Search results for "Cell Cycle"

showing 10 items of 804 documents

JAK3/STAT5/6 Pathway Alterations Are Associated with Immune Deviation in CD8+ T Cells in Renal Cell Carcinoma Patients

2010

To investigate the molecular mechanisms underlying altered T cell response in renal cell carcinoma (RCC) patients, we compared autologous and allogeneic CD8(+) T cell responses against RCC line from RCC patients and their HLA-matched donors, using mixed lymphocyte/tumor cell cultures (MLTCs). In addition, we analyzed the expression of molecules associated with cell cycle regulation. Autologous MLTC responder CD8(+) T cells showed cytotoxic activity against RCC cell lines; however the analysis of the distribution of CD8(+) T-cell subsets revealed that allogenic counterparts mediate superior antitumor efficacy. In RCC patients, a decreased proliferative response to tumor, associated with defe…

Article SubjectCell Survivallcsh:Biotechnologylcsh:MedicineEnzyme-Linked Immunosorbent AssayE2F4 Transcription FactorCD8-Positive T-Lymphocytesurologic and male genital diseaseslcsh:TP248.13-248.65Chromium IsotopesSTAT5 Transcription FactorTumor Cells CulturedHumansCarcinoma Renal CellInhibitor of Differentiation Protein 2Microscopy Confocallcsh:RCell CycleIntracellular Signaling Peptides and ProteinsJanus Kinase 3Flow Cytometryfemale genital diseases and pregnancy complicationsKidney NeoplasmsGene Expression Regulation NeoplasticCase-Control StudiesLymphocyte Culture Test MixedSTAT6 Transcription FactorCyclin-Dependent Kinase Inhibitor p27Research ArticleSignal TransductionJournal of Biomedicine and Biotechnology
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Septins 2, 7 and 9 and MAP4 colocalize along the axoneme in the primary cilium and control ciliary length

2013

International audience; Septins are a large, evolutionarily conserved family of GTPases that form hetero-oligomers and interact with the actin-based cytoskeleton and microtubules. They are involved in scaffolding functions, and form diffusion barriers in budding yeast, the sperm flagellum and the base of primary cilia of kidney epithelial cells. We investigated the role of septins in the primary cilium of retinal pigmented epithelial (RPE) cells, and found that SEPT2 forms a 1:1:1 complex with SEPT7 and SEPT9 and that the three members of this complex colocalize along the length of the axoneme. Similar to observations in kidney epithelial cells, depletion of cilium-localized septins by siRN…

AxonemeAxonemeMicrotubule-associated protein[SDV]Life Sciences [q-bio]DIFFUSION BARRIERTUBULINCell Cycle Proteinsmacromolecular substancesORGANIZATIONCYTOSKELETONBiologySeptinMicrotubulesRetinaCell Line03 medical and health sciences0302 clinical medicineMicrotubuleCiliogenesisHumansCiliaCytoskeletonMolecular BiologyAFFINITY-REGULATING KINASEActin030304 developmental biologyCILIOGENESIS0303 health sciencesPrimary ciliumCOMPLEXSperm flagellumCilium030302 biochemistry & molecular biologyColocalizationEpithelial CellsAnatomyCell BiologyActinsCell biology[SDV] Life Sciences [q-bio]MAMMALIAN SEPTINSMAP4CELLSbiological phenomena cell phenomena and immunityMicrotubule-Associated Proteins030217 neurology & neurosurgerySeptinsDevelopmental BiologyResearch Article
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Translational readthrough of ciliopathy genes BBS2 and ALMS1 restores protein, ciliogenesis and function in patient fibroblasts

2021

Abstract Background Ciliary dysfunction underlies a range of genetic disorders collectively termed ciliopathies, for which there are no treatments available. Bardet-Biedl syndrome (BBS) is characterised by multisystemic involvement, including rod-cone dystrophy and renal abnormalities. Together with Alstrom syndrome (AS), they are known as the ‘obesity ciliopathies’ due to their common phenotype. Nonsense mutations are responsible for approximately 11% and 40% of BBS and AS cases, respectively. Translational readthrough inducing drugs (TRIDs) can restore full-length protein bypassing in-frame premature termination codons, and are a potential therapeutic approach for nonsense-mediated ciliop…

BBS2AdultMaleMedicine (General)AdolescentNonsense mutationAminopyridinesCell Cycle ProteinsCiliopathiesGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundR5-920AtalurenCiliogenesismedicineHumansReceptors SomatostatinBardet-Biedl SyndromeAlstrom SyndromeCells CulturedOxadiazolesbusiness.industryTumor Suppressor ProteinsTranslational readthroughRProteinsGeneral MedicineFibroblastsmedicine.diseaseNonsense suppressionCiliopathiesAtalurenCiliopathyALMS1chemistryCodon NonsenseAmlexanoxCancer researchMedicineBBS2businessAlström syndromeResearch PaperEBioMedicine
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Pathogenic correlation between mosaic variegated aneuploidy 1 (MVA1) and a novel BUB1B variant: a reappraisal of a severe syndrome.

2022

Funder: Università degli Studi di Catania

BUB1B gene Epileptic seizure Microcephaly Mosaic variegated aneuploidy 1 (MVA1) syndrome Ovary cystMosaicismCell Cycle ProteinsOvary cystDermatologyGeneral MedicineSyndromeBUB1B geneProtein Serine-Threonine KinasesAneuploidyPsychiatry and Mental healthSeizuresMosaic variegated aneuploidy 1 (MVA1) syndromeMutationEpileptic seizureMicrocephalyHumansNeurology (clinical)Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Performance of QuantiFERON-TB Gold Plus for detection of latent tuberculosis infection in pregnant women living in a tuberculosis- and HIV-endemic se…

2017

We evaluated the performance of QuantiFERON-TB Gold Plus (QFT-Plus), which includes two Mycobacterium tuberculosis antigen formulations (TB1 and TB2), for detection of latent tuberculosis infection during pregnancy. Eight-hundred-twenty-nine Ethiopian pregnant women (5.9% HIV-positive) were tested with QFT-Plus, with bacteriological sputum analysis performed for women with clinically suspected tuberculosis and HIV-positive women irrespective of clinical presentation. QFT-Plus read-out was categorized according to the conventional cut-off (0.35 IU/ml) for both antigen formulations. In addition, we analysed the distribution of QFT-Plus results within a borderline zone (0.20–0.70 IU/ml), and i…

Bacterial DiseasesRNA virusesPhysiologyMaternal Healthlcsh:MedicineHIV InfectionsPathology and Laboratory MedicineGastroenterologyWhite Blood Cells0302 clinical medicineImmunodeficiency VirusesPregnancyAnimal CellsMedicine and Health SciencesCell Cycle and Cell Division030212 general & internal medicinePregnancy Complications InfectiousYoung adultlcsh:ScienceMultidisciplinarybiologyLatent tuberculosisT CellsObstetrics and GynecologyGestational ageActinobacteriaInfectious DiseasesMedical MicrobiologyCell ProcessesViral PathogensVirusesFemalePathogensCellular Typesmedicine.symptomResearch ArticleAdultmedicine.medical_specialtyTuberculosisImmune CellsImmunologyViral diseasesMicrobiologyMycobacterium tuberculosisInterferon-gammaYoung Adult03 medical and health sciencesAntigenLatent TuberculosisInternal medicineRetrovirusesmedicineHumansTuberculosisMicrobial PathogensSecretionPregnancyBlood CellsBacteriaTuberculin Testbusiness.industryLentiviruslcsh:ROrganismsHIVBiology and Life SciencesMycobacterium tuberculosisCell BiologyTropical Diseasesbiology.organism_classificationmedicine.disease030228 respiratory systemWomen's HealthSputumlcsh:QEthiopiaMitogensPhysiological ProcessesbusinessInterferon-gamma Release TestsPLOS ONE
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Synthesis, antiproliferative activity, and mechanism of action of new benzamido derivatives

2011

The cinnamoyl anthranilamides represent a class of biological active substances of great importance in medicinal chemistry. Moreover, despite their wide range of biological activities, a review of the literature revealed that no anticancer activity is described for this kind of substances. Starting from the 2-cinnamamido-5-iodobenzamide, resulted able to inhibit the leukemic cell line K-562 proliferation with a percent of inhibition of 74% at 10M concentration, we undertake the following structural modifications on cinnamamidobenzamide skeleton: the introduction of various substituents both on the benzamido and the cinnamamido moieties, the substitution of olefinic bond with the ethane, et…

Benzamido derivatives antiproliferative activity cell cycleSettore CHIM/08 - Chimica Farmaceutica
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Synthesis and Biological Properties of Benzothiazole, Benzoxazole, and Chromen-4-one Analogues of the Potent Antitumor Agent 2-(3,4-Dimethoxyphenyl)-…

2008

New fluorinated 2-aryl-benzothiazoles, -benzoxazoles, and -chromen-4-ones have been synthesized and their activity against MCF-7 and MDA 468 breast cancer cell lines compared with the potent antitumor benzothiazole 5. Analogues such as 9a, b and 12a, d yielded submicromolar GI50 values in both cell lines; however, none of the new compounds approached 5 in terms of antitumor potency. For 5, binding to the aryl hydrocarbon receptor appeared to be necessary but not sufficient for growth inhibition.

BenzoxazolesBicyclic moleculebiologyStereochemistryCell CycleAntineoplastic AgentsBreast NeoplasmsBenzoxazoleAryl hydrocarbon receptorChemical synthesisIn vitroStructure-Activity Relationshipchemistry.chemical_compoundReceptors Aryl HydrocarbonchemistryBenzothiazoleCell Line TumorDrug Discoverybiology.proteinHumansMolecular MedicineStructure–activity relationshipBenzopyransBenzothiazolesGrowth inhibitionJournal of Medicinal Chemistry
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TORC1 coordinates the conversion of Sic1 from a target to an inhibitor of cyclin-CDK-Cks1

2017

Eukaryotic cell cycle progression through G(1)-S is driven by hormonal and growth-related signals that are transmitted by the target of rapamycin complex 1 (TORC1) pathway. In yeast, inactivation of TORC1 restricts G(1)-S transition due to the rapid clearance of G(1) cyclins (Cln) and the stabilization of the B-type cyclin (Clb) cyclin-dependent kinase (CDK) inhibitor Sic1. The latter mechanism remains mysterious but requires the phosphorylation of Sic1-Thr(173) by Mpk1 and inactivation of the Sic1-pThr(173)-targeting phosphatase (PP2A(Cdc55)) through greatwall kinase-activated endosulfines. Here we show that the Sic1-pThr(173) residue serves as a specific docking site for the CDK phospho-a…

BioquímicaBiologiaCDK inhibitor (CDKI)Rim15Sic1cyclin-dependent protein kinase (CDK)G1 cell cycle arrestgreatwall kinase pathwayG(1) cell cycle arrestCks1Articletarget of rapamycin complex 1 (TORC1)Cell Discovery
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TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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