Search results for "Mutation."

showing 10 items of 2808 documents

Body Weight, Physical Activity, and Risk of Cancer in Lynch Syndrome

2021

Simple Summary Lifestyle modifies cancer risk in the general public. How lifestyle modifies cancer risk in individuals carrying the inherited pathogenic gene variants in DNA mismatch repair genes (Lynch syndrome) remains understudied. We conducted a retrospective study with cancer register data to investigate associations between body weight, physical activity, and cancer risk among Finnish Lynch syndrome carriers (n = 465, 54% women). The results of our study indicated that longitudinal weight gain increases cancer risk, whereas being highly physically active during adulthood could decrease cancer risk in men. Further, women were observed to be less prone to lifestyle-related risk factors …

elintavatperinnölliset tauditMENOPAUSElifestyleMUTATIONS3122 Cancershereditary non-polyposis colorectal cancerylipainoEXERCISEsuolistosyövätriskitekijätlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282ArticleCOLORECTAL-CANCERESTROGENADIPOSE-TISSUEMASS INDEXAGEDEFINED FAMILIAL RISKepidemiologyepidemiologiaLynchin oireyhtymäfyysinen aktiivisuusASSOCIATIONSCancers
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Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity

2014

Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regul…

endocrine system diseasesMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesGene ExpressionRNA-binding proteinResveratrolBiologyp38 Mitogen-Activated Protein KinasesMicechemistry.chemical_compoundCell Line TumorStilbenesGene expressionGeneticsAnimalsHumansddc:610RNA Messengerskin and connective tissue diseasesMice KnockoutMessenger RNAGene knockdownExosome Multienzyme Ribonuclease Complexorganic chemicalsAnti-Inflammatory Agents Non-SteroidalGene regulation Chromatin and EpigeneticsRNA-Binding Proteinsfood and beveragesMolecular biology3. Good healthCell biologychemistryResveratrolMutationTrans-ActivatorsPhosphorylationInflammation Mediatorshormones hormone substitutes and hormone antagonistsNucleic Acids Research
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L‐Aspartate as a high‐quality nitrogen source in Escherichia coli : Regulation of L‐aspartase by the nitrogen regulatory system and interaction of L‐…

2020

Escherichia coli uses the C4-dicarboxylate transporter DcuA for L-aspartate/fumarate antiport, which results in the exploitation of L-aspartate for fumarate respiration under anaerobic conditions and for nitrogen assimilation under aerobic and anaerobic conditions. L-Aspartate represents a high-quality nitrogen source for assimilation. Nitrogen assimilation from L-aspartate required DcuA, and aspartase AspA to release ammonia. Ammonia is able to provide by established pathways the complete set of intracellular precursors (ammonia, L-aspartate, L-glutamate, and L-glutamine) for synthesizing amino acids, nucleotides, and amino sugars. AspA was regulated by a central regulator of nitrogen meta…

endocrine system diseasesNitrogenGlutaminePII Nitrogen Regulatory ProteinsNitrogen assimilationDeaminationGlutamic AcidBiologymedicine.disease_causeAspartate Ammonia-LyaseMicrobiology03 medical and health sciencesBacterial ProteinsAmmoniaEscherichia colimedicineProtein Interaction Domains and MotifsNucleotideMolecular BiologyEscherichia coliNitrogen cycle030304 developmental biologyDicarboxylic Acid Transporterschemistry.chemical_classificationAspartic Acid0303 health sciences030306 microbiologyEscherichia coli ProteinsAssimilation (biology)Gene Expression Regulation BacterialAmino acidEnzymechemistryBiochemistryMutationKetoglutaric AcidsMetabolic Networks and PathwaysMolecular Microbiology
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Molecular Approaches Fighting Nonsense

2021

Nonsense mutations are the result of single nucleotide substitutions in the DNA that change a sense codon (coding for an amino acid) to a nonsense or premature termination codon (PTC) within the coding region of the mRNA [...]

endocrine system diseasesQH301-705.5media_common.quotation_subjectNonsenseNonsense mutationBiologyCatalysisInorganic ChemistrySense Codonchemistry.chemical_compoundHumansCoding regionNucleotideBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopymedia_commonchemistry.chemical_classificationGeneticsMessenger RNAOrganic ChemistryGenetic Diseases InbornSettore CHIM/06 - Chimica OrganicaGeneral MedicineNonsense Mediated mRNA DecayComputer Science ApplicationsAmino acidChemistryn/aEditorialchemistryCodon NonsenseGenetic DiseasesProtein BiosynthesisMutationsense organsDNAInternational Journal of Molecular Sciences
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Measuring mutagenicity in ecotoxicology: A case study of Cd exposure in Chironomus riparius.

2021

Abstract Existing mutagenicity tests for metazoans lack the direct observation of enhanced germline mutation rates after exposure to anthropogenic substances, therefore being inefficient. Cadmium (Cd) is a metal described as a mutagen in mammalian cells and listed as a group 1 carcinogenic and mutagenic substance. But Cd mutagenesis mechanism is not yet clear. Therefore, in the present study, we propose a method coupling short-term mutation accumulation (MA) lines with subsequent whole genome sequencing (WGS) and a dedicated data analysis pipeline to investigate if chronic Cd exposure on Chironomus riparius can alter the rate at which de novo point mutations appear. Results show that Cd exp…

endocrine system010504 meteorology & atmospheric sciencesHealth Toxicology and Mutagenesisved/biology.organism_classification_rank.speciesMutagen010501 environmental sciencesBiologyToxicologymedicine.disease_causeEcotoxicology01 natural sciencesChironomidaeGermline mutationmedicineAnimalsCarcinogen0105 earth and related environmental sciencesChironomus ripariusGeneticsved/biologyMutagenicity TestsPoint mutationfungiMutagenesisfood and beveragesGeneral MedicineMutation AccumulationPollutionmedicine.anatomical_structureMutagenesisGerm cellCadmiumMutagensEnvironmental pollution (Barking, Essex : 1987)
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De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome

2014

Activating mutations in genes encoding phosphatidylinositol 3-kinase (PI3K)-AKT pathway components cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH, OMIM 603387)(1-3). Here we report that individuals with MPPH lacking upstream PI3K-AKT pathway mutations carry de novo mutations in CCND2 (encoding cyclin D2) that are clustered around a residue that can be phosphorylated by glycogen synthase kinase 313 (GSK-3 beta)(4). Mutant CCND2 was resistant to proteasomal degradation in vitro compared to wild-type CCND2. The PI3K-AKT pathway modulates GSK-3 beta activity(4), and cells from individuals with PIK3CA, PIK3R2 or AKT3 mutations showed similar CCND2 accumulation. CCND…

endocrine systemBlotting WesternMolecular Sequence DataMutantMedizinBiologymedicine.disease_causeArticleAKT3Mice03 medical and health sciences0302 clinical medicineCyclin D2GSK-3GeneticsmedicineAnimalsCyclin D2HumansAbnormalities MultipleExomeMegalencephalyPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesMutationBase SequenceSequence Analysis DNASyndromeCell cyclemedicine.diseaseImmunohistochemistryMolecular biologyMegalencephalyMalformations of Cortical DevelopmentPolydactylyElectroporationHEK293 CellsBromodeoxyuridineMicroscopy FluorescenceMutagenesis Site-DirectedFemale030217 neurology & neurosurgeryHydrocephalusNature Genetics
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Extensive nuclear gyration and pervasive non-genic transcription during primordial germ cell development in zebrafish.

2020

ABSTRACT Primordial germ cells (PGCs) are the precursors of germ cells, which migrate to the genital ridge during early development. Relatively little is known about PGCs after their migration. We studied this post-migratory stage using microscopy and sequencing techniques, and found that many PGC-specific genes, including genes known to induce PGC fate in the mouse, are only activated several days after migration. At this same time point, PGC nuclei become extremely gyrated, displaying general broad opening of chromatin and high levels of intergenic transcription. This is accompanied by changes in nuage morphology, expression of large loci (PGC-expressed non-coding RNA loci, PERLs) that ar…

endocrine systemRNA UntranslatedTranscription GeneticZygotePiwi-interacting RNApiRNABiology03 medical and health sciences0302 clinical medicineGyrationTranscription (biology)Primordial germ cellmedicineAnimalsRNA Small InterferingMolecular BiologyZebrafishGeneZebrafish030304 developmental biologyCell NucleusNuage0303 health sciencesGonadal ridgeurogenital systemNuclear morphologyGene Expression Regulation DevelopmentalDNA-Directed RNA PolymerasesZygotic activationZebrafish Proteinsbiology.organism_classificationChromatinCell biologyUp-Regulationmedicine.anatomical_structureGerm CellsGenetic Loci207FertilizationMutationIntergenic transcriptionDNA Transposable ElementsDNA Intergenic030217 neurology & neurosurgeryGerm cellBiogenesisDevelopmental BiologyResearch ArticleDevelopment (Cambridge, England)
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EZH2 mutations are frequent and represent an early event in follicular lymphoma

2013

Gain of function mutations in the H3K27 methyltransferase EZH2 represent a promising therapeutic target in germinal center lymphomas. In this study, we assessed the frequency and distribution of EZH2 mutations in a large cohort of patients with follicular lymphoma (FL) (n = 366) and performed a longitudinal analysis of mutation during the disease progression from FL to transformed FL (tFL) (n = 33). Mutations were detected at 3 recurrent mutation hot spots (Y646, A682, and A692) in 27% of FL cases with variant allele frequencies (VAF) ranging from 2% to 61%. By comparing VAF of EZH2 with other mutation targets (CREBBP, MLL2, TNFRSF14, and MEF2B), we were able to distinguish patients harbori…

endocrine systemTime FactorsMethyltransferasemedicine.medical_treatmentDNA Mutational AnalysisImmunologyFollicular lymphomaKaplan-Meier Estimatemacromolecular substancesBiologymedicine.disease_causeBiochemistryTargeted therapyCohort StudiesGene Frequencyhemic and lymphatic diseasesBiomarkers TumormedicineHumansEnhancer of Zeste Homolog 2 ProteinLymphoma FollicularAllele frequencyMutationLymphoid NeoplasiaMEF2 Transcription FactorsGene Expression ProfilingEZH2Polycomb Repressive Complex 2Germinal centerCell BiologyHematologymedicine.diseaseCREB-Binding ProteinLymphomaMutationDisease ProgressionCancer researchReceptors Tumor Necrosis Factor Member 14Blood
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Developmental Abnormalities of the Thyroid

2010

Publisher Summary This chapter explores the abnormalities in the development of the thyroid gland during organogenesis referred to as thyroid dysgenesis. Permanent primary congenital hypothyroidism (CH) is mentioned to be the most common congenital endocrine disorder as estimated from systematic biochemical screening of newborns. The functional disorders of the thyroid gland are known as thyroid dyshormonogenesis and this disorder is typically inherited in an autosomal recessive manner and common in populations with a high degree of consanguinity. It briefly reviews the single gene disorders that cause CH from thyroid dysgenesis, and mutations that activate the thyrotropin receptor (TSH) re…

endocrine systemmedicine.medical_specialtyGoiterendocrine system diseasesThyroidThyroid Transcription Factor 1BiologyGene mutationmedicine.diseaseThyroid dysgenesisCongenital hypothyroidismThyroid dyshormonogenesismedicine.anatomical_structureEndocrinologyInternal medicinemedicinePAX8
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Absence of mutations in the WT1 gene in patients with XY gonadal dysgenesis

1995

The WT1 gene is normally expressed during gonadal development and specific mutations in heterozygous form cause Drash syndrome, characterized by male pseudohermaphroditism and gonadal dysgenesis, renal failure and a predisposition for Wilms' tumour. These observations prompted us to test whether WT1 mutations are involved in isolated gonadal dysgenesis, being the most severe form of disturbance in gonadal differentiation. We studied 27 cases of 46,XY females with gonadal dysgenesis who had previously been screened for and found not to carry SRY gene mutations. We performed mutational screening of the WT1 gene with denaturing gradient gel electrophoresis. In one of these patients, a heterozy…

endocrine systemmedicine.medical_specialtyGonadGonadal dysgenesisBiologymedicine.disease_causePolymerase Chain ReactionXY gonadal dysgenesisExonInternal medicineGeneticsmedicineHumansGenetics (clinical)Gonadal Dysgenesis 46XYGeneticsMutationurogenital systemPoint mutationDNAExonsmedicine.diseaseEndocrinologymedicine.anatomical_structureTestis determining factorMutationMale pseudohermaphroditismFemaleHuman Genetics
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