Search results for "MUTATION"

showing 10 items of 2830 documents

Immunoprofiles and DNA methylation of inflammatory marker genes in ulcerative colitis-associated colorectal tumorigenesis

2021

Immunological and epigenetic changes are interconnected and contribute to tumorigenesis. We determined the immunoprofiles and promoter methylation of inflammation-related genes for colitis-associated colorectal carcinomas (CA-CRC). The results were compared with Lynch syndrome (LS)-associated colorectal tumors, which are characterized by an active immune environment through inherited mismatch repair defects. CA-CRCs (n = 31) were immunohistochemically evaluated for immune cell scores (ICSs) and PDCD1 and CD274 expression. Seven inflammation-associated genes (CD274, NTSR1, PPARG, PTGS2, PYCARD, SOCS1, and SOCS2), the repair gene MGMT, and eight standard marker genes for the CpG Island Methyl…

MaleCarcinogenesismedicine.disease_causeBiochemistry0302 clinical medicineIntestinal MucosaDNA Modification Methylases0303 health sciencesMUCOSADNA methylationtulehdusinflammation-associated genesPYCARDMethylationMiddle AgedLynch syndromeQR1-502EPIGENETICS3. Good healthDNA-metylaatioGene Expression Regulation NeoplasticPhenotypecolon cancerepigenetiikka030220 oncology & carcinogenesisimmuunivasteDNA methylationFemaleColorectal NeoplasmsCANCERSINSTABILITYsuolistosyövätBiology3121 Internal medicineMicrobiologyArticle03 medical and health sciencesmedicineHumansEpigeneticsLynchin oireyhtymäMolecular Biologyneoplasms030304 developmental biologypaksusuolisyöpäulcerative colitisInflammationCpG Island Methylator PhenotypeTumor Suppressor Proteinshaavainen koliittimedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseasesDNA Repair EnzymesLynch syndrome3121 General medicine internal medicine and other clinical medicineMutationimmune cell scoreCancer research1182 Biochemistry cell and molecular biologyColitis UlcerativeCpG IslandsField cancerizationCarcinogenesisBiomarkers
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Structural and functional characterization of a human IgG monoclonal antiphospholipid antibody

2009

Antiphospholipid antibodies (aPL) are likely involved in the pathogenesis of the antiphospholipid syndrome (APS). This study analyzes the structural and functional characteristics of a human monoclonal aPL (HL7G) from the IgG2 subtype with λ light chains generated from a patient with primary APS and recurrent cerebral microemboli. DNA encoding the variable region of heavy and light chains of the antibody was sequenced, analyzed, and compared to HL5B a previously described monoclonal aPL from the same patient. Both antibodies are derived from the same germline genes. HL7G had similar but more extensive somatic mutations in the CDR1 and 2 regions than HL5B, indicating that both antibodies are…

MaleCardiolipinsmedicine.drug_classImmunologySomatic hypermutationComplementarity determining regionMonoclonal antibodyImmunoglobulin light chainThromboplastinAntigenimmune system diseasesAntiphospholipid syndromemedicineHumansImmunology and AllergyneoplasmsCells CulturedMolecular StructurebiologyAntibodies MonoclonalT-Lymphocytes Helper-InducerHematologyMiddle AgedAntiphospholipid Syndromemedicine.diseaseComplementarity Determining RegionsMolecular biologybeta 2-Glycoprotein IImmunoglobulin GImmunologyMonoclonalAntibodies Antiphospholipidbiology.proteinSomatic Hypermutation ImmunoglobulinAntibodyImmunobiology
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KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron

2012

Familial hyperkalemic hypertension (FHHt) is a Mendelian form of arterial hypertension that is partially explained by mutations in WNK1 and WNK4 that lead to increased activity of the Na(+)-Cl(-) cotransporter (NCC) in the distal nephron. Using combined linkage analysis and whole-exome sequencing in two families, we identified KLHL3 as a third gene responsible for FHHt. Direct sequencing of 43 other affected individuals revealed 11 additional missense mutations that were associated with heterogeneous phenotypes and diverse modes of inheritance. Polymorphisms at KLHL3 were not associated with blood pressure. The KLHL3 protein belongs to the BTB-BACK-kelch family of actin-binding proteins tha…

MaleCarrier Proteins/geneticsPseudohypoaldosteronism/genetics/metabolism/physiopathologyPseudohypoaldosteronism[SDV]Life Sciences [q-bio]Blood Pressure030204 cardiovascular system & hematologyNephrons/metabolismKidney0302 clinical medicineMissense mutationChildComputingMilieux_MISCELLANEOUSGeneticsddc:616Aged 80 and over0303 health sciencesbiologyMicrofilament ProteinsMiddle AgedWNK1PhenotypeSodium Chloride SymportersWNK4Ubiquitin ligaseFemaleSignal TransductionAdultmedicine.medical_specialtyAdolescentBlood Pressure/geneticsIon Transport/geneticsMolecular Sequence DataPolymorphism Single Nucleotide03 medical and health sciencesYoung AdultInternal medicineGeneticsmedicineHumansAmino Acid SequenceSodium Chloride Symporters/genetics/metabolism030304 developmental biologyAdaptor Proteins Signal TransducingAgedIon TransportBase Sequenceurogenital systemPseudohypoaldosteronismKidney metabolismNephronsSequence Analysis DNAmedicine.diseaseKidney/metabolismEndocrinologyIon homeostasisbiology.proteinCarrier Proteins
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p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1.

2007

Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 i…

MaleCell signalingmedicine.medical_treatmentImmunologyBone Marrow CellsGATA3 Transcription FactorBiologyp38 Mitogen-Activated Protein KinasesTransactivationMiceTh2 CellsmedicineAnimalsGATA1 Transcription FactorMast CellsRNA MessengerPhosphorylationPromoter Regions GeneticMolecular BiologyInterleukin 5Mice Inbred BALB CGATA2Interleukin-9Mast cellCell biologyInterleukin 33GATA2 Transcription FactorCytokinemedicine.anatomical_structureGene Expression RegulationInterleukin 15MutationFemaleMolecular immunology
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Morphological studies on CLN2

2001

Electron microscopic, fluorescence microscopic, and immunohistochemical studies earlier performed on archivalcerebral tissue from Max Bielchowsky's original three patients revealed curvilinear bodies rich in subunit C of mitochondrial ATP synthase (SCMAS). Recent progress in the elucidation of CLN2, i.e. identification of the defective lysosomal enzyme tripeptidyl-peptidase I (TPP-I) and mutations in the CLN2 gene have further corroborated earlier data. Immunohistochemically the absence of the TPP-I protein could be confirmed in the archival tissues using pathological controls. Unlike biochemistry, immunohistochemistry enables examination of these archival tissues elucidating the causative …

MaleCell typePathologymedicine.medical_specialtyProtein subunitEncephalopathyBiologymedicine.disease_causeAminopeptidasesNeuronal Ceroid-LipofuscinosesChloroquineEndopeptidasesmedicineHumansChildDipeptidyl-Peptidases and Tripeptidyl-PeptidasesMyopathyGeneMutationTripeptidyl-Peptidase 1BrainGeneral MedicineMitochondrial Proton-Translocating ATPasesmedicine.diseaseImmunohistochemistryProton-Translocating ATPasesMutationPediatrics Perinatology and Child HealthImmunohistochemistryFemaleNeurology (clinical)Serine Proteasesmedicine.symptomPeptide Hydrolasesmedicine.drugEuropean Journal of Paediatric Neurology
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A novel compound heterozygous mutation in GALC associated with adult-onset Krabbe disease: case report and literature review

2021

Krabbe disease (KD) is a rare autosomal recessive lipid storage leukodystrophy. It is caused by deficient enzyme activity resulting from mutations of the β-galactocerebrosidase (GALC) gene. KD is distinguished into subtypes based on the age of onset; these are early infantile, late infantile, juvenile, and adult-onset. We report a case of a 47-year-old Caucasian man with a 2-year history of muscle atrophy and weakness in both hands associated with pyramidal signs and mild spasticity in the lower limbs. An extensive work-up led this motor neuron disease-like disorder to be diagnosed as adult-onset KD. The patient was found to be compound heterozygous for two GALC mutations (p.G286D and p.Y49…

MaleCellular and Molecular NeuroscienceHeterozygoteMutationGeneticsHumansSettore MED/26 - NeurologiaMiddle AgedGenetics (clinical)Compound heterozygous mutation GALC Adult-onset Krabbe disease Peripheral neuropathyGalactosylceramidaseLeukodystrophy Globoid Cell
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Aspartoacylase-lacZ knockin mice: an engineered model of Canavan disease.

2011

Canavan Disease (CD) is a recessive leukodystrophy caused by loss of function mutations in the gene encoding aspartoacylase (ASPA), an oligodendrocyte-enriched enzyme that hydrolyses N-acetylaspartate (NAA) to acetate and aspartate. The neurological phenotypes of different rodent models of CD vary considerably. Here we report on a novel targeted aspa mouse mutant expressing the bacterial β-Galactosidase (lacZ) gene under the control of the aspa regulatory elements. X-Gal staining in known ASPA expression domains confirms the integrity of the modified locus in heterozygous aspa lacZ-knockin (aspa(lacZ/+)) mice. In addition, abundant ASPA expression was detected in Schwann cells. Homozygous (…

MaleCentral Nervous SystemCerebellumPathologyAnatomy and PhysiologyCanavan DiseaseMouseMutantlcsh:MedicineNeural HomeostasisBiochemistryMiceNeurobiology of Disease and Regenerationlcsh:ScienceSex CharacteristicsMultidisciplinaryNeuromodulationNeurochemistryGenomicsAnimal ModelsFunctional Genomicsmedicine.anatomical_structureLac OperonNeurologyHomeostatic MechanismsMedicineFemaleNeurochemicalsGenetic EngineeringResearch ArticleNervous System PhysiologyBiotechnologymedicine.medical_specialtyTransgeneCentral nervous systemNeurophysiologyMice TransgenicNeuroimagingBiologyNeurological SystemAmidohydrolasesWhite matterModel OrganismsGeneticsmedicineAnimalsBiologyNeuropeptidesLeukodystrophylcsh:RComputational Biologymedicine.diseaseMolecular biologyCanavan diseaseAspartoacylaseDisease Models AnimalMetabolismnervous systemSmall MoleculesCellular NeuroscienceMetabolic DisordersMutationGenetics of DiseaseNervous System Componentslcsh:QGene FunctionMolecular NeuroscienceAnimal GeneticsNeurosciencePLoS ONE
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Immunohistochemical marker for Na+ CP type Vα (C-20) and heterozygous nonsense SCN5A mutation W822X in a sudden cardiac death induced by mild anaphyl…

2009

A sudden death likely due to mild anaphylactic reaction in a young man is described. Autoptic, histologic, immunohistochemical, and laboratory findings were strongly consistent with the diagnosis of a mild anaphylactic reaction. Genetic molecular analysis, performed on formalin-fixed, paraffin-embedded tissues, showed a mutation described as W822X in a family with electrocardiographic pattern typical of Brugada Syndrome. It results in a nonsense mutation generating a truncated form of the channel protein. The mutation is due to a point substitution of a guanine with an adenine residue (G2466A). Immunohistochemistry and laser scanning confocal microscopy on sections from heart formalin-fixed…

MaleChannellopathies; Confocal laser scanning microscopy; Immunohistochemistry; Na+ CP type Vα (C-20); Sodium channel; Sudden cardiac death; W822X; Adult; Anaphylaxis; Brugada Syndrome; Fatal Outcome; Humans; Male; Muscle Proteins; Myocardium; Myocytes Cardiac; NAV1.5 Voltage-Gated Sodium Channel; Peanut Hypersensitivity; Sodium Channels; Death Sudden Cardiac; Mutation Missense; 2734; Medical Laboratory Technology; HistologyMuscle Proteinsmedicine.disease_causeSodium ChannelsSudden cardiac deathNAV1.5 Voltage-Gated Sodium ChannelNa+ CP type V[alpha] (C-20)Fatal OutcomeMissense mutationMyocytes CardiacConfocal laser scanning microscopyCP type Vα (C-20)Cellular localizationBrugada syndromeBrugada SyndromeMutationChemistrySodium channelChannellopathiesImmunohistochemistryChannellopathies; Confocal laser scanning microscopy; Immunohistochemistry; Na; +; CP type Vα (C-20); Sodium channel; Sudden cardiac death; W822XDeathMedical Laboratory TechnologyCardiologyCardiacAdultmedicine.medical_specialtyHistologyNa+ CP type V[alpha] (C-20) confocal laser scanning microscopy immunohistochemistry sodium channel channellopathies W822X sudden cardiac deathNonsense mutation2734Mutation MissenseSocio-culturaleNa+ CP type Vα (C-20)+Sudden deathPathology and Forensic MedicineInternal medicinemedicineHumansPeanut HypersensitivityNacardiovascular diseasesW822XAnaphylaxisMyocytesSodium channelMyocardiummedicine.diseaseMolecular biologySuddenSudden cardiac deathDeath Sudden CardiacMutationMissenseNa+ CP type V[alpha] (C-20); confocal laser scanning microscopy; immunohistochemistry; sodium channel; channellopathies; W822X; sudden cardiac death
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A very mild phenotype of Charcot-Marie-Tooth disease type 4H caused by two novel mutations in FGD4

2019

Abstract Background Mutations in the FGD4 gene cause an autosomal recessive demyelinating peripheral neuropathy referred to as CMT4H, characterized by its onset in infancy or early-childhood and its slow progression. Methods The clinical and genetic status of two patients with CMT4H was studied, performing genetic testing with a panel of genes and analysing FGD4 mRNA expression by quantitative PCR. Results Two novel FGD4 variants (c.514delG and c.2211dupA) were identified in two mildly affected Spanish siblings with CMT4H, and with disease onset in late adolescence/adulthood (one of them remaining asymptomatic at 20). On examination, foot deformity was observed without weakness or sensory i…

MaleCharcot-Marie-ToothPathologymedicine.medical_specialtyAdolescentFGD4medicine.disease_causeAsymptomaticYoung Adult03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseCharcot-Marie-Tooth disease type 4HCMT4HmedicineHumans030212 general & internal medicineAlleleFrameshift MutationGeneAllelesGenetic testingMutationmedicine.diagnostic_testbusiness.industrySiblingsCMTMicrofilament Proteinsmedicine.diseasePhenotypePedigreeNeuropathyPhenotypePeripheral neuropathyNeurologyFemaleNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgeryJournal of the Neurological Sciences
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Analysis of the C9orf72 gene in patients with amyotrophic lateral sclerosis in Spain and different populations worldwide.

2013

The C9ORF72 Spanish Study Group, et al.

MaleChinaHeterozygoteDNA Mutational AnalysisChromosome 9Kaplan-Meier EstimateBiologyPolymorphism Single NucleotideAsian PeopleGene FrequencyJapanC9orf72GeneticsmedicineEthnicityHumansGenetic Predisposition to DiseaseFamily historyAlleleAmyotrophic lateral sclerosisGenetics (clinical)AgedGeneticsAged 80 and overDNA Repeat ExpansionC9orf72 ProteinHaplotypeAmyotrophic Lateral SclerosisProteinsmedicine.diseaseEuropeHaplotypesSpainAfricaMutationFemaleTrinucleotide repeat expansionFrontotemporal dementia
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