Search results for "5'"

showing 10 items of 358 documents

CCDC 868802: Experimental Crystal Structure Determination

2012

Related Article: A.Cornia, F.Felluga, V.Frenna, F.Ghelfi, A.F.Parsons, M.Pattarozzi, F.Roncaglia, D.Spinelli|2012|Tetrahedron|68|5863|doi:10.1016/j.tet.2012.04.117

66'-Diethyl-77'-diphenyl-22'33'-tetrahydro-5H5'H-7a7a'-bipyrrolo[21-b][13]thiazole-55'-dioneSpace GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death

2011

Abstract Extracellular adenosine (ADO), generated from ATP or ADP through the concerted action of the ectoenzymes CD39 and CD73, elicits autocrine and paracrine effects mediated by type 1 purinergic receptors. We have tested whether the expression of CD39 and CD73 by chronic lymphocytic leukemia (CLL) cells activates an adenosinergic axis affecting growth and survival. By immunohistochemistry, CD39 is widely expressed in CLL lymph nodes, whereas CD73 is restricted to proliferation centers. CD73 expression is highest on Ki-67+ CLL cells, adjacent to T lymphocytes, and is further localized to perivascular areas. CD39+/CD73+ CLL cells generate ADO from ADP in a time- and concentration-dependen…

AdenosineCellular differentiationChronic lymphocytic leukemia5'-Nucleotidase; Adenosine; Adenosine Diphosphate; Adenosine Triphosphate; Antigens CD; Antineoplastic Agents Phytogenic; Apyrase; Autocrine Communication; Cell Death; Cell Differentiation; Cell Movement; Cell Survival; Etoposide; Extracellular Space; GPI-Linked Proteins; Humans; Leukemia Lymphocytic Chronic B-Cell; Paracrine Communication; Receptor Adenosine A2A; Tumor Cells Cultured; Biochemistry; Immunology; Hematology; Cell BiologyMICROENVIRONMENTCD38BiochemistryACTIVATIONAdenosine TriphosphateCell MovementPhytogenichemic and lymphatic diseasesTumor Cells CulturedChronic5'-NucleotidaseEtoposideLeukemiaCulturedCell DeathTUMOR-GROWTHApyrasePurinergic receptorCell DifferentiationHematologyLymphocyticCDTumor CellsCell biologyAdenosine DiphosphateAutocrine CommunicationLeukemiaReceptorIMMUNE SUPPRESSIONReceptor Adenosine A2ACell SurvivalImmunologyAntineoplastic AgentsAdenosinergicBiologyGPI-Linked ProteinsDAMAGE-INDUCED APOPTOSISAdenosine A2AParacrine signallingAntigens CDParacrine CommunicationmedicineHumansAntigensAutocrine signallingImmunobiologyB-CellCell BiologyDAMAGE-INDUCED APOPTOSIS; T-CELLS; IMMUNE SUPPRESSION; ZAP-70 EXPRESSION; TUMOR-GROWTH; RECEPTOR; CD73; ACTIVATION; CD38; MICROENVIRONMENTmedicine.diseaseAntineoplastic Agents PhytogenicLeukemia Lymphocytic Chronic B-CellSettore MED/15 - MALATTIE DEL SANGUET-CELLSCD73Extracellular SpaceZAP-70 EXPRESSIONCD38Blood
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Production of Adenosine by Ectonucleotidases: A Key Factor in Tumor Immunoescape

2012

It is now well known that tumor immunosurveillance contributes to the control of cancer growth. Many mechanisms can be used by cancer cells to avoid the antitumor immune response. One such mechanism relies on the capacity of cancer cells or more generally of the tumor microenvironment to generate adenosine, a major molecule involved in antitumor T cell response suppression. Adenosine is generated by the dephosphorylation of extracellular ATP released by dying tumor cells. The conversion of ATP into adenosine is mediated by ectonucleotidase molecules, namely, CD73 and CD39. These molecules are frequently expressed in the tumor bed by a wide range of cells including tumor cells, regulatory T …

AdenosineStromal cellArticle SubjectHealth Toxicology and Mutagenesislcsh:Biotechnologylcsh:MedicineAntineoplastic AgentsBiologyPharmacology5'-nucleotidaseDephosphorylationImmune systemNeoplasmslcsh:TP248.13-248.65GeneticsmedicineAnimalsHumansEctonucleotidaseMolecular Targeted Therapy5'-NucleotidaseMolecular BiologyImmune EvasionTumor microenvironmentlcsh:RGeneral MedicineAdenosineCancer cellCancer researchMolecular MedicineResearch ArticleBiotechnologymedicine.drugJournal of Biomedicine and Biotechnology
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Controversies on the role of Th17 in cancer: a TGF-β-dependent immunosuppressive activity?

2012

The immune system has important roles in limiting the spread of cancer and shaping the tumor microenvironment. Although the contributions of T helper 17 (Th17) cells (a subtype of CD4(+) T lymphocytes) to autoimmunity and allergy response are well known, their roles in cancer remain ambiguous. Despite adoptive transfer studies indicating that mouse Th17 cells support anticancer immunity, the Th17 cells that naturally infiltrate experimental tumors appear to have a tumor-promoting effect. These contradictory properties can be related to the high degree of plasticity inherent in Th17 cells and their capacity to differentiate into tumoricidal Th1-like cells. Mouse Th17 cells induced by transfo…

Adoptive cell transferAngiogenesisAntigen-Presenting Cellschemical and pharmacologic phenomenaBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciences0302 clinical medicineImmune systemAntigenAntigens CDTransforming Growth Factor betaImmunityNeoplasmsImmune TolerancemedicineAnimals5'-NucleotidaseMolecular Biology030304 developmental biologyImmunity Cellular0303 health sciencesTumor microenvironmentNeovascularization PathologicApyraseModels ImmunologicalCell DifferentiationTh1 Cells3. Good health030220 oncology & carcinogenesisImmunologyCancer researchTh17 CellsMolecular MedicineTransforming growth factorTrends in Molecular Medicine
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Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
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Thymidylate synthase gene promoter polymorphisms are associated with TSmRNA expressions but not with microsatellite instability in colorectal cancer

2005

Abstract BACKGROUND: Microsatellite instability (MSI) is a biological characteristic of most tumours, being involved in 85% of hereditary non-polyposis colorectal cancer (HNPCC). It also occurs in 10-15% of sporadic colorectal cancers (CRC). HNPCC appears to be caused by germline mutations in mismatch repair (MMR) genes, which are responsible for repairing single base-pair mismatches. MSI is also associated with a better response of CRC to adjuvant chemotherapy with fluoropyrimidines. We investigated any relationship between the MSI status and the TSmRNA expression, the polymorphisms of 5-Fluorouracil (5-FU cellular target, the enzyme thymidylate synthase (TS) and TS expression evaluated by…

AdultAged 80 and overMalePolymorphism GeneticAntibodies MonoclonalThymidylate SynthaseMiddle AgedSettore MED/08 - Anatomia PatologicaImmunohistochemistryGenomic InstabilityHumansFemaleColorectal cancer thymidylate synthase pharmacogenomic microsatellite instability polymorphism molecular therapeutic.RNA Messenger5' Untranslated RegionsColorectal NeoplasmsPromoter Regions GeneticAgedMicrosatellite Repeats
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β-Adrenoceptor stimulation up-regulates phosphodiesterase 4 activity and reduces prostaglandin E 2 -inhibitory effects in human neutrophils

2000

Human neutrophils were treated for 4 h with a combination of salbutamol (1 µM), a β2-adrenoceptor agonist, and rolipram (30 µM), a selective phosphodiesterase 4 inhibitor, to investigate whether this treatment produces up-regulation of phosphodiesterase activity with functional consequences. Anion-exchange chromatography coupled with the use of selective activators and inhibitors demonstrated that a phosphodiesterase activity with characteristics of the isoenzyme type 4 was increased in drug-treated cells. Kinetic analysis showed a ~1.5-fold increase in V max without alteration of K m values. The augmented phosphodiesterase activity in drug-treated cells was abolished by actinomycin D. Cycl…

AdultAgonistmedicine.medical_specialtyNeutrophilsmedicine.drug_classStimulationIn Vitro TechniquesBiologyDinoprostoneNeutrophil Activationchemistry.chemical_compoundPDE4BDownregulation and upregulationSuperoxidesInternal medicineCyclic AMPmedicineHumansAlbuterolRNA MessengerEnzyme InhibitorsProstaglandin E2RolipramPharmacologyReverse Transcriptase Polymerase Chain ReactionSuperoxideZymosanZymosanGeneral MedicineAdrenergic AgonistsCyclic Nucleotide Phosphodiesterases Type 4Up-RegulationEndocrinologychemistry3'5'-Cyclic-AMP PhosphodiesterasesReceptors Adrenergic beta-2Roliprammedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Relaxation and cyclic GMP levels in response to sildenafil in human pulmonary arteries from donors.

2005

We measured cyclic GMP formation and relaxation response to sildenafil given either alone or in combination with sodium nitroprusside (SNP) in pulmonary arteries obtained from 13 multi-organ donors. Sildenafil (10(-9)-10(-4) M) caused concentration-dependent relaxations and amplified the relaxation induced by SNP. Relaxation was unaffected by endothelium removal or by pre-treatment with the inhibitor of nitric oxide synthase L-NMMA (10(-4) M). SNP (10(-7) M) caused elevation of cyclic GMP levels that was potentiated by sildenafil (10(-6) M). Thus, the enhancement of SNP-induced relaxation by sildenafil is mainly due to an increase in cyclic GMP accumulation.

AdultMaleNitroprussideEndotheliumSildenafilPhosphodiesterase InhibitorsVasodilator AgentsVasodilationPharmacologyIn Vitro TechniquesPulmonary ArteryPiperazinesSildenafil CitrateNitric oxidechemistry.chemical_compound3'5'-Cyclic-GMP PhosphodiesterasesmedicineHumansNitric Oxide DonorsSulfonesCyclic GMPPharmacologybiologyChemistryDrug SynergismMiddle Agedrespiratory tract diseasesNitric oxide synthaseVasodilationmedicine.anatomical_structureBiochemistryEnzyme inhibitorPurinesCirculatory systemcardiovascular systembiology.proteinFemaleSodium nitroprussidemedicine.drugEuropean journal of pharmacology
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Analysis of genetic variations of protein tyrosine kinase fyn and their association with alcohol dependence in two independent cohorts.

2003

Abstract Background Decreased sensitivity to and increased tolerance for the effects of alcohol is a phenotype, which was shown to be associated with an increased risk for alcoholism in humans and was observed in protein tyrosine kinase (PTK) fyn knockout mice. Methods We performed an association study of genetic variations of PTK fyn in 430 alcohol-dependent patients and 365 unrelated control subjects from two independent samples. Results In a combined analysis, we found an association of alcohol dependence with the single nucleotide polymorphism (SNP) T137346C in the 5′ untranslated region (UTR) of the gene. A relevant association could be excluded for the remaining two informative SNPs. …

AdultMaleThreonineLinkage disequilibriumGenotypeGlycineSingle-nucleotide polymorphismBiologyProto-Oncogene Proteins c-fynPolymorphism Single NucleotideCohort StudiesFYNGene FrequencyProto-Oncogene ProteinsGenotypeSNPHumansCysteineAlleleBiological PsychiatryGeneticsAlanineChi-Square DistributionAlcohol dependenceGenetic VariationMiddle AgedAlcoholismCase-Control StudiesFemale5' Untranslated RegionsTyrosine kinaseBiological psychiatry
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Associations between polymorphisms in the thymidylate synthase gene, the expression of thymidylate synthase mRNA and the microsatellite instability p…

2004

Microsatellite instability (MSI) is a characteristic feature of up to 15% of colorectal cancers (CRC) and is associated with better response to adjuvant chemotherapy with 5-fluorouracil (5-FU). In this study we have investigated the association between the MSI status and the mRNA expression as well as the polymorphisms of the cellular target of 5-FU therapy, thymidylate synthase. Polymorphisms in the 3'- and the 5'-UTR of the TS gene were determined by a PCR assay in 53 colorectal cancer tissues. TS mRNA was quantified by real-time RT-PCR. Data were correlated with the MSI phenotype. There was neither a significant correlation between the polymorphisms in the TS gene and the MSI phenotype n…

AdultMaleUntranslated regionCancer ResearchGene ExpressionBiologyThymidylate synthaseGene expressionGenotypeBiomarkers TumormedicineHumansRNA MessengerGeneAgedAged 80 and overPolymorphism GeneticMicrosatellite instabilityCancerThymidylate SynthaseGeneral MedicineMiddle AgedPrognosismedicine.diseasePhenotypeMolecular biologydigestive system diseasesOncologyChemotherapy Adjuvantbiology.proteinCancer researchFemaleFluorouracil5' Untranslated RegionsColorectal NeoplasmsMicrosatellite RepeatsOncology Reports
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