Search results for "PROTEIN-KINASE-C"

showing 4 items of 4 documents

Muscarinic type-1 receptors contribute to I-K,I-ACh in human atrial cardiomyocytes and are upregulated in patients with chronic atrial fibrillation

2018

Background: Basal and acetylcholine-gated inward-rectifier K+-currents (I-K1 and I-K,I-ACh, respectively) are altered in atrial fibrillation (AF). G(i)-protein-coupled muscarinic (M) receptors type-2 are considered the predominant receptors activating I-K,I-ACh. Although a role for G(q)-coupled non-M-2-receptor subtypes has been suggested, the precise regulation of I-K,I-ACh by multiple M-receptor subtypes in the human atrium is unknown. Here, we investigated M-1-receptor-mediated I-K,I-ACh regulation and its remodeling in chronic AF (cAF). Methods and results: M-1-receptor mRNA and protein abundance were increased in atrial cardiomyocyte fractions and atrial homogenates from cAF patients, …

0301 basic medicineAgonistEXPRESSIONmedicine.medical_specialtyCarbacholmedicine.drug_classMedizin030204 cardiovascular system & hematologyPertussis toxinSUBTYPES03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicinePROTEIN-KINASE-CReceptorAcetylcholine receptorK+-CURRENTACETYLCHOLINE-RECEPTORSCHANNELSCONGESTIVE-HEART-FAILUREbusiness.industryMuscarinic receptor subtypesInward-rectifier K+-channelELECTROPHYSIOLOGYPirenzepineAtrial fibrillationDEPENDENT REGULATIONPOTASSIUM CURRENTS030104 developmental biologyEndocrinologyCardiology and Cardiovascular MedicinebusinessAcetylcholinemedicine.drug
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PED Mediates AKT-Dependent Chemoresistance in Human Breast Cancer Cells

2005

Abstract Killing of tumor cells by cytotoxic therapies, such as chemotherapy or gamma-irradiation, is predominantly mediated by the activation of apoptotic pathways. Refractoriness to anticancer therapy is often due to a failure in the apoptotic pathway. The mechanisms that control the balance between survival and cell death in cancer cells are still largely unknown. Tumor cells have been shown to evade death signals through an increase in the expression of antiapoptotic molecules or loss of proapoptotic factors. We aimed to study the involvement of PED, a molecule with a broad antiapoptotic action, in human breast cancer cell resistance to chemotherapeutic drugs–induced cell death. We show…

EXPRESSIONAdultCancer ResearchProgrammed cell deathmedicine.medical_treatmentINHIBITIONApoptosisBreast NeoplasmsProtein Serine-Threonine KinasesDNA AntisenseACTIVATIONBreast cancerTransduction GeneticCell Line TumorProto-Oncogene ProteinsComplementary DNAmedicineHumansCytotoxic T cellPROTEIN-KINASE-CProtein kinase BAgedNeoplasm StagingChemotherapybusiness.industryDEATHIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesIN-VITROCHEMOTHERAPYMiddle AgedPhosphoproteinsmedicine.diseasePED/PEA-15Up-RegulationEnzyme ActivationOncologyDrug Resistance NeoplasmApoptosisCancer cellImmunologyCancer researchFemalePTEN GENEApoptosis Regulatory ProteinsbusinessProto-Oncogene Proteins c-aktCancer Research
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Role of calcineurin in Ca2+-induced release of catecholamines and neuropeptides

1998

Neurotransmission requires rapid docking, fusion, and recycling of neurotransmitter vesicles. Several of the proteins involved in this complex Ca2+-regulated mechanism have been identified as substrates for protein kinases and phosphatases, e.g., the synapsins, synaptotagmin, rabphilin3A, synaptobrevin, munc18, MARCKS, dynamin I, and B-50/GAP-43. So far most attention has focused on the role of kinases in the release processes, but recent evidence indicates that phosphatases may be as important. Therefore, we investigated the role of the Ca2+/calmodulin-dependent protein phosphatase calcineurin in exocytosis and subsequent vesicle recycling. Calcineurin-neutralizing antibodies, which blocke…

MaleSynaptobrevinCYCLOSPORINE-APhosphataseCalcineurin InhibitorsB-50 GAP-43Biologydynamin IBiochemistryBRAIN NERVE-TERMINALSExocytosisSynaptotagmin 1SincalidephosphataseGeneeskundeCellular and Molecular NeuroscienceNorepinephrineBacterial ProteinsPERMEATED SYNAPTOSOMESAnimalsratNEUROTRANSMITTER RELEASEMARCKSEnzyme InhibitorsRats WistarPROTEIN-KINASE-CDynaminCalcineurinTRANSMITTER RELEASEDYNAMIN-ISynapsinPhosphoric Monoester HydrolasesRatsINDUCED NORADRENALINE RELEASECalcineurinBiochemistryImmunoglobulin GStreptolysinsCalciumexocytosisCALMODULIN-BINDINGSynaptosomes
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The pharmacological rationale for combining muscarinic receptor antagonists and beta-adrenoceptor agonists in the treatment of airway and bladder dis…

2014

Highlights • Muscarinic receptors increase smooth muscle tone in airways and urinary bladder. • β-Adrenoceptors relax smooth muscle tone and oppose muscarinic contraction. • Opposition involves transmitter release, signal transduction and receptor expression. • This supports the combined use of muscarinic antagonists and β-adrenoceptor agonists.

medicine.medical_specialtyUrologyDiseaseMuscarinic AntagonistsPharmacologyArticleβ adrenoceptorchemistry.chemical_compoundInternal medicineReceptors Adrenergic betaMuscarinic acetylcholine receptorDrug DiscoveryMuscarinic acetylcholine receptor M4RAT URINARY-BLADDERMedicineAnimalsHumansCyclic adenosine monophosphateADRENERGIC RELAXATIONLung Diseases ObstructivePROTEIN-KINASE-CReceptorTRACHEAL SMOOTH-MUSCLEPharmacologybusiness.industryUrinary Bladder DiseasesMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2ACETYLCHOLINE-RELEASEAdrenergic beta-Agonistsmedicine.diseaseReceptors MuscarinicEndocrinologyNONNEURONAL CHOLINERGIC SYSTEMchemistryGUINEA-PIG TRACHEADrug Therapy CombinationCYCLIC ADENOSINE-MONOPHOSPHATECA2+-ACTIVATED K+ CHANNELAirwaybusinessUrinary bladder diseaseAUTORADIOGRAPHIC VISUALIZATIONAcetylcholinemedicine.drug
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