Search results for "tyrosine phosphatases"

showing 2 items of 22 documents

Diabetes Antibody Standardization Program: evaluation of assays for autoantibodies to glutamic acid decarboxylase and islet antigen-2

2008

Aims/hypothesis Islet autoantibodies are important in diabetes classification and risk assessment, and as endpoints in observational studies. The Diabetes Autoantibody Standardization Program (DASP) aims to improve and standardise measurement of autoantibodies associated with type 1 diabetes. We report results for glutamic acid decarboxylase autoantibodies (GADA) and islet antigen-2 autoantibodies (IA-2A) from three DASP workshops (2002–2005). Methods Up to 60 laboratories in 18 countries participated in each workshop. Participants received coded serum aliquots from 50 patients with newly diagnosed type 1 diabetes (median age 18 years, range 9–35 years) and 100 blood donor controls. Results…

medicine.medical_specialtyEndocrinology Diabetes and MetabolismGlutamate decarboxylaseThe Environmental Determinants of Diabetes in the YoungGastroenterologySensitivity and SpecificityAntigenInterquartile rangeDiabetes mellitusInternal medicineInternal MedicinemedicineDiabetes MellitusHumansReceptor-Like Protein Tyrosine Phosphatases Class 8AutoantibodiesType 1 diabetesReceiver operating characteristicbusiness.industryGlutamate DecarboxylaseAutoantibodymedicine.diseaseAdjusted sensitivity AUC GAD autoantibodies IA-2 autoantibodies Islet autoantibodies Prediction Sensitivity SpecificityROC CurveImmunologybusiness
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Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

rac1 GTP-Binding ProteinProgrammed cell deathSmall interfering RNAGlutathione reductaseDown-RegulationAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle ProteinsBiologyPeptides CyclicImmediate-Early ProteinsMembrane Potentialschemistry.chemical_compoundMiceDownregulation and upregulationDepsipeptidesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseGlutathione DisulfideJNK Mitogen-Activated Protein KinasesProtein phosphatase 1Dual Specificity Phosphatase 1Cell BiologyGlutathioneCell biologyEnzyme ActivationOxidative StressGlutathione ReductasechemistryMitochondrial MembranesGlutathione disulfideCalciumProtein Tyrosine PhosphatasesReactive Oxygen SpeciesCopperHeLa CellsCell Death and Differentiation
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