Search results for "CDC"

showing 10 items of 88 documents

GTPases of the Rho Subfamily Are Required for Brucella abortus Internalization in Nonprofessional Phagocytes

2001

Members of the genus Brucella are intracellular -Proteobacteria responsible for brucellosis, a chronic disease of humans and animals. Little is known about Brucella virulence mechanisms, but the abilities of these bacteria to invade and to survive within cells are decisive factors for causing disease. Transmission electron and fluorescence microscopy of infected nonprofessional phagocytic HeLa cells revealed minor membrane changes accompanied by discrete recruitment of F-actin at the site of Brucella abortus entry. Cell uptake of B. abortus was negatively affected to various degrees by actin, actin-myosin, and microtubule chemical inhibitors. Modulators of MAPKs and protein-tyrosine kinases…

biologymedia_common.quotation_subjectIntracellular parasiteBRUCELLA ABORTUSVirulenceCell BiologyCDC42BrucellaGTPasebiology.organism_classificationBiochemistryMicrobiologyBRUCELOSISCytotoxic T cellBRUCELLAESCHERICHIA COLIBACTERIASInternalizationMolecular BiologyIntracellularmedia_commonJournal of Biological Chemistry
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On Cancer Cell Cycle and Universal Apoptosis Parameters Signaling Unravelled In Silico

2010

Here, cell cycle in higher eukaryotes and their molecular networks signals both in G1/S and G2/M transitions are in silico replicated. Systems control theory is employed to design multi-nestled digital layers to simulate protein-to- protein activation and inhibition in the cancer cell cycle dynamics in presence of damaged genome. Sequencing and controlling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage; p21mRNA/cyclin-CDK complex; CDK/CDC25/wee1/SKP2/APC/CKI and apoptosis target genes system) paved the way for unravelling the participants and their by-products having the task to execute (or not) cell death. The results of the proposed cell digital multi-layers…

Programmed cell deathWee1Cell signalingCell cycle checkpointbiologyCdc25Cyclin-dependent kinaseIn silicobiology.proteinCell cycleCell biologyThe Open Conference Proceedings Journal
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MCC1019, a selective inhibitor of the Polo-box domain of Polo-like kinase 1 as novel, potent anticancer candidate

2019

Polo-like kinase (PLK1) has been identified as a potential target for cancer treatment. Although a number of small molecules have been investigated as PLK1 inhibitors, many of which showed limited selectivity. PLK1 harbors a regulatory domain, the Polo box domain (PBD), which has a key regulatory function for kinase activity and substrate recognition. We report on 3-bromomethyl-benzofuran-2-carboxylic acid ethyl ester (designated: MCC1019) as selective PLK1 inhibitor targeting PLK1 PBD. Cytotoxicity and fluorescence polarization-based screening were applied to a library of 1162 drug-like compounds to identify potential inhibitors of PLK1 PBD. The activity of compound MC1019 against the PLK1…

PBD Polo box domainMTD maximal tolerance doseCDC25 cell division cycle 25HIF-1α hypoxia-inducible factor 1 αMST microscale thermophoresisIC50 50% inhibition concentrationMFP M phase promoting factorPARP-1 poly(ADP-ribose) polymerase-10302 clinical medicineFOXO forkhead box ONec-1 necrostatin 1CDC2 cell division cycle protein 2 homologGeneral Pharmacology Toxicology and PharmaceuticsMitotic catastropheCDK cyclin-dependent kinase0303 health sciencesChemistryPolo-like kinaseMono-targeted therapyCell cycleBUBR1 budding uninhibited by benzimidazole-related 1Polo box domain030220 oncology & carcinogenesisPLK1 Polo-like kinaseNecroptosisSpindle damagePLK1IHC immunohistochemistryOriginal articleNecroptosisCell cyclePLK1APC/C anaphase-promoting complex/cyclosomePLK3ABC avidin-biotin complexPI propidium iodide03 medical and health sciencesFBS fetal bovine serumPDB Protein Data BankKd the dissociation constantKinase activity030304 developmental biologyAkt/PKB signaling pathwayCell growthlcsh:RM1-950LC3 light chain 3lcsh:Therapeutics. PharmacologyCancer researchDAPKs death-associated protein kinase3-MA 3-methyladenineDAPI 4′6-diamidino-2-phenylindoleSAC spindle assembly checkpointActa Pharmaceutica Sinica B
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Ikaros-1 couples cell cycle arrest of late striatal precursors with neurogenesis of enkephalinergic neurons

2010

et al.

Cyclin-Dependent Kinase Inhibitor p21CalbindinsEnkephalinNeurogenesiseducationCentral nervous systemCell Cycle ProteinsStriatumSubstance PBiologyEfferent PathwaysCalbindinIkaros Transcription FactorMiceS100 Calcium Binding Protein GmedicineAnimalsProgenitor cellTranscription factorhealth care economics and organizationsHomeodomain ProteinsMice KnockoutNeuronsStem CellsGeneral NeuroscienceNeurogenesisCell DifferentiationEnkephalinsCell cycleCorpus StriatumGenes cdcMice Inbred C57BLmedicine.anatomical_structurenervous systemTrans-ActivatorsNeuroscienceTranscription FactorsThe Journal of Comparative Neurology
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Rho GTPases in human breast tumours: expression and mutation analyses and correlation with clinical parameters

2002

In the present study, we addressed the question of a putative relevance of Rho proteins in tumour progression by analysing their expression on protein and mRNA level in breast tumours. We show that the level of RhoA, RhoB, Rac1 and Cdc42 protein is largely enhanced in all tumour samples analysed (n=15) as compared to normal tissues originating from the same individual. The same is true for 32P-ADP-ribosylation of Rho proteins which is catalysed by Clostridium botulinum exoenzyme C3. Also the amount of Rho-GDI and ERK2 as well as the level of overall 32P-GTP binding acvitity was tumour-specific elevated, yet to a lower extent than Rho proteins. Although the amount of Rho proteins was enhance…

rac1 GTP-Binding Proteinrho GTP-Binding ProteinsCancer ResearchRHOAProliferation indexRHOBBlotting WesternDNA Mutational AnalysisRhoCGene ExpressionBreast NeoplasmsRAC1breast tumoursCDC42Polymerase Chain ReactionRho GTPasesRhoB GTP-Binding ProteinHumansBreastRNA Messengercdc42 GTP-Binding ProteinrhoB GTP-Binding Proteinmutation analysisADP Ribose TransferasesMitogen-Activated Protein Kinase 1biologyGenetics and GenomicsMolecular biologyOncologyCdc42 GTP-Binding ProteinMutationtumour progressionDisease Progressionbiology.proteinFemaleGuanosine TriphosphaterhoA GTP-Binding ProteinBritish Journal of Cancer
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Translocation of cdk2 to the nucleus during G1-phase in PDGF-stimulated human fibroblasts.

1997

We studied the subcellular distribution of cdk2 in synchronized, PDGF-stimulated human fibroblasts (FH109). After contact inhibition and serum depletion, more than 95% of FH109 cells were arrested in G0/G1-phase. PDGF-AB led to a 16-fold increase in proliferation compared with untreated cells. Cell cycle progression was studied by flow cytometric analysis, [3H]thymidine incorporation, and phosphorylation of the retinoblastoma gene product, pRB. Using Western blot analysis after subcellular fractionation, we revealed that after PDGF stimulation the phosphorylated (Thr 160), i.e., activated, form of cdk2 (33 kDa) first appeared in the nucleus at late G1-phase and persisted throughout until to…

CytoplasmFluorescent Antibody TechniqueProtein Serine-Threonine KinasesmedicineCDC2-CDC28 KinasesHumansCells CulturedCell NucleusPlatelet-Derived Growth FactorbiologyKinaseCyclin-dependent kinase 2Cyclin-Dependent Kinase 2G1 PhaseContact inhibitionBiological TransportCell BiologyCell cycleFibroblastsMolecular biologyCyclin-Dependent KinasesCell biologyCell CompartmentationCytosolmedicine.anatomical_structurebiology.proteinCell fractionationNucleusPlatelet-derived growth factor receptorCyclin-Dependent Kinase-Activating KinaseExperimental cell research
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In silico identification of small molecules as new cdc25 inhibitors through the correlation between chemosensitivity and protein expression pattern

2021

The cell division cycle 25 (Cdc25) protein family plays a crucial role in controlling cell proliferation, making it an excellent target for cancer therapy. In this work, a set of small molecules were identified as Cdc25 modulators by applying a mixed ligand-structure-based approach and taking advantage of the correlation between the chemosensitivity of selected structures and the protein expression pattern of the proposed target. In the first step of the in silico protocol, a set of molecules acting as Cdc25 inhibitors were identified through a new ligand-based protocol and the evaluation of a large database of molecular structures. Subsequently, induced-fit docking (IFD) studies allowed us…

0301 basic medicineHepG2Protein familyCdc25In silicoAntiproliferative activityCell cycleLigandsCatalysisArticleInorganic Chemistrylcsh:Chemistry03 medical and health sciencesCdc250302 clinical medicineCDC2 Protein KinaseDrug DiscoveryHumanscdc25 PhosphatasesComputer SimulationMolecular Targeted TherapyPhysical and Theoretical ChemistryPhosphorylationMolecular Biologylcsh:QH301-705.5DRUDITSpectroscopyBinding SitesbiologyCell growthChemistryOrganic ChemistryGeneral MedicineHep G2 CellsCell cycleAntiproliferative activity; Cdc25; Cell cycle; DRUDIT; HepG2; Molecular dockingLigand (biochemistry)Small moleculeComputer Science Applications030104 developmental biologyBiochemistrylcsh:Biology (General)lcsh:QD1-999Docking (molecular)030220 oncology & carcinogenesisMolecular dockingbiology.proteinDrug Screening Assays Antitumor
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Resveratrol, a chemopreventive agent, disrupts the cell cycle control of human SW480 colorectal tumor cells

2002

Resveratrol is a natural polyphenolic compound produced by a number of plants and found in high amount in peanuts, seeds, grapes or berries as source of human nutrition. Epidemiological studies strongly suggest that resveratrol may act as a cancer chemopreventive compound. The mechanism by which resveratrol inhibits cell proliferation was studied in human colorectal tumor SW480 cell line. The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner. Resveratrol appears to block the cell cycle at the transition --> G2/M since inhibition of [(3)H]-thymidine incorporation is not observed, while there is an increase of the c…

DNA Replicationendocrine system diseasesCellCyclin AAdenocarcinomaCyclin BProtein Serine-Threonine KinasesResveratrolS Phasechemistry.chemical_compoundCDC2 Protein KinaseStilbenesCDC2-CDC28 KinasesTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansCyclin B1Phosphorylationskin and connective tissue diseasesCyclinCyclin-dependent kinase 1biologyKinaseCell growthorganic chemicalsCell CycleCyclin-Dependent Kinase 2Cyclin-dependent kinase 2food and beveragesGeneral MedicineCell cycleFlow CytometryCyclin-Dependent KinasesGrowth InhibitorsNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureBiochemistrychemistryResveratrolEnzyme Inductionbiology.proteinCancer researchColorectal NeoplasmsProtein Processing Post-TranslationalCell DivisionInternational Journal of Molecular Medicine
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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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