Search results for "G proteins"

showing 10 items of 992 documents

The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes

2003

Azathioprine and its metabolite 6-mercaptopurine (6-MP) are immunosuppressive drugs that are used in organ transplantation and autoimmune and chronic inflammatory diseases such as Crohn disease. However, their molecular mechanism of action is unknown. In the present study, we have identified a unique and unexpected role for azathioprine and its metabolites in the control of T cell apoptosis by modulation of Rac1 activation upon CD28 costimulation. We found that azathioprine and its metabolites induced apoptosis of T cells from patients with Crohn disease and control patients. Apoptosis induction required costimulation with CD28 and was mediated by specific block- ade of Rac1 activation thro…

AdultCD4-Positive T-LymphocytesSTAT3 Transcription Factorrac1 GTP-Binding Proteinmedicine.medical_specialtyApoptosisRAC1AzathioprineProtein Serine-Threonine KinasesBiologyLymphocyte ActivationOrgan transplantationTioguanineCD28 AntigensAzathioprinemedicineHumansPhosphorylationProtein kinase ACells CulturedAgedKinaseCD28General MedicineMiddle AgedI-kappa B KinaseDNA-Binding ProteinsApoptosisImmunologyTrans-ActivatorsCommentaryCancer researchImmunosuppressive Agentsmedicine.drugJournal of Clinical Investigation
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Azathioprine suppresses ezrin-radixin-moesin-dependent T cell-APC conjugation through inhibition of Vav guanosine exchange activity on rac proteins

2006

Abstract We have shown recently that the azathioprine metabolite 6-Thio-GTP causes immunosuppression by blockade of GTPase activation in T lymphocytes. In the present study, we describe a new molecular mechanism by which 6-Thio-GTP blocks GTPase activation. Although 6-Thio-GTP could bind to various small GTPases, it specifically blocked activation of Rac1 and Rac2 but not of closely related Rho family members such as Cdc42 and RhoA in primary T cells upon stimulation with αCD28 or fibronectin. Binding of 6-Thio-GTP to Rac1 did not suppress Rac effector coupling directly but blocked Vav1 exchange activity upon 6-Thio-GTP hydrolysis, suggesting that 6-Thio-GTP loading leads to accumulation of…

AdultCD4-Positive T-LymphocytesVAV1RHOAT cellImmunologyBlotting WesternAntigen-Presenting CellsFluorescent Antibody TechniqueRAC1ApoptosisEnzyme-Linked Immunosorbent AssayGTPaseCell CommunicationBiologyArticleAzathioprinemedicineImmunology and AllergyHumansAntigen-presenting cellProto-Oncogene Proteins c-vavNeurofibromin 2Flow CytometryMolecular biologyCell biologyrac GTP-Binding ProteinsRac GTP-Binding ProteinsEnzyme Activationmedicine.anatomical_structurebiology.proteinSignal transductionImmunosuppressive Agents
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Prospective study on cervical neoplasia IV. Presence of HPV antibodies.

1999

Sera collected in the course of a prospective study carried out in Prague in 1975–1983 were assayed for the presence of human papillomavirus (HPV) antibodies. Women with cervical neoplasia proven by biopsy at enrollment possessed antibodies to peptides derived from E2, E4 and E7 proteins of HPV16 and to virus-like particles (VLPs) of HPV16, -18 and -33 significantly more frequently than matched controls. Women without cervical neoplasia at enrollment who developed the disease in the course of the study differed from matched controls by a higher prevalence of antibodies against VLPs of HPV16 and -18 but not against early antigens of HPV16. In 19 of the latter subjects, paired serum specimens…

AdultCancer Researchmedicine.medical_specialtyvirusesPapillomavirus E7 ProteinsUterine Cervical NeoplasmsAntibodies ViralGastroenterologySerologyAntigenInternal medicineBiopsymedicineHumansProspective StudiesSeroconversionProspective cohort studyPapillomaviridaebiologymedicine.diagnostic_testbusiness.industryvirus diseasesCancerOncogene Proteins ViralMiddle Agedmedicine.diseasefemale genital diseases and pregnancy complicationsDNA-Binding ProteinsOncologyImmunologybiology.proteinFemaleViral diseaseAntibodybusinessBiomarkersInternational journal of cancer
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Potential effects of age-associated oxidative stress on mammalian oocytes/embryos

1996

This bioessay aims to explain the different effects of maternal ageing and postovulatory oocyte ageing on mammalian oocytes/embryos under the scope of 'the oxygen radical-mitochondrial injury hypothesis of ageing'. This hypothesis assumes a key role in the senescent process of oxygen radical damage to mitochondrial DNA, proteins and lipids. It is proposed that a decrease in intracellular ATP concentrations and glutathione (GSH)/glutathione disulphide (GSSG) ratio together with a concomitant increase in cytosolic Ca2+ are major factors causing the observed detrimental effects of ageing on cytoskeletal fibres, fertilization and embryo development.

AdultFetal ProteinsEmbryologyBiologymedicine.disease_causeDNA MitochondrialCongenital AbnormalitiesMicechemistry.chemical_compoundAdenosine TriphosphateNeoplasmsGeneticsmedicineAnimalsHumansMolecular BiologyCellular SenescenceCytoskeletonMammalsEgg ProteinsEmbryogenesisObstetrics and GynecologyEmbryoCell BiologyGlutathioneEmbryo MammalianOocyteGlutathioneCell biologyOxidative StressCytosolFertilitymedicine.anatomical_structureReproductive MedicineBiochemistrychemistryAgeingFertilizationOocytesReactive Oxygen SpeciesOxidation-ReductionIntracellularOxidative stressMaternal AgeDevelopmental BiologyMolecular Human Reproduction
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Cardiomyopathy due to PRDM16 mutation: First description of a fetal presentation, with possible modifier genes

2020

PRDM16 (positive regulatory domain 16) is localized in the critical region for cardiomyopathy in patients with deletions of chromosome 1p36, as defined by Gajecka et al., American Journal of Medical Genetics, 2010, 152A, 3074-3083, and encodes a zinc finger transcription factor. We present the first fetal case of left ventricular non-compaction (LVNC) with a PRDM16 variant. The third-trimester obstetric ultrasound revealed a hydropic fetus with hydramnios and expanded hypokinetic heart. After termination of pregnancy, foetopathology showed a eutrophic fetus with isolated cardiomegaly. Endocardial fibroelastosis was associated with non-compaction of the myocardium of the left ventricle. Exom…

AdultHeart Defects CongenitalMalemedicine.medical_specialtyCardiomyopathyBiologyLabor PresentationGenetic HeterogeneityPregnancyExome SequencingGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseGenetics (clinical)Exome sequencingGeneticsFetusGenes ModifierGenetic heterogeneityInfant NewbornEndocardial fibroelastosisMiddle AgedFetal Presentationmedicine.diseasePedigreeDNA-Binding ProteinsMutationMedical geneticsFemaleCardiomyopathiesTranscription FactorsAmerican Journal of Medical Genetics Part C: Seminars in Medical Genetics
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Genotype and phenotype analysis of Friedreich's ataxia compound heterozygous patients

2000

Friedreich's ataxia is caused by mutations in the FRDA gene that encodes frataxin, a nuclear-encoded mitochondrial protein. Most patients are homozygous for the expansion of a GAA triplet repeat within the FRDA gene, but a few patients show compound heterozygosity for a point mutation and the GAA-repeat expansion. We analyzed DNA samples from a cohort of 241 patients with autosomal recessive or isolated spinocerebellar ataxia for the GAA triplet expansion. Patients heterozygous for the GAA expansion were screened for point mutations within the FRDA coding region. Molecular analyses included the single-strand conformation polymorphism analysis, direct sequencing, and linkage analysis with FR…

AdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaGenotypeGenetic LinkageDNA Mutational AnalysisGenes RecessiveCompound heterozygosityLoss of heterozygosityTrinucleotide RepeatsIron-Binding ProteinsGenotypeGeneticsmedicineHumansPoint MutationAge of OnsetAlleleChildAllelesPolymorphism Single-Stranded ConformationalGenetics (clinical)Family HealthGeneticsbiologynutritional and metabolic diseasesmedicine.diseasePedigreePhosphotransferases (Alcohol Group Acceptor)PhenotypeFriedreich AtaxiaChild PreschoolFrataxinbiology.proteinSpinocerebellar ataxiamedicine.symptomTrinucleotide Repeat ExpansionTrinucleotide repeat expansionMicrosatellite Repeats
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Circulating levels of adipose products and differences in fat distribution in the ovulatory and anovulatory phenotypes of polycystic ovary syndrome.

2009

Central fat distribution is increased in anovulatory women with polycystic ovary syndrome (PCOS) compared with ovulatory PCOS and matched controls. Among secreted adipocytokines, this is reflected mainly in lower levels of adiponectin.

AdultLeptinOvulationmedicine.medical_specialtySettore MED/09 - Medicina Internaendocrine system diseasesmedia_common.quotation_subjectAdipokineAdipose tissueBiologyAnovulationInsulin resistanceAdipokinesInternal medicinemedicineBody Fat DistributionHumansNicotinamide PhosphoribosyltransferaseOvulationmedia_commonAdiponectinLeptinnutritional and metabolic diseasesObstetrics and Gynecologymedicine.diseasePolycystic ovaryfat distribution; polycystic ovary syndromeLipidsfemale genital diseases and pregnancy complicationsEndocrinologyC-Reactive ProteinPhenotypeReproductive Medicinefat distributionCase-Control StudiesFemaleAdiponectinInsulin ResistanceWaist CircumferenceRetinol-Binding Proteins PlasmaAnovulationPolycystic Ovary SyndromeFertility and sterility
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Anti-tissue transglutaminase antibodies in patients with abnormal liver tests: is it always coeliac disease?

2005

Coeliac disease (CD) is found in 5-10% of patients with chronically abnormal liver tests and no obvious cause of liver disease. In this population the efficacy of screening for CD by anti-tissue transglutaminase (anti-tTG) may be impaired by the high rate of positive anti-tTG found in chronic liver disease.To evaluate the prevalence of coeliac disease and the role of anti-tTG in patients with non-viral, non-autoimmune chronic and no obvious cause of liver damage.Out of 2,512 consecutive patients with abnormal liver tests, 168 (118 men, 50 women; mean age 40.7 +/- 12.6 years) were defined, on the basis of clinical data and liver biopsy, as NAFLD or cryptogenic chronic hepatitis. All were tes…

AdultLiver CirrhosisMalePathologymedicine.medical_specialtyAdolescentTissue transglutaminaseDuodenumBiopsyGastroenterologyCoeliac diseaseGTP-Binding ProteinsInternal medicineBiopsymedicineHumansMass ScreeningIn patientProtein Glutamine gamma Glutamyltransferase 2Aspartate AminotransferasesDuodenoscopyMass screeningAgedAutoantibodiesHepatitis ChronicHepatitisTransglutaminasesHepatologybiologymedicine.diagnostic_testbusiness.industryLiver DiseasesGastroenterologynutritional and metabolic diseasesAlanine TransaminaseMiddle Agedmedicine.diseasedigestive system diseasesImmunoglobulin AFatty LiverCeliac DiseaseLiverImmunoglobulin Gbiology.proteinFemaleAbnormal liverAntibodybusinessThe American journal of gastroenterology
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Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay…

AdultLiver CirrhosisMaleendocrine systemmedicine.medical_specialtyTriiodothyronine Reverseendocrine system diseasesEndocrinology Diabetes and MetabolismPulsatile flowThyrotropinBiologyThyroxine-Binding ProteinsEndocrinologyRhythmHypothyroidismThyrotropic cellNeoplasmsInternal medicinemedicineHumansCircadian rhythmTriiodothyroninePulse (signal processing)ThyroidGeneral MedicineMiddle AgedCircadian RhythmThyroxineEndocrinologymedicine.anatomical_structurePulsatile FlowTriiodothyronineFemaleHormoneEuropean Journal of Endocrinology
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