Search results for " protein tyrosine phosphatases"

showing 6 items of 6 documents

Islet autoantibodies in Latvian subjects with non-insulin-dependent diabetes mellitus: slow-onset type 1 diabetes or polyendocrine autoimmunity?

2006

In Latvia diabetes mellitus is diagnosed using the WHO's clinical criteria; assays for the detection of autoantibodies are not available, and hence slowly progressive autoimmune diabetes is likely to be missed. Autoantibodies against glutamic acid decarboxylase (GAD65) and protein tyrosine phosphatase (IA-2) among patients with clinically diagnosed NIDDM identify group of patients with slow-onset type 1 diabetes or LADA. The aim of this study was to estimate the risk of polyendocrine autoimmunity among clinically diagnosed NIDDM patients from Latvia. One hundred NIDDM patients and 100 healthy controls were tested for GAD65 and IA-2 autoantibodies as well as 21-hydroxylase (21-OH) and tissue…

AdultMalemedicine.medical_specialtyendocrine system diseasesAdolescentTissue transglutaminasemedicine.medical_treatmentOverweightmedicine.disease_causeAutoantigensGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityDiagnosis DifferentialHistory and Philosophy of ScienceInternal medicineDiabetes mellitusmedicineHumansReceptor-Like Protein Tyrosine Phosphatases Class 8ChildPolyendocrinopathies AutoimmuneAutoantibodiesProtein Tyrosine Phosphatase Non-Receptor Type 1Type 1 diabetesbiologybusiness.industryGlutamate DecarboxylaseGeneral NeuroscienceInsulinAutoantibodynutritional and metabolic diseasesMembrane Proteinsmedicine.diseaseLatviaIsoenzymesEndocrinologyDiabetes Mellitus Type 1Child Preschoolbiology.proteinFemalemedicine.symptomProtein Tyrosine PhosphatasesbusinessBody mass indexBiomarkersAnnals of the New York Academy of Sciences
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A novel regulatory mechanism of MAP kinases activation and nuclear translocation mediated by PKA and the PTP-SL tyrosine phosphatase

1999

Protein tyrosine phosphatase PTP-SL retains mitogen-activated protein (MAP) kinases in the cytoplasm in an inactive form by association through a kinase interaction motif (KIM) and tyrosine dephosphorylation. The related tyrosine phosphatases PTP-SL and STEP were phosphorylated by the cAMP-dependent protein kinase A (PKA). The PKA phosphorylation site on PTP-SL was identified as the Ser231 residue, located within the KIM. Upon phosphorylation of Ser231, PTP-SL binding and tyrosine dephosphorylation of the MAP kinases extracellular signal–regulated kinase (ERK)1/2 and p38α were impaired. Furthermore, treatment of COS-7 cells with PKA activators, or overexpression of the Cα catalytic subunit …

Cytoplasmanimal structuresRecombinant Fusion ProteinsCèl·lulesAmino Acid MotifsNerve Tissue ProteinsProtein tyrosine phosphataseSH2 domainTransfectionenvironment and public healthModels Biologicalp38 Mitogen-Activated Protein KinasesReceptor tyrosine kinaseSH3 domainCell LinePhosphoserinetyrosine phosphatasesAnimalsHumansProtein phosphorylationPKAReceptor-Like Protein Tyrosine Phosphatases Class 7PhosphorylationPTP-SLCell NucleusMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyBrief ReportIntracellular Signaling Peptides and ProteinsBiological TransportCell BiologyProtein Tyrosine Phosphatases Non-ReceptorCyclic AMP-Dependent Protein KinasesEnzyme Activationenzymes and coenzymes (carbohydrates)MAP kinasesBiochemistryMitogen-activated protein kinaseCOS CellsMutationbiology.proteinPhosphorylationMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesEnzimssignal transductionProto-oncogene tyrosine-protein kinase Src
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UNC-52/perlecan affects gonadal leader cell migrations in C. elegans hermaphrodites through alterations in growth factor signaling.

2003

0012-1606 doi: DOI: 10.1016/S0012-1606(03)00014-9; The unc-52 gene of Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecu…

Malemedicine.medical_treatmentOrganogenesisCellDisorders of Sex DevelopmentReceptor-Like Protein Tyrosine PhosphatasesFibroblast growth factorAnimals Genetically ModifiedCell MovementNetrinGrowth SubstancesGenes HelminthGeneticsMusclesCell migrationsWnt signaling pathwayHelminth Proteinsmedicine.anatomical_structurePhenotypeLarvaC. elegansFemaleNetrinsProteoglycansSignal transductionSignal TransductionUNC-52Nerve Tissue ProteinsReceptors Cell SurfacePerlecanmacromolecular substancesBiologymedicineAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGonadsGeneMolecular BiologyGrowth factorfungiMembrane ProteinsCell BiologyPerlecanReceptors Fibroblast Growth Factornervous systemMutationbiology.proteinProtein Tyrosine PhosphatasesDevelopmental BiologyDevelopmental biology
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Role of PTPRJ genotype in papillary thyroid carcinoma risk

2010

The strong genetic predisposition to papillary thyroid carcinoma (PTC) might be due to a combination of low-penetrance susceptibility variants. Thus, the research into gene variants involved in the increase of susceptibility to PTC is a relevant field of investigation. The gene coding for the receptor-type tyrosine phosphatase PTPRJ has been proposed as a cancer susceptibility gene, and its role as a tumor suppressor gene is well established in thyroid carcinogenesis. In this study, we want to ascertain the role of PTPRJ genotype in the risk for PTC. We performed a case–control study in which we determined the PTPRJ genotype for the non-synonymous Gln276Pro and Asp872Glu polymorphisms by PC…

RiskOncologyCancer Researchmedicine.medical_specialtyGenotypeendocrine system diseasesEndocrinology Diabetes and MetabolismBiologyPolymerase Chain ReactionArticleSettore MED/13 - EndocrinologiaThyroid carcinomaEndocrinologyGene FrequencyInternal medicineGenotypeOdds RatiomedicineGenetic predispositionHumansGenetic Predisposition to DiseaseThyroid NeoplasmsAlleleAllele frequencyAllelesGenetic Association StudiesPapillay thyroid carcinomaGeneticsChi-Square DistributionPolymorphism GeneticReceptor-Like Protein Tyrosine Phosphatases Class 3ThyroidCase-control studyCarcinoma PapillaryGenotype frequencymedicine.anatomical_structureOncologyCase-Control Studies
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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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