Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Ent…

DNA Replicationendocrine system diseasesDNA damagereplication stressQH301-705.5RNR Inhibitor COH29Antineoplastic AgentsCell Cycle ProteinsRNRAtaxia Telangiectasia Mutated ProteinsArticle03 medical and health scienceschemistry.chemical_compoundAtaxia TelangiectasiaMice0302 clinical medicineHDACAnimalscancerPDAC cellsRibonucleotide Reductase SubunitEnzyme InhibitorsBiology (General)030304 developmental biology0303 health sciencesbiologyChemistryEntinostatDNA replicationapoptosisGeneral Medicine3. Good healthPancreatic NeoplasmsHistoneRibonucleotide reductase030220 oncology & carcinogenesisATMbiology.proteinCancer researchDNA damageHistone deacetylaseCells
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Myosin VIIa, harmonin and cadherin 23, three Usher I gene products that cooperate to shape the sensory hair cell bundle

2002

Deaf-blindness in three distinct genetic forms of Usher type I syndrome (USH1) is caused by defects in myosin VIIa, harmonin and cadherin 23. Despite being critical for hearing, the functions of these proteins in the inner ear remain elusive. Here we show that harmonin, a PDZ domain-containing protein, and cadherin 23 are both present in the growing stereocilia and that they bind to each other. Moreover, we demonstrate that harmonin b is an F-actin-bundling protein, which is thus likely to anchor cadherin 23 to the stereocilia microfilaments, thereby identifying a novel anchorage mode of the cadherins to the actin cytoskeleton. Moreover, harmonin b interacts directly with myosin VIIa, and i…

DNA ComplementaryCadherin Related ProteinsCell Cycle Proteinsmacromolecular substancesMyosinsBiologyTransfectionMicrofilamentGeneral Biochemistry Genetics and Molecular BiologyCell LineMiceCDH23Two-Hybrid System TechniquesHair Cells Auditoryotorhinolaryngologic diseasesmedicineAnimalsHumansProtein IsoformsRats WistarMolecular BiologyActinAdaptor Proteins Signal TransducingGene LibraryGeneral Immunology and MicrobiologyCadherinGeneral NeuroscienceStereociliaDyneinsCell DifferentiationArticlesCadherinsActin cytoskeletonActinsProtein Structure TertiaryRatsCell biologyCytoskeletal ProteinsMicroscopy Electronmedicine.anatomical_structureMicroscopy FluorescenceMyosin VIIasense organsCarrier ProteinsTip linkPCDH15HeLa CellsProtein BindingThe EMBO Journal
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Ofd1, a Human Disease Gene, Regulates the Length and Distal Structure of Centrioles

2010

SUMMARYCentrosomes and their component centrioles represent the principal microtubule organizing centers of animal cells. Here we show that the gene underlying Orofaciodigital Syndrome 1, Ofd1, is a component of the distal centriole that controls centriole length. In the absence of Ofd1, distal regions of centrioles, but not procentrioles, elongate abnormally. These long centrioles are structurally similar to normal centrioles, but contain destabilized microtubules with abnormal post-translational modifications. Ofd1 is also important for centriole distal appendage formation and centriolar recruitment of the intraflagellar transport protein Ift88. To model OFD1 Syndrome in embryonic stem ce…

G2 PhaseCentrioleMicrotubule-associated proteinMutation MissenseHUMDISEASECell Cycle ProteinsBiologyMicrotubulesModels BiologicalArticleGeneral Biochemistry Genetics and Molecular BiologyCentriole elongationCell LineMiceIntraflagellar transportCiliogenesisAnimalsHumansBasal bodyMolecular BiologyEmbryonic Stem CellsCentriolesTumor Suppressor ProteinsProteinsCell BiologyOrofaciodigital SyndromesPhosphoproteinsRecombinant ProteinsCell biologyCentrosomeCELLBIOCentriolar satelliteMicrotubule-Associated ProteinsDevelopmental Biology
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GADD45a physically and functionally interacts with TET1

2015

AbstractDNA demethylation plays a central role during development and in adult physiology. Different mechanisms of active DNA demethylation have been established. For example, Growth Arrest and DNA Damage 45-(GADD45) and Ten-Eleven-Translocation (TET) proteins act in active DNA demethylation but their functional relationship is unresolved. Here we show that GADD45a physically interacts – and functionally cooperates with TET1 in methylcytosine (mC) processing. In reporter demethylation GADD45a requires endogenous TET1 and conversely TET1 requires GADD45a. On GADD45a target genes TET1 hyperinduces 5-hydroxymethylcytosine (hmC) in the presence of GADD45a, while 5-formyl-(fC) and 5-carboxylcyto…

Gadd45Cancer ResearchDNA damageCell Cycle ProteinsBiologyDNA-binding proteinArticleMixed Function OxygenaseshmCchemistry.chemical_compoundCytosineLC–MS/MSProto-Oncogene ProteinsHumansImmunoprecipitationMolecular BiologyDemethylationGadd45Nuclear ProteinsOxidative DNA demethylationCell BiologyDNA MethylationDNA-Binding Proteins5-MethylcytosineDNA demethylationHEK293 CellschemistryBiochemistryGene Knockdown TechniquesDNA methylationDNA demethylation5-MethylcytosineOxidation-ReductionTETProtein BindingDevelopmental BiologyDifferentiation
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The “Janus” Role of C/EBPs Family Members in Cancer Progression

2020

CCAAT/enhancer-binding proteins (C/EBPs) constitute a family of transcription factors composed of six members that are critical for normal cellular differentiation in a variety of tissues. They promote the expression of genes through interaction with their promoters. Moreover, they have a key role in regulating cellular proliferation through interaction with cell cycle proteins. C/EBPs are considered to be tumor suppressor factors due to their ability to arrest cell growth (contributing to the terminal differentiation of several cell types) and for their role in cellular response to DNA damage, nutrient deprivation, hypoxia, and genotoxic agents. However, C/EBPs can elicit completely opposi…

Gene isoformCell typeDNA damagetumor suppressorCellular differentiationReviewBiologyCatalysisInorganic Chemistrylcsh:ChemistryStructure-Activity RelationshipSettore BIO/13 - Biologia ApplicataNeoplasmsAnimalsHumansProtein IsoformscancerPhysical and Theoretical ChemistryCell Cycle ProteinMolecular BiologyTranscription factorlcsh:QH301-705.5SpectroscopyCell growthOrganic Chemistrytumor promoterPromoterGeneral MedicineC/EBPComputer Science ApplicationsCell biologyGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999Multigene FamilyCCAAT-Enhancer-Binding ProteinsDisease ProgressionDisease SusceptibilityProtein BindingSignal TransductionInternational Journal of Molecular Sciences
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Gene Repair of an Usher Syndrome Causing Mutation by Zinc-Finger Nuclease Mediated Homologous Recombination

2012

PURPOSE. Human Usher syndrome (USH) is the most frequent cause of inherited deaf-blindness. It is clinically and genetically heterogeneous, assigned to three clinical types of which the most severe type is USH1. No effective treatment for the ophthalmic component of USH exists. Gene augmentation is an attractive strategy for hereditary retinal diseases. However, several USH genes, like USH1C, are expressed in various isoforms, hampering gene augmentation. As an alternative treatment strategy, we applied the zinc-finger nuclease (ZFN) technology for targeted gene repair of an USH1C, causing mutation by homologous recombination. METHODS. We designed ZFNs customized for the p.R31X nonsense mut…

Gene isoformNonsense mutationCell Cycle ProteinsBiologyRetinaCell Linechemistry.chemical_compoundHumansDNA Breaks Double-StrandedDNA CleavageHomologous RecombinationGeneAdaptor Proteins Signal TransducingZinc fingerGeneticsTargeted Gene RepairfungiZinc FingersDNAEndonucleasesZinc finger nucleaseCytoskeletal ProteinschemistryCodon NonsenseHomologous recombinationUsher SyndromesDNATargeted Gene RepairInvestigative Opthalmology & Visual Science
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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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Role of Gadd45a in Wip1-dependent regulation of intestinal tumorigenesis.

2012

Conversion of intestinal stem cells into tumor-initiating cells is an early step in Apc(Min)-induced polyposis. Wild-type p53-induced phosphatase 1 (Wip1)-dependent activation of a DNA damage response and p53 has a permanent role in suppression of stem cell conversion, and deletion of Wip1 lowers the tumor burden in Apc(Min) mice. Here we show that cyclin-dependent kinase inhibitor 2a, checkpoint kinase 2, and growth arrest and DNA damage gene 45a (Gadd45a) exert critical functions in the tumor-resistant phenotype of Wip1-deficient mice. We further identified Gadd45a as a haploinsufficient gene in the regulation of Wip1-dependent tumor resistance in mice. Gadd45a appears to function through…

Genes APCDNA RepairDNA repairDNA damageApoptosisCell Cycle ProteinsBiologyProtein Serine-Threonine KinasesReceptors G-Protein-CoupledMicePhosphoprotein PhosphatasesGene silencingAnimalsMolecular BiologyCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p16beta CateninMice KnockoutOriginal PaperKinaseIntestinal PolyposisStem CellsJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyCell biologyProtein Phosphatase 2CCheckpoint Kinase 2Cell Transformation NeoplasticCancer researchSignal transductionStem cellTumor Suppressor Protein p53GADD45ASignal TransductionCell death and differentiation
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Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

2001

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC cont…

Genetic Markerscongenital hereditary and neonatal diseases and abnormalitiesBeckwith–Wiedemann syndromeCell Cycle ProteinsBiologyChromosomesEvolution MolecularContig MappingMiceChromosome regionsGene OrderMetalloproteinsGeneticsmedicineAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyOncogene ProteinsGeneticsChromosome 7 (human)Base CompositionChromosomes Human Pair 11Nuclear ProteinsChromosomeSequence Analysis DNALIM Domain ProteinsProtein-Tyrosine Kinasesmedicine.diseaseAT Rich SequenceGC Rich SequenceDNA-Binding ProteinsChromosome 3CpG IslandsChromosome 21Transcription FactorsCytogenetic and Genome Research
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