Search results for "GLI3"

showing 4 items of 4 documents

GLI3 is rarely implicated in OFD syndromes with midline abnormalities

2011

A range of phenotypes including Greig cephalopolysyndactyly and Pallister-Hall syndromes (GCPS, PHS) are caused by pathogenic mutation of the GLI3 gene. To characterize the clinical variability of GLI3 mutations, we present a subset of a cohort of 174 probands referred for GLI3 analysis. Eighty-one probands with typical GCPS or PHS were previously reported, and we report the remaining ninety-three probands here. This includes nineteen probands (twelve mutations) who fulfilled clinical criteria for GCPS or PHS, forty-eight probands (sixteen mutations) with features of GCPS or PHS but who did not meet the clinical criteria (sub-GCPS and sub-PHS), twenty-one probands (six mutations) with featu…

congenital hereditary and neonatal diseases and abnormalitiesPallister-Hall SyndromeKruppel-Like Transcription FactorsNerve Tissue ProteinsBiologyBioinformaticsArticlePolydactylyMutationGLI3Mutation (genetic algorithm)GeneticsHumansAbnormalities MultipleSyndactylyGenetics (clinical)Human Mutation
researchProduct

TCTN3 Mutations Cause Mohr-Majewski Syndrome

2012

Orofaciodigital syndromes (OFDSs) consist of a group of heterogeneous disorders characterized by abnormalities in the oral cavity, face, and digits and associated phenotypic abnormalities that lead to the delineation of 13 OFDS subtypes. Here, by a combined approach of homozygozity mapping and exome ciliary sequencing, we identified truncating TCTN3 mutations as the cause of an extreme form of OFD associated with bone dysplasia, tibial defect, cystic kidneys, and brain anomalies (OFD IV, Mohr-Majewski syndrome). Analysis of 184 individuals with various ciliopathies (OFD, Meckel, Joubert, and short rib polydactyly syndromes) led us to identify four additional truncating TCTN3 mutations in un…

AdolescentFoot Deformities CongenitalMolecular Sequence DataCiliopathiesJoubert syndromeYoung AdultFetusReportCerebellumGLI3medicineGeneticsHumansExomeHedgehog ProteinsGenetics(clinical)Sonic hedgehogChildExomeGenetics (clinical)Adaptor Proteins Signal TransducingCystic kidneyGeneticsBase SequencebiologyHomozygoteIntracellular Signaling Peptides and ProteinsMembrane ProteinsCiliary transition zoneSequence Analysis DNAOrofaciodigital Syndromesmedicine.diseaseCleft PalateCiliopathyPhenotypeMutationbiology.proteinApoptosis Regulatory ProteinsHand Deformities CongenitalSignal TransductionThe American Journal of Human Genetics
researchProduct

Mutations in KIAA0586 Cause Lethal Ciliopathies Ranging from a Hydrolethalus Phenotype to Short-Rib Polydactyly Syndrome

2015

KIAA0586, the human ortholog of chicken TALPID3, is a centrosomal protein that is essential for primary ciliogenesis. Its disruption in animal models causes defects attributed to abnormal hedgehog signaling; these defects include polydactyly and abnormal dorsoventral patterning of the neural tube. Here, we report homozygous mutations of KIAA0586 in four families affected by lethal ciliopathies ranging from a hydrolethalus phenotype to short-rib polydactyly. We show defective ciliogenesis, as well as abnormal response to SHH-signaling activation in cells derived from affected individuals, consistent with a role of KIAA0586 in primary cilia biogenesis. Whereas centriolar maturation seemed una…

Heart Defects CongenitalMolecular Sequence DataCell Cycle ProteinsBiologyShort Rib-Polydactyly SyndromeCiliopathies03 medical and health sciencesFatal OutcomeCiliogenesisReportGLI3GeneticsmedicineHumansGenetics(clinical)Europe EasternGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesLikelihood FunctionsShort rib – polydactyly syndromePolydactylyBase SequenceCilium030305 genetics & hereditySequence Analysis DNAmedicine.diseasePhenotypeHuman geneticsHedgehog signaling pathwayFounder EffectPedigreePhenotypeCodon NonsenseCentriolar satelliteErratumHand Deformities CongenitalCiliary Motility DisordersHydrocephalus
researchProduct

The E3 Ubiquitin Ligase MID1 Catalyzes Ubiquitination and Cleavage of Fu

2014

Sonic Hedgehog (SHH)-GLI signalling plays an important role during embryogenesis and in tumorigenesis. The survival and growth of several types of cancer depend on autonomously activated SHH-GLI signalling. A protein complex containing the ubiquitin-ligase MID1 and protein phosphatase 2A (PP2A) regulates the nuclear localization and transcriptional activity of GLI3, a transcriptional effector molecule of SHH, in cancer cell lines with autonomously activated SHH signalling. However, the exact molecular mechanisms that mediate the interaction between MID1 and GLI3 remained unknown. Here, we show that MID1 catalyses the ubiquitination and proteasomal cleavage of the GLI3-regulator Fu. Our data…

metabolism [Microtubule Proteins]Ubiquitin-conjugating enzymeBiochemistrymetabolism [Protein Serine-Threonine Kinases]Ubiquitinmetabolism [Transcription Factors]Nuclear proteinSonic hedgehogbiologymetabolism [Protein-Serine-Threonine Kinases]Nuclear Proteinsrespiratory systemProtein-Serine-Threonine KinasesUbiquitin ligaseGene Expression Regulation NeoplasticGLI3 protein humanBiochemistryddc:540embryonic structuresMicrotubule Proteinsmetabolism [Hedgehog Proteins]Function and Dysfunction of the Nervous Systemmetabolism [Nuclear Proteins]Signal Transductionmetabolism [Kruppel-Like Transcription Factors]Proteasome Endopeptidase Complexanimal structuresSTK36 protein humanUbiquitin-Protein LigasesKruppel-Like Transcription FactorsNerve Tissue ProteinsProtein Serine-Threonine Kinaseschemistry [Ubiquitin-Protein Ligases]CatalysisZinc Finger Protein Gli3Cell Line TumorGLI3HumansHedgehog Proteinsmetabolism [Proteasome Endopeptidase Complex]metabolism [Cell Nucleus]Molecular Biologychemistry [Lysine]DNA PrimersCell Nucleusmetabolism [Nerve Tissue Proteins]UbiquitinLysineUbiquitinationCell BiologyProtein phosphatase 2chemistry [Ubiquitin]Proteasomebiology.proteinSHH protein humanhuman activitiesMid1 protein humanHeLa CellsTranscription FactorsJournal of Biological Chemistry
researchProduct