Search results for " Cell Cycle Proteins"

showing 5 items of 5 documents

Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
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Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro-uracil sensitivity in human derived colon cancer…

2009

International audience; Epidemiological studies suggested that trans-resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans-resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, epsilon-viniferin and its acetylated form, epsilon-viniferin penta-acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans-resveratrol and epsilon-viniferin. We show here that resveratrol triacetat…

Cancer ResearchCyclin AFluorescent Antibody TechniqueCell Cycle ProteinsMESH: Cell CycleMESH: Flow CytometryMESH : Blotting WesternResveratrolmedicine.disease_causeWine grapeMESH: Drug SynergismImmunoenzyme Techniqueschemistry.chemical_compoundMESH: PhenolsMESH : Cell Cycle ProteinsMESH : Tumor Cells CulturedMESH: StilbenesStilbenesTumor Cells CulturedMESH : Cell ProliferationMESH: Fluorescent Antibody TechniqueMESH: Antimetabolites AntineoplasticbiologyKinaseMESH : Antimetabolites AntineoplasticCell Cyclefood and beveragesDrug SynergismCell cycleFlow CytometryMESH : Colonic NeoplasmsOncologyBiochemistryColonic NeoplasmsMESH : FluorouracilFluorouracilMESH : PhenolsAntimetabolites AntineoplasticMESH : Drug SynergismMESH : Flow CytometryBlotting WesternMESH : ImmunoprecipitationMESH : StilbenesMESH: Cell Cycle ProteinsPhenolsMESH : Immunoenzyme TechniquesMESH: Cell ProliferationMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansImmunoprecipitationMESH: Blotting Western[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Tumor Cells CulturedKinase activityMESH: Immunoenzyme Techniques[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBenzofuransCell ProliferationMESH: Colonic NeoplasmsMESH: HumansMESH : BenzofuransMESH: ImmunoprecipitationMESH : HumansMESH: BenzofuransMESH : Fluorescent Antibody TechniquechemistryResveratrolCell culturebiology.proteinCarcinogenesisMESH: Fluorouracil
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Use of CDC2 from etoposide-treated cells as substrate to assay CDC25 phosphatase activity

1999

International audience; Cyclin-dependent kinases (CDKs) regulate the key transition of the cell cycle in all organisms. In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Here we report that upon Etoposide treatment CDC2 is phosphorylated on tyrosine 15 and is dephosphorylated and activated in vitro by recombinant CDC25 phosphatase. We also show that inactive CDC2 kinase from Etoposide-treated cells can be used as a substrate in a sensitive two-step assay of CDC25 phosphatase. This assay, which is very simple to set-up, is based on the monitoring of CDC2 kinase activity after CDC25-depe…

MESH: HumansMESH: Phosphorylation[SDV]Life Sciences [q-bio]Cell Cycle Proteins[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]MESH: CDC2 Protein KinaseMESH: Tyrosine[SDV] Life Sciences [q-bio]AGENT ANTITUMORALenzymes and coenzymes (carbohydrates)MESH: Cell Cycle ProteinsMESH: cdc25 PhosphatasesCDC2 Protein KinaseMESH: HeLa CellsMESH: Phosphoprotein PhosphatasesPhosphoprotein PhosphatasesHumansTyrosinecdc25 PhosphatasesPhosphorylationbiological phenomena cell phenomena and immunityEtoposideHeLa CellsMESH: Etoposide
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Let-7d miRNA Shows Both Antioncogenic and Oncogenic Functions in Osteosarcoma-Derived 3AB-OS Cancer Stem Cells

2015

Osteosarcoma (OS), an aggressive highly invasive and metastatic bone-malignancy, shows therapy resistance and recurrence, two features that likely depend on cancer stem cells (CSCs), which hold both self-renewing and malignant potential. So, effective anticancer therapies against OS should specifically target and destroy CSCs. We previously found that the let-7d microRNA was downregulated in the 3AB-OS-CSCs, derived from the human OS-MG63 cells. Here, we aimed to assess whether let-7d modulation affected tumorigenic and stemness properties of these OS-CSCs. We found that let-7d-overexpression reduced cell proliferation by decreasing CCND2 and E2F2 cell-cycle-activators and increasing p21 an…

Time FactorsEpithelial-Mesenchymal TransitionTime FactorTranscription FactorPhysiologyClinical BiochemistryDrug ResistanceAntineoplastic AgentsApoptosisBone NeoplasmsCell Cycle ProteinsBone NeoplasmTransfectionCell LineAntineoplastic AgentCell MovementCell Line TumorCell Cycle ProteinHumansNeoplasm InvasivenessCell Self RenewalAntineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Bone Neoplasms; Cell Cycle; Cell Cycle Proteins; Cell Line Tumor; Cell Movement; Cell Self Renewal; Drug Resistance Neoplasm; Epithelial-Mesenchymal Transition; Gene Expression Regulation Neoplastic; Humans; MicroRNAs; Neoplasm Invasiveness; Neoplastic Stem Cells; Osteosarcoma; Phenotype; Signal Transduction; Time Factors; Transcription Factors; Transfection; Physiology; Medicine (all); Clinical Biochemistry; Cell BiologyNeoplasm InvasiveneNeoplasticOsteosarcomaTumorApoptosis Regulatory ProteinMedicine (all)Cell CycleApoptosiMicroRNACell BiologyGene Expression Regulation NeoplasticMicroRNAsPhenotypeGene Expression RegulationDrug Resistance NeoplasmNeoplastic Stem CellsNeoplasmNeoplastic Stem CellApoptosis Regulatory ProteinsTranscription FactorsHumanSignal Transduction
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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