoglycoside NB30 in the Retina

2010

PURPOSE. The human Usher syndrome (USH) is the most frequent cause of inherited combined deaf-blindness. USH is clinically and genetically heterogeneous, assigned to three clinical types. The most severe type is USH1, characterized by profound inner ear defects and retinitis pigmentosa. Thus far, no effective treatment for the ophthalmic component of USH exists. The p.R31X nonsense mutation in USH1C leads to a disease causing premature termination of gene translation. Here, we investigated the capability of the novel synthetic aminoglycoside NB30 for the translational read-through of the USH1C-p.R31X nonsense mutation as a retinal therapy option. METHODS. Read-through of p.R31X by three com…

ParomomycinUsher syndromeBlotting WesternNonsense mutationCell Culture TechniquesGene ExpressionCell Cycle ProteinsParomomycinBiologyPharmacologyTransfectionRetinaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinitis pigmentosaIn Situ Nick-End Labelingotorhinolaryngologic diseasesmedicineAnimalsHumansAdaptor Proteins Signal Transducing030304 developmental biologyGenetics0303 health sciencesRetinaDose-Response Relationship DrugAminoglycosideRetinalmedicine.disease3. Good healthMice Inbred C57BLCytoskeletal ProteinsAminoglycosidesElectroporationHEK293 Cellsmedicine.anatomical_structureMicroscopy FluorescencechemistryCodon NonsenseProtein BiosynthesisGentamicinGentamicins030217 neurology & neurosurgerymedicine.drugInvestigative Opthalmology & Visual Science
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From clinical description, to in vitro and animal studies, and backward to patients: Oxidative stress and mitochondrial dysfunction in Fanconi anemia

2013

Fanconi anemia (FA) is a rare genetic disease associated with deficiencies in DNA repair pathways. A body of literature points to a pro-oxidant state in FA patients, along with evidence for oxidative stress (OS) in the FA phenotype reported by in vitro, molecular, and animal studies. A highlight arises from the detection of mitochondrial dysfunction (MDF) in FA cell lines of complementation groups A, C, D2, and G. As yet lacking, in vivo studies should focus on FA-associated MDF, which may help in the understanding of the mitochondrial basis of OS detected in cells and body fluids from FA patients. Beyond the in vitro and animal databases, the available analytical devices may prompt the dir…

Pathologymedicine.medical_specialtyDNA RepairFree RadicalsDNA repairmitochondrial nutrientsCell Cycle ProteinsFree radicalsDiseaseBiologymedicine.disease_causeBioinformaticsBiochemistryChemopreventionPathogenesis03 medical and health sciencesMice0302 clinical medicineIn vivoFanconi anemiaPhysiology (medical)medicineAnimalsHumans030304 developmental biology0303 health sciencesMitochondrial nutrientNuclear ProteinsFanconi anemia Mitochondrial dysfunction Mitochondrial nutrients Chemoprevention Free radicalsmedicine.diseasePhenotype3. Good healthMitochondriaOxidative StressFanconi Anemia030220 oncology & carcinogenesisFanconi anemiaAnimal studiesReactive Oxygen SpeciesMitochondrial dysfunctionOxidative stress
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Loss of ATM sensitizes against O6-methylguanine triggered apoptosis, SCEs and chromosomal aberrations.

2003

A critical pre-cytotoxic and -apoptotic DNA lesion induced by methylating carcinogens and chemotherapeutic drugs is O6-methylguanine (O6MeG). The mechanism by which O6MeG causes cell death via apoptosis is only partially understood. The current model ascribes a role to DNA replication and mismatch repair, which converts O6MeG into a critical distal lesion (presumably a DNA double-strand break) that is finally responsible for genotoxicity and apoptosis. Here we analysed whether the PI3-like kinase ATM is involved in this process. ATM is a major player in recognizing and signaling DNA breaks, but most reports are limited to ionizing radiation. Comparing mouse ATM knockout fibroblasts (ATM-/-)…

Programmed cell deathGuanineDNA damageApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryMicemedicineCytotoxic T cellAnimalsMolecular BiologyChromosome AberrationsMice KnockoutTumor Suppressor ProteinsCell BiologyTransfectionMolecular biologyDNA-Binding ProteinsCell killingApoptosisDNA mismatch repairSister Chromatid ExchangeGenotoxicityDNA repair
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