Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
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Differential expression of the tumor suppressor A-kinase anchor protein 12 in human diffuse and pilocytic astrocytomas is regulated by promoter methy…

2013

The scaffold protein A-kinase anchor protein 12 (AKAP12) exerts tumor suppressor activity and is downregulated in several tumor entities. We characterized AKAP12 expression and regulation in astrocytomas, including pilocytic and diffusely infiltrating astrocytomas. We examined 194 human gliomas and 23 normal brain white matter samples by immunohistochemistry or immunoblotting for AKAP12 expression. We further performed quantitative methylation analysis of the AKAP12 promoter by MassARRAY® of normal brain, World Health Organization (WHO) grade I to IV astrocytomas, and glioma cell lines. Our results show that AKAP12 is expressed in a perivascular distribution in normal CNS, strongly upregula…

AdultMalePathologymedicine.medical_specialtyAdolescent2804 Cellular and Molecular NeuroscienceA Kinase Anchor ProteinsCell Cycle Proteins610 Medicine & healthAstrocytomaBiologyPathology and Forensic MedicineCellular and Molecular NeuroscienceGliomamedicineHumansChildPromoter Regions GeneticneoplasmsAgedAged 80 and overRegulation of gene expressionPilocytic astrocytomaBrain NeoplasmsInfantAstrocytomaGeneral MedicineMethylationDNA MethylationMiddle AgedAKAP12medicine.diseaseUp-Regulationnervous system diseases10040 Clinic for NeurologyGene Expression Regulation Neoplastic2734 Pathology and Forensic Medicine2728 Neurology (clinical)nervous systemNeurologyChild Preschool2808 NeurologyDNA methylationCancer researchImmunohistochemistryFemaleNeurology (clinical)Neoplasm Grading
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P16INK4A and p15INK4B gene alteration associated with oxidative stress in renal cell carcinomas after the chernobyl accident (pilot study).

2002

Our study was undertaken to better understand the role of G1/S transition abnormalities in the malignant progression of renal cell carcinomas (RCCs), exposed to long-term low doses of ionizing radiation (IR), from patients living in radiocontaminated areas of the Ukraine after the Chernobyl accident. We studied p16 and p15 gene alteration in association with oxidative stress markers, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). We analyzed 88 samples collected from 22 patients with RCCs and with different exposure to IR. Homozygous deletion of the p16 and p15 genes, as well as hypermethylation of the 5CpG island in the promoter region of the same genes, were…

AdultMalePathologymedicine.medical_specialtyAdolescentCellCell Cycle ProteinsPilot Projectsmedicine.disease_causePolymerase Chain ReactionPathology and Forensic MedicineImmunoenzyme TechniquesCarcinomamedicineBiomarkers TumorHumansMolecular BiologyCarcinoma Renal CellCyclin-Dependent Kinase Inhibitor p16AgedCyclin-Dependent Kinase Inhibitor p15Neoplasm Stagingbiologybusiness.industryTumor Suppressor ProteinsPromoterCell BiologyDNA NeoplasmDNA MethylationMiddle Agedmedicine.diseaseKidney NeoplasmsNitric oxide synthaseOxidative Stressmedicine.anatomical_structureDNA methylationbiology.proteinImmunohistochemistryHistopathologyFemalebusinessRadioactive Hazard ReleaseUkraineOxidative stressPower PlantsDiagnostic molecular pathology : the American journal of surgical pathology, part B
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Mutations in FAM111B Cause Hereditary Fibrosing Poikiloderma with Tendon Contracture, Myopathy, and Pulmonary Fibrosis

2013

Congenital poikiloderma is characterized by a combination of mottled pigmentation, telangiectasia, and epidermal atrophy in the first few months of life. We have previously described a South African European-descent family affected by a rare autosomal-dominant form of hereditary fibrosing poikiloderma accompanied by tendon contracture, myopathy, and pulmonary fibrosis. Here, we report the identification of causative mutations in FAM111B by whole-exome sequencing. In total, three FAM111B missense mutations were identified in five kindreds of different ethnic backgrounds. The mutation segregated with the disease in one large pedigree, and mutations were de novo in two other pedigrees. All thr…

AdultMalePathologymedicine.medical_specialtyContractureAdolescentPulmonary FibrosisPoikilodermaCell Cycle Proteinsmedicine.disease_causeTendonssymbols.namesakeYoung AdultMuscular DiseasesReportPulmonary fibrosismedicineGeneticsMissense mutationHumansGenetics(clinical)MyopathyChildRothmund–Thomson syndromeGenetics (clinical)Sanger sequencingMutationbusiness.industryInfant NewbornRothmund-Thomson SyndromeInfantmedicine.diseasePedigreePhenotypeChild PreschoolMutationsymbolsFemalemedicine.symptomContracturebusiness
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DNA-fragmentation and apoptosis-related proteins of muscle cells in motor neuron disorders

2009

Apoptosis has been described as one of the mechanisms of muscle fiber loss in infantile spinal muscular atrophy. In order to investigate if muscle fiber-apoptosis plays a role in other denervating disorders as well, we studied DNA-fragmentation, a hallmark of apoptosis, by the TUNEL-method and, moreover, the expression patterns of apoptosis-related proteins in 2 patients suffering from ALS and in 6 patients with polyneuropathy. We identified DNA-cleavage in muscle fibers of all these patients. Furthermore, we found strong expression of bax and ICE promoting apoptosis in muscle fibers. However, also strong expression of the anti-apoptotic factor bcl-2 was found. Our findings indicate that de…

AdultMalePathologymedicine.medical_specialtyMuscle Fibers SkeletalApoptosisCell Cycle ProteinsDNA FragmentationBiologyProto-Oncogene ProteinsGene expressionmedicineHumansMyocytefas ReceptorMotor Neuron DiseaseAmyotrophic lateral sclerosisMuscle SkeletalActinAgedReceptors Leukocyte-AdhesionAmyotrophic Lateral SclerosisPeripheral Nervous System DiseasesGeneral MedicineMiddle AgedMotor neuronmedicine.diseaseCell biologyCysteine Endopeptidasesmedicine.anatomical_structureNeurologyApoptosisNerve DegenerationDNA fragmentationFemaleNeurology (clinical)AtrophyPolyneuropathyActa Neurologica Scandinavica
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Depletion of alloreactive T cells via CD69: implications on antiviral, antileukemic and immunoregulatory T lymphocytes

2005

Selective depletion of alloreactive T cells from stem-cell allografts should abrogate graft-versus-host disease while preserving beneficial T cell specificities to facilitate engraftment and immune reconstitution. We therefore explored a refined immunomagnetic separation strategy to effectively deplete alloreactive donor lymphocytes expressing the activation antigen CD69 upon stimulation, and examined the retainment of antiviral, antileukemic, and immunoregulatory T cells. In addition to the CD69high T cell fraction, our studies retrieved two T cell subsets based on residual CD69 expression. Whereas, truly CD69(neg) cells were devoid of detectable alloresponses to original stimulators, CD69…

Antigens Differentiation T-LymphocyteCD4-Positive T-LymphocytesEpstein-Barr Virus InfectionsHerpesvirus 4 HumanT cellCytomegalovirusGraft vs Host DiseaseCell Cycle Proteinschemical and pharmacologic phenomenaStreptamerBiologyLymphocyte ActivationLymphocyte DepletionCell LineInterleukin 21Antigens CDmedicineHumansTransplantation HomologousCytotoxic T cellLectins C-TypeIL-2 receptorAntigen-presenting cellTransplantationHematopoietic Stem Cell TransplantationNuclear ProteinsForkhead Transcription FactorsReceptors Interleukin-2hemic and immune systemsHematologyT lymphocyteNatural killer T cellDNA-Binding Proteinsmedicine.anatomical_structureCytomegalovirus InfectionsImmunologyRNA Splicing FactorsCarrier ProteinsImmunologic MemoryBone Marrow Transplantation
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Septins 2, 7 and 9 and MAP4 colocalize along the axoneme in the primary cilium and control ciliary length

2013

International audience; Septins are a large, evolutionarily conserved family of GTPases that form hetero-oligomers and interact with the actin-based cytoskeleton and microtubules. They are involved in scaffolding functions, and form diffusion barriers in budding yeast, the sperm flagellum and the base of primary cilia of kidney epithelial cells. We investigated the role of septins in the primary cilium of retinal pigmented epithelial (RPE) cells, and found that SEPT2 forms a 1:1:1 complex with SEPT7 and SEPT9 and that the three members of this complex colocalize along the length of the axoneme. Similar to observations in kidney epithelial cells, depletion of cilium-localized septins by siRN…

AxonemeAxonemeMicrotubule-associated protein[SDV]Life Sciences [q-bio]DIFFUSION BARRIERTUBULINCell Cycle Proteinsmacromolecular substancesORGANIZATIONCYTOSKELETONBiologySeptinMicrotubulesRetinaCell Line03 medical and health sciences0302 clinical medicineMicrotubuleCiliogenesisHumansCiliaCytoskeletonMolecular BiologyAFFINITY-REGULATING KINASEActin030304 developmental biologyCILIOGENESIS0303 health sciencesPrimary ciliumCOMPLEXSperm flagellumCilium030302 biochemistry & molecular biologyColocalizationEpithelial CellsAnatomyCell BiologyActinsCell biology[SDV] Life Sciences [q-bio]MAMMALIAN SEPTINSMAP4CELLSbiological phenomena cell phenomena and immunityMicrotubule-Associated Proteins030217 neurology & neurosurgerySeptinsDevelopmental BiologyResearch Article
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Translational readthrough of ciliopathy genes BBS2 and ALMS1 restores protein, ciliogenesis and function in patient fibroblasts

2021

Abstract Background Ciliary dysfunction underlies a range of genetic disorders collectively termed ciliopathies, for which there are no treatments available. Bardet-Biedl syndrome (BBS) is characterised by multisystemic involvement, including rod-cone dystrophy and renal abnormalities. Together with Alstrom syndrome (AS), they are known as the ‘obesity ciliopathies’ due to their common phenotype. Nonsense mutations are responsible for approximately 11% and 40% of BBS and AS cases, respectively. Translational readthrough inducing drugs (TRIDs) can restore full-length protein bypassing in-frame premature termination codons, and are a potential therapeutic approach for nonsense-mediated ciliop…

BBS2AdultMaleMedicine (General)AdolescentNonsense mutationAminopyridinesCell Cycle ProteinsCiliopathiesGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundR5-920AtalurenCiliogenesismedicineHumansReceptors SomatostatinBardet-Biedl SyndromeAlstrom SyndromeCells CulturedOxadiazolesbusiness.industryTumor Suppressor ProteinsTranslational readthroughRProteinsGeneral MedicineFibroblastsmedicine.diseaseNonsense suppressionCiliopathiesAtalurenCiliopathyALMS1chemistryCodon NonsenseAmlexanoxCancer researchMedicineBBS2businessAlström syndromeResearch PaperEBioMedicine
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Pathogenic correlation between mosaic variegated aneuploidy 1 (MVA1) and a novel BUB1B variant: a reappraisal of a severe syndrome.

2022

Funder: Università degli Studi di Catania

BUB1B gene Epileptic seizure Microcephaly Mosaic variegated aneuploidy 1 (MVA1) syndrome Ovary cystMosaicismCell Cycle ProteinsOvary cystDermatologyGeneral MedicineSyndromeBUB1B geneProtein Serine-Threonine KinasesAneuploidyPsychiatry and Mental healthSeizuresMosaic variegated aneuploidy 1 (MVA1) syndromeMutationEpileptic seizureMicrocephalyHumansNeurology (clinical)Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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