Search results for " Non-Receptor"

showing 10 items of 22 documents

Endocytosis of the glutamate transporter 1 is regulated by laforin and malin: Implications in Lafora disease.

2020

Postprint 36 páginas, 7 figuras

0301 basic medicineArrestinsAmino Acid Transport System X-AGPhosphataseProgressive myoclonus epilepsyBiologyEndocytosisLafora diseaseArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineUbiquitinmedicineAnimalsNedd4.2Lafora diseaseGlutamate receptorUbiquitinationTransportermedicine.diseaseProtein Tyrosine Phosphatases Non-ReceptorEndocytosisCell biologyGLT-1030104 developmental biologyNeurologyLafora Diseasebiology.proteinGlutamateLaforin030217 neurology & neurosurgeryGlia
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PTP1B phosphatase as a novel target of oleuropein activity in MCF-7 breast cancer model.

2019

Phosphatase PTP1B has become a therapeutic target for the treatment of type 2-diabetes, whereas recent studies have revealed that PTP1B plays a pivotal role in pathophysiology and development of breast cancer. Oleuropein is a natural, phenolic compound with anticancer activity. The aim of this study was to address the question whether PTP1B constitutes a target for oleuropein in breast cancer MCF-7 cells. The cellular MCF-7 breast cancer model was used in the study. The experiments were performed using cellular viability tests, Elisa assays, immunoprecipitation, flow cytometry analyses and computer modelling. Herein, we evidenced that the reduced activity of phosphatase PTP1B after treatmen…

0301 basic medicineCell cycle checkpointImmunoprecipitationCell Survivalmedicine.medical_treatmentPhosphataseIridoid GlucosidesAntineoplastic AgentsBreast NeoplasmsAdenocarcinomaMolecular Dynamics SimulationToxicologyFlow cytometry03 medical and health scienceschemistry.chemical_compoundbreast cancer0302 clinical medicineBreast cancerOleuropeinmedicineHumansPTP1B phosphataseIridoidsskin and connective tissue diseasesSettore CHIM/02 - Chimica FisicaCell ProliferationOleuropeinProtein Tyrosine Phosphatase Non-Receptor Type 1MCF-7 cellmedicine.diagnostic_testAnticancer therapyGeneral Medicinemedicine.disease030104 developmental biologychemistryMCF-7Settore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSettore BIO/14 - FarmacologiaCancer researchMCF-7 CellsAdjuvanthormones hormone substitutes and hormone antagonistsToxicology in vitro : an international journal published in association with BIBRA
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Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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Assessing the biological activity of the glucan phosphatase laforin

2016

Glucan phosphatases are a recently discovered family of enzymes that dephosphorylate either starch or glycogen and are essential for proper starch metabolism in plants and glycogen metabolism in humans. Mutations in the gene encoding the only human glucan phosphatase, laforin, result in the fatal, neurodegenerative, epilepsy known as Lafora disease. Here, we describe phosphatase assays to assess both generic laforin phosphatase activity and laforin's unique glycogen phosphatase activity.

0301 basic medicinePhosphataseLafora diseaseArticleSubstrate SpecificityNitrophenols03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsDual-specificity phosphatasemedicineHumansGlucanEnzyme Assayschemistry.chemical_classificationGlycogenbiologyfood and beveragesBiological activitymedicine.diseaseFluoresceinsProtein Tyrosine Phosphatases Non-Receptor030104 developmental biologyEnzymechemistryBiochemistryLafora Diseasebiology.proteinLaforin030217 neurology & neurosurgeryGlycogen
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PTPN22 and CTLA-4 Polymorphisms Are Associated With Polyglandular Autoimmunity

2017

Context Single nucleotide polymorphisms (SNPs) of various genes increase susceptibility to monoglandular autoimmunity. Data on autoimmune polyglandular syndromes (APSs) are scarce. Objective Evaluate potential associations of eight SNPs with APSs. Setting Academic referral endocrine clinic. Patients A total of 543 patients with APS and monoglandular autoimmunity and controls. Intervention The SNP protein tyrosine phosphatase nonreceptor type 22 (PTPN22) rs2476601 (+1858); cytotoxic T-lymphocyte‒associated antigen 4 (CTLA-4) rs3087243 (CT60) and rs231775 (AG49); vitamin D receptor (VDR) rs1544410 (Bsm I), rs7975232 (Apa I), rs731236 (Taq I); tumor necrosis factor α rs1800630 (-863); and inte…

AdultMale0301 basic medicinemedicine.medical_specialtyGenotypeEndocrinology Diabetes and MetabolismGraves' diseaseClinical Biochemistry030209 endocrinology & metabolismSingle-nucleotide polymorphismPolymorphism Single NucleotideBiochemistryCalcitriol receptorPTPN22Young Adult03 medical and health sciences0302 clinical medicineEndocrinologyGene FrequencyInternal medicinemedicineHumansCTLA-4 AntigenGenetic Predisposition to DiseasePolyendocrinopathies AutoimmuneAllele frequencyGenetic Association Studiesbusiness.industryBiochemistry (medical)HaplotypeCase-control studyProtein Tyrosine Phosphatase Non-Receptor Type 22Odds ratioMiddle Agedmedicine.disease030104 developmental biologyEndocrinologyCase-Control StudiesFemalebusinessThe Journal of Clinical Endocrinology & Metabolism
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Autoimmune associations and autoantibody screening show focused recognition in patient subgroups with generalized myasthenia gravis

2013

Autoimmune associations in myasthenia gravis (MG)-patients and their relatives have not been re-assessed since their separation into early- or late-onset MG (EOMG, LOMG), or thymoma-associated MG. Here, we analysed 226 EOMG-, 97 LOMG-, and 150 thymoma-patients for autoimmune disorders in themselves and their relatives. From 283 of them sera were tested for different organ- and non-organ-specific autoantibodies (autoAbs) by immunofluorescence test (IFT) and ELISA; genotyping was performed in 213 patients. Relatives with autoimmune disorders were reported by more patients with EOMG (40% of 210) than LOMG (20% of 89; p0.01) than thymomas (8% of 150; p0.001). In 150 genotyped EOMG-females, the …

AdultMaleAdolescentGenotypeThymomaAnti-nuclear antibodyImmunologyPTPN22Young AdultPrimary biliary cirrhosisPopulation GroupsMyasthenia GravismedicineHumansImmunology and AllergyAge of OnsetChildAgedAutoantibodiesAged 80 and overProtein Tyrosine Phosphatase Non-Receptor Type 2Neuromyelitis opticabusiness.industryMultiple sclerosisAutoantibodyGeneral MedicineMiddle Agedmedicine.diseaseMuscle StriatedMyasthenia gravisPedigreeOrgan SpecificityChild PreschoolRheumatoid arthritisImmunologyAdrenal CortexFemalebusinessHuman Immunology
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The PTPN22gain-of-function+1858T(+) genotypes correlate with low IL-2 expression in thymomas and predispose to myasthenia gravis

2009

Protein tyrosine phosphatase, non-receptor type 22 (PTPN22) inhibits T-cell activation and interleukin-2 (IL-2) production. The PTPN22(gain-of-function)+1858T(+) genotypes predispose to multiple autoimmune diseases, including early-onset (non-thymomatous) myasthenia gravis (MG). The disease association and the requirement of IL-2/IL-2 receptor signaling for intrathymic, negative T-cell selection have suggested that these genotypes may weaken T-cell receptor (TCR) signaling and impair the deletion of autoreactive T cells. Evidence for this hypothesis is missing. Thymoma-associated MG, which depends on intratumorous generation and export of mature autoreactive CD4(+) T cells, is a model of au…

AdultMalemedicine.medical_specialtyThymomaAdolescentGenotypeThymomaImmunologyBiologymedicine.disease_causePolymorphism Single NucleotideWhite PeopleAutoimmunityPTPN22Young AdultAntigens CDInternal medicineMyasthenia GravisCentral tolerance inductionGeneticsmedicineHumansCTLA-4 AntigenGenetic Predisposition to DiseaseReceptorGenetics (clinical)AgedAged 80 and overT-cell receptorProtein Tyrosine Phosphatase Non-Receptor Type 22Thymus NeoplasmsMiddle Agedmedicine.diseaseMyasthenia gravisEndocrinologyImmunologyInterleukin-2FemaleCentral toleranceGenes & Immunity
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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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Role of SHP2 for FLT3-dependent proliferation and transformation in 32D cells.

2008

Fms-like tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase, which plays a role in proliferation and differentiation of B-cell progenitors, myelomonocytic and dendritic cells, as well as in the maintenance of pluripotent hematopoietic stem cells (reviewed in Stirewalt and Radich,1and Schmidt-Arras et al.2). Recently, FLT3 has received much attention as an important oncoprotein. Mutations in FLT3 that lead to constitutive activation are among the most common molecular lesions found in acute myeloid leukemia.3 The most prevalent type of mutations result in internal tandem duplications (ITD) of amino-acid stretches in the juxtamembrane domain of FLT3. FLT3-ITD is constitutively a…

Cancer ResearchMyeloidProtein Tyrosine Phosphatase Non-Receptor Type 11Biologymedicine.disease_causeReceptor tyrosine kinaseCell LineMicefluids and secretionshemic and lymphatic diseasesmedicineAnimalsHumansRNA Small InterferingCell ProliferationMice Inbred C3Hhemic and immune systemsHematologyHaematopoiesismedicine.anatomical_structureCell Transformation NeoplasticOncologyfms-Like Tyrosine Kinase 3Trk receptorembryonic structuresCancer researchbiology.proteinStem cellSignal transductionCarcinogenesisTyrosine kinaseSignal TransductionLeukemia
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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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