Search results for "Arachnodactyly"

showing 4 items of 4 documents

Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
researchProduct

3q27.3 microdeletional syndrome: a recognisable clinical entity associating dysmorphic features, marfanoid habitus, intellectual disability and psych…

2013

Abstract: Background Since the advent of array-CGH, numerous new microdeletional syndromes have been delineated while others remain to be described. Although 3q29 subtelomeric deletion is a well-described syndrome, there is no report on 3q interstitial deletions. Methods We report for the first time seven patients with interstitial deletions at the 3q27.3q28 locus gathered through the Decipher database, and suggest this locus as a new microdeletional syndrome. Results The patients shared a recognisable facial dysmorphism and marfanoid habitus, associated with psychosis and mild to severe intellectual disability (ID). Most of the patients had no delay in gross psychomotor acquisition, but ha…

AdultMalePsychosisCandidate genePediatricsmedicine.medical_specialtyAdolescentLocus (genetics)ArachnodactylyYoung AdultIntellectual DisabilityIntellectual disabilityGeneticsMedicineHumansAbnormalities MultipleGenetics (clinical)GeneticsComparative Genomic Hybridizationbusiness.industryMood DisordersMarfanoidChromosome MappingFaciesInfantSyndromemedicine.diseasePhenotypeMood disordersChild PreschoolBone maturationFemaleHuman medicineChromosomes Human Pair 3Chromosome DeletionbusinessJournal of medical genetics
researchProduct

The FBN2 gene: new mutations, locus-specific database (Universal Mutation Database FBN2), and genotype-phenotype correlations.

2009

International audience; Congenital contractural arachnodactyly (CCA) is an extremely rare disease, due to mutations in the FBN2 gene encoding fibrillin-2. Another member of the fibrillin family, the FBN1 gene, is involved in a broad phenotypic continuum of connective-tissue disorders including Marfan syndrome. Identifying not only what is in common but also what differentiates these two proteins should enable us to better comprehend their respective functions and better understand the multitude of diseases in which these two genes are involved. In 1995 we created a locus-specific database (LSDB) for FBN1 mutations with the Universal Mutation Database (UMD) tool. To facilitate comparison of …

Fibrillin-2MESH : Polymorphism GeneticFibrillin-1DNA Mutational AnalysisMESH : Genotype[SDV.GEN] Life Sciences [q-bio]/Geneticscomputer.software_genreMESH: Genotype0302 clinical medicineGenotypeDatabases GeneticMissense mutationCongenital contractural arachnodactylyMESH: DNA Mutational AnalysisGenetics (clinical)MESH: Databases GeneticRegulation of gene expressionGenetics0303 health sciencesDatabaseMESH : Gene Expression RegulationMicrofilament ProteinsPhenotypeMESH: Gene Expression RegulationBeals-Hecht syndrome3. Good healthINCMESH : PhenotypePhenotypeMESH : MutationFibrillinmusculoskeletal diseasesMESH: MutationGenotypeMESH : Microfilament Proteinsdatabase OFFICIAL JOURNAL wwwhgvsorg & 2008 WILEY-LISSLocus (genetics)fibrillinMESH : DNA Mutational AnalysisBiologyFibrillinsMESH: PhenotypeMESH: Sequence Homology Nucleic Acidcongenital contractural arachnodactyly03 medical and health sciencesMESH: Microfilament ProteinsSequence Homology Nucleic AcidMESH: Polymorphism GeneticGeneticsmedicineHumansMESH : Sequence Homology Nucleic AcidFBN2CCAMESH : Databases GeneticGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsPolymorphism GeneticMESH: HumansMESH : Humansmedicine.diseaseGene Expression RegulationMutation[ SDV.GEN ] Life Sciences [q-bio]/Geneticscomputer030217 neurology & neurosurgery
researchProduct

In-Frame Mutations in Exon 1 of SKI Cause Dominant Shprintzen-Goldberg Syndrome

2012

International audience; Shprintzen-Goldberg syndrome (SGS) is characterized by severe marfanoid habitus, intellectual disability, camptodactyly, typical facial dysmorphism, and craniosynostosis. Using family-based exome sequencing, we identified a dominantly inherited heterozygous in-frame deletion in exon 1 of SKI. Direct sequencing of SKI further identified one overlapping heterozygous in-frame deletion and ten heterozygous missense mutations affecting recurrent residues in 18 of the 19 individuals screened for SGS; these individuals included one family affected by somatic mosaicism. All mutations were located in a restricted area of exon 1, within the R-SMAD binding domain of SKI. No mut…

MaleModels Molecularmedicine.disease_cause[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMarfan SyndromeArachnodactylyExon0302 clinical medicineGene OrderMissense mutationGenetics(clinical)Child[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)Exome sequencingGenes DominantGenetics0303 health sciencesMutationShprintzen–Goldberg syndromeExonsPhenotypePedigreeDNA-Binding ProteinsPhenotypeChild PreschoolFemalemedicine.symptomAdultAdolescentMolecular Sequence Data[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics03 medical and health sciencesCamptodactylyCraniosynostosesYoung Adultstomatognathic systemReportProto-Oncogene ProteinsmedicineGeneticsHumansAmino Acid Sequence030304 developmental biologyFacies[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyProtein Structure TertiaryArachnodactyly[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationSequence Alignmenthuman activities030217 neurology & neurosurgery
researchProduct