Search results for " adenosine"

showing 10 items of 64 documents

Production of Extracellular Adenosine by CD73+ Dendritic Cells Is Crucial for Induction of Tolerance in Contact Hypersensitivity Reactions

2019

Dendritic cells (DCs) express the ecto-5′-nucleotidase CD73 that generates immunosuppressive adenosine (Ado) by dephosphorylation of extracellular Ado monophosphate and diphosphate. To investigate whether CD73-derived Ado has immune-suppressive activity, 2,4-dinitrothiocyanobenzene (DNTB) was applied to skin of wild-type (WT) or CD73-deficient (CD73–/–) mice, followed by sensitization and challenge with 2,4-dinitrofluorobenzene. In this model, we show the induction of tolerance by DNTB against 2,4-dinitrofluorobenzene only in WT but not in CD73–/– mice. Analysis of skin DCs showed increased expression of CD73 after application of DNTB in WT mice. That was accompanied by elevated concentrati…

0301 basic medicineAdenosine monophosphateLangerhans cellRegulatory T cellTransgeneCell BiologyDermatologyDendritic cellBiochemistryAdenosineCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structurechemistry030220 oncology & carcinogenesisExtracellularmedicineCyclic adenosine monophosphateMolecular Biologymedicine.drugJournal of Investigative Dermatology
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Singular Location and Signaling Profile of Adenosine A2A-Cannabinoid CB1 Receptor Heteromers in the Dorsal Striatum

2018

The dorsal striatum is a key node for many neurobiological processes such as motor activity, cognitive functions, and affective processes. The proper functioning of striatal neurons relies critically on metabotropic receptors. Specifically, the main adenosine and endocannabinoid receptors present in the striatum, ie, adenosine A(2A) receptor (A(2A)R) and cannabinoid CB1 receptor (CB1R), are of pivotal importance in the control of neuronal excitability. Facilitatory and inhibitory functional interactions between striatal A(2A)R and CB1R have been reported, and evidence supports that this cross-talk may rely, at least in part, on the formation of A(2A)R-CB1R heteromeric complexes. However, th…

0301 basic medicineCannabinoid receptorAdenosineReceptor Adenosine A2Amedicine.medical_treatmentAdenosinaAdenosine A2A receptormediated inhibitionStriatumBiologyhuntingtons-disease micecannabinoid CB1Mice03 medical and health sciencesglutamatergic neurotransmission0302 clinical medicineReceptor Cannabinoid CB1NeurobiologyNeural PathwaysBasal gangliamedicineAnimalsHumansendocannabinoid systemGenetically modified animalProtein Structure QuaternaryA(2A) receptorsPharmacologyEndocannabinoid systemCorpus Striatumprotein-coupled receptorsProtein SubunitsPsychiatry and Mental healthtransgenic mouse modelHuntington Disease030104 developmental biologyMetabotropic receptornervous systembasal gangliaCannabinoidallosteric interactionsNeuroscience030217 neurology & neurosurgeryNeurobiologiaSignal Transduction
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Feedback Regulation of Syk by Protein Kinase C in Human Platelets

2019

The spleen tyrosine kinase (Syk) is essential for immunoreceptor tyrosine-based activation motif (ITAM)-dependent platelet activation, and it is stimulated by Src-family kinase (SFK)-/Syk-mediated phosphorylation of Y352 (interdomain-B) and Y525/526 (kinase domain). Additional sites for Syk phosphorylation and protein interactions are known but remain elusive. Since Syk S297 phosphorylation (interdomain-B) was detected in platelets, we hypothesized that this phosphorylation site regulates Syk activity via protein kinase C (PKC)-and cyclic adenosine monophosphate (cAMP)-dependent pathways. ADP, the GPVI-agonist convulxin, and the GPIb&alpha

0301 basic medicineIndolesPlatelet AggregationSyk030204 cardiovascular system & hematologyenvironment and public healthMaleimideslcsh:Chemistrychemistry.chemical_compound0302 clinical medicinePhosphorylationlcsh:QH301-705.5SpectroscopyFeedback PhysiologicalKinaseConvulxinhemic and immune systemsGeneral MedicineComputer Science ApplicationsCell biologyAdenosine DiphosphateplateletsPhosphorylationbiological phenomena cell phenomena and immunityBlood Plateletschemical and pharmacologic phenomenaViper Venomsspleen tyrosine kinase (Syk)CatalysisArticleInorganic Chemistryglycoprotein VIglycoprotein Ibα03 medical and health sciencesCrotalid VenomsHumansSyk KinaseCyclic adenosine monophosphateLectins C-TypePlatelet activationPhysical and Theoretical ChemistryMolecular BiologyProtein kinase CPhospholipase C gammaOrganic Chemistryenzymes and coenzymes (carbohydrates)030104 developmental biologyProtein kinase domainchemistrylcsh:Biology (General)lcsh:QD1-999Calciumcyclic adenosine monophosphate (cAMP)protein kinase CInternational Journal of Molecular Sciences
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The role of extracellular calcium in bone metastasis

2016

AbstractThis review summarizes the role of extracellular calcium, as found present in the bone tissue, in the process of bone metastasis.

0301 basic medicinelcsh:Diseases of the musculoskeletal systemIGF insulin-like growth factorPGE-2 prostaglandin E-2Bone tissueFibroblast growth factorM-CSF macrophage colony-stimulating factorPDGF platelet-derived growth factorBone remodelingSK3 small conductance calcium-activated potassium channel 30302 clinical medicineERK extracellular signal-regulated kinaseTGFβ transforming growth factor betaBMP's bone morphogenetic proteinsbiologyAKT AKT8 virus oncogene cellular homologBone metastasislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenshumanitiescAMP cyclic adenosine monophosphatemedicine.anatomical_structureOncologyRANKL030220 oncology & carcinogenesisIon channelsCaSR calcium-sensing receptorPTHrP parathyroid hormone-related proteinPlatelet-derived growth factor receptorResearch PaperTRP transient receptor potentialmedicine.medical_specialtychemistry.chemical_elementCalciumRANKL receptor activator of NF-κB ligandlcsh:RC254-28203 medical and health sciencesPLC phospholipase CInternal medicinemedicineExtracellularCaSRET-1 endothelin-1PTEN phosphatase and tensin homolog deleted on chromosome 10business.industryBone metastasismedicine.diseaseFGF fibroblast growth factor030104 developmental biologyEndocrinologyPSA prostate specific antigenchemistryCOPD chronic obstructive pulmonary diseasebiology.proteinCancer researchJNK jun N-terminal kinasePKA protein kinase ARANK receptor activator of NF-κBCalciumlcsh:RC925-935businessMAPK mitogen-activated protein kinaseJournal of Bone Oncology
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The cAMP pathway as therapeutic target in autoimmune and inflammatory diseases

2016

Nucleotide signaling molecules contribute to the regulation of cellular pathways. In the immune system, cyclic adenosine monophosphate (cAMP) is well established as a potent regulator of innate and adaptive immune cell functions. Therapeutic strategies to interrupt or enhance cAMP generation or effects have immunoregulatory potential in autoimmune and inflammatory disorders. Here, we provide an overview of the cyclic AMP axis and its role as a regulator of immune functions and discuss the clinical and translational relevance of interventions with these processes.

0301 basic medicinelcsh:Immunologic diseases. AllergyCell signalingT regulatory cellsImmunologyRegulatorT cellsTregsInflammationAutoimmunityReviewmedicine.disease_causeAutoimmunity03 medical and health scienceschemistry.chemical_compoundImmune systemmedicineCyclic AMPImmunology and AllergyCyclic adenosine monophosphateTregs; T regulatory CellsInflammationbusiness.industryCellular pathwaystargeted therapiesCell biology030104 developmental biologychemistryImmunologycAMP-dependent pathwaymedicine.symptombusinesslcsh:RC581-607Frontiers in Immunology
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Binding mode analysis of ABCA7 for the prediction of novel Alzheimer's disease therapeutics

2021

Graphical abstract

ATP Adenosine-triphosphateNBD nucleotide binding domainGSH reduced glutathionePolypharmacologyAlzheimer’s disease (AD)ATP-binding cassette transporterHTS high-throughput screeningBiochemistryABCA7Structural BiologyPLIF protein ligand interactionMSD membrane spanning domainPDB protein data bankTM transmembrane helixABC ATP-binding cassetteMultitarget modulation (PANABC)RMSD root mean square distanceABC transporter (ABCA1 ABCA4 ABCA7)Computer Science ApplicationsMOE Molecular Operating EnvironmentPharmacophoreSNP single-nucleotide polymorphismBiotechnologyResearch ArticleBBB blood-brain barrierBiophysicsDrug designComputational biologyBiologyAD Alzheimer’s diseasePET positron emission tomographyIC intracellular helixAPP amyloid precursor proteincryo-EM cryogenic-electron microscopyGeneticsHomology modelingBinding siteRational drug design and developmentComputingMethodologies_COMPUTERGRAPHICSNBD-cholesterol 7-nitro-2-13-benzoxadiazol-4-yl-cholesterolTransporterPSO particle swarm optimizationPET tracer (PETABC)ECD extracellular domainR-domain/region regulatory domain/regionABCA1biology.proteinEH extracellular helixTP248.13-248.65BODIPY-cholesterol 44-difluoro-4-bora-3a4a-diaza-s-indacene-cholesterolComputational and Structural Biotechnology Journal
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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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Regulatory T cell-derived adenosine induces dendritic cell migration through the Epac-Rap1 pathway.

2014

Abstract Dendritic cells (DC) are one target for immune suppression by regulatory T cells (Treg), because their interaction results in reduced T cell stimulatory capacity and secretion of inhibitory cytokines in DC. We show that DC in the presence of Treg are more mobile as compared with cocultures with conventional CD4+ T cells and form DC–Treg aggregates within 2 h of culture. The migration of DC was specifically directed toward Treg, as Treg, but not CD4+ T cells, attracted DC in Boyden chambers. Treg deficient for the ectonucleotidase CD39 were unable to attract DC. Likewise, addition of antagonists for A2A adenosine receptors abolished the formation of DC–Treg clusters, indicating a ro…

AdenosineRegulatory T cellT cellImmunologyMedizinchemical and pharmacologic phenomenaCell CommunicationBiologyT-Lymphocytes RegulatoryMiceAdenosine TriphosphateAntigens CDCell MovementmedicineImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsDendritic cell migrationReceptors Adenosine A2Apyraserap1 GTP-Binding Proteinshemic and immune systemsDendritic CellsActin cytoskeletonAdenosineAdenosine receptorCell biologyActin Cytoskeletonmedicine.anatomical_structureRap1Signal transductionmedicine.drugSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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NOseq: amplicon sequencing evaluation method for RNA m6A sites after chemical deamination

2020

Abstract Methods for the detection of m6A by RNA-Seq technologies are increasingly sought after. We here present NOseq, a method to detect m6A residues in defined amplicons by virtue of their resistance to chemical deamination, effected by nitrous acid. Partial deamination in NOseq affects all exocyclic amino groups present in nucleobases and thus also changes sequence information. The method uses a mapping algorithm specifically adapted to the sequence degeneration caused by deamination events. Thus, m6A sites with partial modification levels of ∼50% were detected in defined amplicons, and this threshold can be lowered to ∼10% by combination with m6A immunoprecipitation. NOseq faithfully d…

AdenosineSequence analysisAcademicSubjects/SCI00010Bisulfite sequencingDeaminationAdenosine/analogs & derivatives; Adenosine/analysis; Algorithms; Animals; Chromatography Liquid; Deamination; Drosophila melanogaster/genetics; HEK293 Cells; HeLa Cells; High-Throughput Nucleotide Sequencing/methods; Humans; RNA/chemistry; RNA Long Noncoding/chemistry; RNA Messenger/chemistry; RNA Ribosomal 18S/chemistry; Sequence Alignment; Sequence Analysis RNA/methods; Tandem Mass SpectrometrySequence alignmentComputational biologyBiology010402 general chemistry[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology01 natural sciencesTranscriptome03 medical and health sciencesNarese/13Tandem Mass Spectrometry[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]GeneticsRNA Ribosomal 18SAnimalsHumansRNA MessengerComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesSequence Analysis RNARNAHigh-Throughput Nucleotide Sequencing[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyAmpliconRibosomal RNA0104 chemical sciencesDrosophila melanogasterHEK293 CellsDeaminationMethods OnlineRNA[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]RNA Long NoncodingSequence AlignmentAlgorithmsChromatography LiquidHeLa Cells
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A Highly Decreased Binding of Cyclic Adenosine Monophosphate to Protein Kinase A in Erythrocyte Membranes is Specific for Active Psoriasis

2002

A cyclic adenosine monophosphate binding abnormality in psoriatic erythrocytes that could be corrected by retinoid treatment has been reported. It was tested whether this binding abnormality is specific for psoriasis and the effects of treatment were compared with etretinate, cyclosporine A, or anthralin on 2-(3)H-8-N(3)-cyclic adenosine monophosphate binding to the regulatory subunit of protein kinase A in erythrocyte membranes. One hundred and fifteen individuals were evaluated, including: (i) 34 healthy persons; (ii) 15 patients with nonatopic inflammatory skin diseases (eczema, erythroderma, tinea, Grover's disease, erysipelas, urticaria); (iii) eight with other dermatoses mediated by i…

AdultMaleAzidesmedicine.medical_specialtyAdolescentmedicine.drug_classAdministration TopicalAnti-Inflammatory AgentsErythrodermaEtretinateDermatologySeverity of Illness IndexBiochemistryRetinoidschemistry.chemical_compoundPsoriasis Area and Severity IndexKeratolytic AgentsPsoriasis Area and Severity IndexPsoriasisInternal medicineCyclic AMPmedicineHumansPsoriasisCyclic adenosine monophosphateRetinoidMolecular BiologydermatitisAgedErythema nodosumbusiness.industryErythrocyte MembraneAffinity LabelsCell BiologyAtopic dermatitisAnthralinMiddle Agedmedicine.diseaseCyclic AMP-Dependent Protein KinasesEndocrinologychemistryEtretinateCyclosporineFemaleDermatologic Agentsbusinesscyclosporine AProtein Bindingmedicine.drugJournal of Investigative Dermatology
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