Search results for "mutation."

showing 10 items of 2808 documents

Updated Field Synopsis and Systematic Meta-Analyses of Genetic Association Studies in Cutaneous Melanoma: The MelGene Database

2015

We updated a field synopsis of genetic associations of cutaneous melanoma (CM) by systematically retrieving and combining data from all studies in the field published as of August 31, 2013. Data were available from 197 studies, which included 83,343 CM cases and 187,809 controls and reported on 1,126 polymorphisms in 289 different genes. Random-effects meta-analyses of 81 eligible polymorphisms evaluated in4 data sets confirmed 20 single-nucleotide polymorphisms across 10 loci (TYR, AFG3L1P, CDK10, MYH7B, SLC45A2, MTAP, ATM, CLPTM1L, FTO, and CASP8) that have previously been published with genome-wide significant evidence for association (P5 × 10(-8)) with CM risk, with certain variants pos…

SLC45A2Skin NeoplasmsLocus (genetics)DermatologyPolymorphism Single NucleotideBiochemistryLinkage DisequilibriumGermlineStatistical significanceDatabases GeneticOdds RatioHumansGenetic Predisposition to DiseaseMelanomaGeneMolecular BiologyGerm-Line MutationGenetic associationGeneticsbiologyChromosome MappingGenetic VariationCell BiologyGene Expression Regulation NeoplasticCutaneous melanomabiology.proteinGenome-Wide Association StudyJournal of Investigative Dermatology
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AP5Z1/SPG4 8 frequency in autosomal recessive and sporadic spastic paraplegia

2014

Hereditary spastic paraplegias (HSP) constitute a rare and highly heterogeneous group of neurodegenerative disorders, defined clinically by progressive lower limb spasticity and pyramidal weakness. Autosomal recessive HSP as well as sporadic cases present a significant diagnostic challenge. Mutations in AP5Z1, a gene playing a role in intracellular membrane trafficking, have been recently reported to be associated with spastic paraplegia type 48 (SPG48). Our objective was to determine the relative frequency and clinical relevance of AP5Z1 mutations in a large cohort of 127 HSP patients. We applied a targeted next-generation sequencing approach to analyze all coding exons of the AP5Z1 gene. …

SPG48Nonsynonymous substitutionHereditary spastic paraplegiaGene mutationBioinformaticsDeep sequencing03 medical and health sciencesExon0302 clinical medicinetargeted next-generation sequencingGeneticsSpasticmedicineddc:610hereditary spastic paraplegiaMolecular BiologyGeneGenetics (clinical)030304 developmental biologyGenetic testingGenetics0303 health sciencesClinical Reportmedicine.diagnostic_testbusiness.industrymedicine.disease3. Good healthAP5Z1business030217 neurology & neurosurgeryMolecular Genetics & Genomic Medicine
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Direct Identification of Each Specific Mutation in Codon 12 and 13 of ci-ki-ras2 by SSCP Analysis

1998

We compared the SSCP behaviour of the DNA fragments containing c-ki-ras 2 wild type 12 and 13 codons or each of the 12 possible point mutated sequences in these two codons. We found that a single electrophoresis condition was sufficient to distinguish each specific mutation from the other 11 and from the wild type sequence. This observation makes it possible to identify each specific mutation directly by SSCP without any need for reamplification and sequencing.

SSCP analysisBiophysicsBiologyBiochemistryFrameshift mutationProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundGene FrequencyHumansCloning MolecularRas2CodonMolecular BiologyPolymorphism Single-Stranded ConformationalSequence (medicine)GeneticsSpecific mutationCarcinomaWild typeSingle-strand conformation polymorphismDNA NeoplasmCell BiologyMolecular biologyGenes raschemistryMutationElectrophoresis Polyacrylamide GelColorectal NeoplasmsDNABiochemical and Biophysical Research Communications
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PARD3 Inactivation in Lung Squamous Cell Carcinomas Impairs STAT3 and Promotes Malignant Invasion.

2015

Abstract Correct apicobasal polarization and intercellular adhesions are essential for the appropriate development of normal epithelia. Here, we investigated the contribution of the cell polarity regulator PARD3 to the development of lung squamous cell carcinomas (LSCC). Tumor-specific PARD3 alterations were found in 8% of LSCCs examined, placing PARD3 among the most common tumor suppressor genes in this malignancy. Most PAR3-mutant proteins exhibited a relative reduction in the ability to mediate formation of tight junctions and actin-based protrusions, bind atypical protein kinase C, activate RAC1, and activate STAT3 at cell confluence. Thus, PARD3 alterations prevented the formation of c…

STAT3 Transcription Factorrac1 GTP-Binding ProteinCancer ResearchLung NeoplasmsCellMice NudeRAC1Cell Cycle ProteinsBiologyArticleCell MovementCell Line TumorCell polaritymedicineAnimalsHumansNeoplasm InvasivenessProtein Kinase CAdaptor Proteins Signal TransducingCell ProliferationConfluencyTight junctionBase SequenceCell growthLiver NeoplasmsMembrane ProteinsSequence Analysis DNACell biologymedicine.anatomical_structureOncologyCell cultureMutationCancer researchCarcinoma Squamous CellTranscriptomeIntracellularNeoplasm TransplantationCancer research
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Adjuvant Imatinib in Patients with GIST Harboring Exon 9 KIT Mutations : Results from a Multi-institutional European Retrospective Study

2022

[Purpose] The effect of high-dose imatinib (800 mg/day) on survival in the adjuvant treatment of patients with resected KIT exon 9–mutated gastrointestinal stromal tumors (GIST) is not established. Here, the association of dose and other clinicopathologic variables with survival was evaluated in a large multi-institutional European cohort.

STRUCTURAL BASISEXPRESSIONOncologyCancer Researchmedicine.medical_specialtyGastrointestinal Stromal Tumors3122 CancersMedizinAntineoplastic Agentsexon 9Adjuvants ImmunologicInternal medicinemedicineHumansFAILURERetrospective StudiesRISKRECEPTORGiSTProportional hazards modelbusiness.industryGASTROINTESTINAL STROMAL TUMORSHazard ratioImatinibRetrospective cohort studyExonsAdjuvant treatmentConfidence intervalGENOTYPEProto-Oncogene Proteins c-kitOncologyChemotherapy AdjuvantMutationPropensity score matchingCohortImatinib MesylateNeoplasm Recurrence LocalTYROSINE KINASE INHIBITORbusinessRare cancers Radboud Institute for Health Sciences [Radboudumc 9]medicine.drugGIST
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A Multivariate Analysis of HIV-1 Protease Inhibitors and Resistance Induced by Mutation

2005

This paper describes the use of the multivariate statistical procedure principal component analysis as a tool to explore the inhibitory activity of classes of protease inhibitors (PIs) against HIV-1 viruses (wild type and more-frequent single mutants, V82A, V82F, and I84V) and against protease enzymes. The analysis of correlations between biological activity and molecular descriptors or similarity indexes allowed a reliable classification of the 51 derivatives considered in this study. The best results were obtained in the case of the I84V mutant for which a high number of predictions was achieved. On this basis, this statistical approach is proposed as a reliable method for the prediction …

STRUCTURE-BASED DESIGNMultivariate analysisGeneral Chemical Engineeringmedicine.medical_treatmentMutantComputational biologyLibrary and Information SciencesModels BiologicalStructure-Activity RelationshipHIV-1 proteaseMolecular descriptorDrug Resistance ViralmedicineHIV Protease InhibitorBIOLOGICAL EVALUATIONGeneticschemistry.chemical_classificationProteasebiologyWild typeBiological activityANTIVIRAL ACTIVITYGeneral ChemistryHIV Protease InhibitorsGeneral MedicineD-AMINO ACIDSIN-VITROComputer Science ApplicationsORALLY BIOAVAILABLE INHIBITOREnzymechemistryRAY CRYSTAL-STRUCTUREMultivariate AnalysisMutationHUMAN-IMMUNODEFICIENCY-VIRUSHIV-1biology.proteinTYPE-1 PROTEASEQUANTITATIVE STRUCTURESoftware
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Protein kinase C controls activation of the DNA integrity checkpoint

2014

The protein kinase C (PKC) superfamily plays key regulatory roles in numerous cellular processes. Saccharomyces cerevisiae contains a single PKC, Pkc1, whose main function is cell wall integrity maintenance. In this work, we connect the Pkc1 protein to the maintenance of genome integrity in response to genotoxic stresses. Pkc1 and its kinase activity are necessary for the phosphorylation of checkpoint kinase Rad53, histone H2A and Xrs2 protein after deoxyribonucleic acid (DNA) damage, indicating that Pkc1 is required for activation of checkpoint kinases Mec1 and Tel1. Furthermore, Pkc1 electrophoretic mobility is delayed after inducing DNA damage, which reflects that Pkc1 is post-translatio…

Saccharomyces cerevisiae ProteinsCell cycle checkpointCell Cycle ProteinsProtein Serine-Threonine KinasesGenome Integrity Repair and ReplicationBiologyGeneticsHumansCHEK1Kinase activityCheckpoint Kinase 2Protein Kinase CProtein kinase CDNA-PKcsDNA integrity checkpointIntracellular Signaling Peptides and ProteinsG2-M DNA damage checkpointCell biologyCheckpoint Kinase 2Protein Kinase C-deltaBiochemistryMutationProtein Processing Post-TranslationalDNA DamageHeLa CellsMutagensNucleic Acids Research
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Role of glycine-82 as a pivot point during the transition from the inactive to the active form of the yeast Ras2 protein

1991

AbstractRas proteins bind either GDP or GTP with high affinity. However, only the GTP-bound form of the yeast Ras2 protein is able to stimulate adenylyl cyclase. To identify amino acid residues that play a role in the conversion from the GDP-bound to the GTP-bound state of Ras proteins, we have searched for single amino acid substitutions that selectively affected the binding of one of the two nucleotides. We have found that the replacement of glycine-82 of the Ras2 protein by serine resulted in an increased rate of dissociation of Gpp(NH)p, a nonhydrolysable analog of GTP, while the GDP dissociation rate was not significantly modified. Glycine-82 resides in a region that is highly conserve…

Saccharomyces cerevisiae ProteinsGTP'Guanosine diphosphateProtein ConformationRestriction MappingGlycineBiophysicsSaccharomyces cerevisiaeBiochemistryFungal ProteinsGTP-binding protein regulatorsProtein structureGTP-Binding ProteinsStructural BiologyEscherichia coliGeneticsRHO protein GDP dissociation inhibitorAmino Acid SequenceRas2Binding siteMolecular BiologyPeptide sequencechemistry.chemical_classificationGuanylyl ImidodiphosphateBinding SitesPoint mutationChemistryCell BiologyGuanosine triphosphateRecombinant ProteinsAmino acidModels StructuralBiochemistryMutagenesis Site-Directedras ProteinsS. cerevisaePlasmidsRasFEBS Letters
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Rot1 plays an antagonistic role to Clb2 in actin cytoskeleton dynamics throughout the cell cycle.

2007

ROT1 is an essential gene whose inactivation causes defects in cell cycle progression and morphogenesis in budding yeast. Rot1 affects the actin cytoskeleton during the cell cycle at two levels. First, it is required for the maintenance of apical growth during bud growth. Second, Rot1 is necessary to polarize actin cytoskeleton to the neck region at the end of mitosis; because of this defect, rot1 cells do not properly form a septum to complete cell division. The inability to polarize the actin cytoskeleton at the end of mitosis is not due to a defect in the recruitment of the polarisome scaffold protein Spa2 or the actin cytoskeleton regulators Cdc42 and Cdc24 in the neck region. Previous …

Saccharomyces cerevisiae ProteinsGenes FungalArp2/3 complexmacromolecular substancesSaccharomyces cerevisiaeCyclin BActin remodeling of neuronsGene Expression Regulation FungalCDC2-CDC28 KinasesCytoskeletonCytoskeletonPolarisomebiologyCell CycleActin remodelingCell PolarityMembrane ProteinsCell BiologyActin cytoskeletonActinsCell biologyProfilinParacytophagyMutationbiology.proteinMolecular ChaperonesJournal of cell science
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The MAPK Hog1 recruits Rpd3 histone deacetylase to activate osmoresponsive genes

2003

Regulation of gene expression by mitogen-activated protein kinases (MAPKs) is essential for proper cell adaptation to extracellular stimuli. Exposure of yeast cells to high osmolarity results in rapid activation of the MAPK Hog1, which coordinates the transcriptional programme required for cell survival on osmostress. The mechanisms by which Hog1 and MAPKs in general regulate gene expression are not completely understood, although Hog1 can modify some transcription factors. Here we propose that Hog1 induces gene expression by a mechanism that involves recruiting a specific histone deacetylase complex to the promoters of genes regulated by osmostress. Cells lacking the Rpd3-Sin3 histone deac…

Saccharomyces cerevisiae ProteinsGenes FungalSaccharomyces cerevisiaeBiologySAP30Histone DeacetylasesOsmotic PressureGene Expression Regulation FungalPromoter Regions GeneticOligonucleotide Array Sequence AnalysisHistone deacetylase 5MultidisciplinaryHistone deacetylase 2HDAC11HDAC10HDAC9Molecular biologyHDAC4Cell biologyRepressor ProteinsMutationHistone deacetylase complexRNA Polymerase IIMitogen-Activated Protein KinasesProtein BindingTranscription FactorsNature
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