Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Impaired DNA demethylation of C/EBP sites causes premature aging

2018

Changes in DNA methylation are among the best-documented epigenetic alterations accompanying organismal aging. However, whether and how altered DNA methylation is causally involved in aging have remained elusive. GADD45α (growth arrest and DNA damage protein 45A) and ING1 (inhibitor of growth family member 1) are adapter proteins for site-specific demethylation by TET (ten-eleven translocation) methylcytosine dioxygenases. Here we show that Gadd45a/Ing1 double-knockout mice display segmental progeria and phenocopy impaired energy homeostasis and lipodystrophy characteristic of Cebp (CCAAT/enhancer-binding protein) mutants. Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers …

0301 basic medicinePremature agingAgingLipodystrophyDNA damageCell Cycle ProteinsBiology03 medical and health sciencesMiceGeneticsAnimalsHomeostasisEpigeneticsCells CulturedDemethylationMice KnockoutNuclear ProteinsAging PrematureMethylationCell biologyChromatinDNA Demethylation030104 developmental biologyDNA demethylationDNA methylationCCAAT-Enhancer-Binding ProteinsInhibitor of Growth Protein 1Developmental BiologyResearch Paper
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Acute depletion of telomerase components DKC1 and NOP10 induces oxidative stress and disrupts ribosomal biogenesis via NPM1 and activation of the P53…

2020

Mutations in DKC1, NOP10, and TINF2 genes, coding for proteins in telomerase and shelterin complexes, are responsible for diverse diseases known as telomeropathies and ribosomopathies, including dyskeratosis congenita (DC, ORPHA 1775). These genes contribute to the DC phenotype through mechanisms that are not completely understood. We previously demonstrated in models of DC that oxidative stress is an early and independent event that occurs prior to telomere shortening. To clarify the mechanisms that induce oxidative stress, we silenced genes DKC1, NOP10, and TINF2 with siRNA technology. With RNA array hybridisation, we found several altered pathways for each siRNA model. Afterwards, we ide…

0301 basic medicineTelomeraseTelomere-Binding ProteinsCell Cycle ProteinsShelterin ComplexCell LineAdherens junction03 medical and health sciences0302 clinical medicineRibonucleoproteins Small NucleolarmedicineRNA Small InterferingMolecular BiologyTelomeraseTelomere ShorteningRibonucleoproteinChemistryRNANuclear ProteinsCell BiologyTelomereShelterinmedicine.diseaseCell biologyTelomereOxidative Stress030104 developmental biology030220 oncology & carcinogenesisMutationTumor Suppressor Protein p53NucleophosminRibosomesDyskeratosis congenitaBiogenesisBiochimica et biophysica acta. Molecular cell research
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Dom34 Links Translation to Protein O-mannosylation.

2016

In eukaryotes, Dom34 upregulates translation by securing levels of activatable ribosomal subunits. We found that in the yeast Saccharomyces cerevisiae and the human fungal pathogen Candida albicans, Dom34 interacts genetically with Pmt1, a major isoform of protein O-mannosyltransferase. In C. albicans, lack of Dom34 exacerbated defective phenotypes of pmt1 mutants, while they were ameliorated by Dom34 overproduction that enhanced Pmt1 protein but not PMT1 transcript levels. Translational effects of Dom34 required the 5′-UTR of the PMT1 transcript, which bound recombinant Dom34 directly at a CA/AC-rich sequence and regulated in vitro translation. Polysomal profiling revealed that Dom34 stimu…

0301 basic medicineUntranslated regionCancer ResearchGlycosylationMolecular biologyHydrolasesOligonucleotidesGene ExpressionRNA-binding proteinCell Cycle ProteinsYeast and Fungal ModelsPathology and Laboratory MedicineMannosyltransferasesBiochemistryTranscription (biology)Untranslated RegionsCandida albicansMedicine and Health SciencesProtein IsoformsGenetics (clinical)CandidaFungal PathogensNucleotidesMessenger RNACell biologyEnzymesNucleic acidsDenaturationPhenotypesPhenotypeMedical MicrobiologySaccharomyces CerevisiaePathogensResearch ArticleGene isoformSaccharomyces cerevisiae Proteinslcsh:QH426-470NucleasesSaccharomyces cerevisiaeMycologyBiologyResearch and Analysis MethodsMicrobiology03 medical and health sciencesSaccharomycesModel OrganismsRibonucleasesDownregulation and upregulationEndoribonucleasesDNA-binding proteinsGeneticsHumansGeneMicrobial PathogensEcology Evolution Behavior and Systematics030102 biochemistry & molecular biologyOrganismsFungiBiology and Life SciencesProteinsRibosomal RNAbiology.organism_classificationMolecular biologyYeastRNA denaturationlcsh:Genetics030104 developmental biologyMolecular biology techniquesProtein BiosynthesisEnzymologyRNAProtein TranslationRibosomesPLoS Genetics
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Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
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Artesunate Impairs Growth in Cisplatin-Resistant Bladder Cancer Cells by Cell Cycle Arrest, Apoptosis and Autophagy Induction

2020

Cisplatin, which induces DNA damage, is standard chemotherapy for advanced bladder cancer (BCa). However, efficacy is limited due to resistance development. Since artesunate (ART), a derivative of artemisinin originating from Traditional Chinese Medicine, has been shown to exhibit anti-tumor activity, and to inhibit DNA damage repair, the impact of artesunate on cisplatin-resistant BCa was evaluated. Cisplatin-sensitive (parental) and cisplatin-resistant BCa cells, RT4, RT112, T24, and TCCSup, were treated with ART (1&ndash

0301 basic medicineautophagyRMCell cycle checkpointDNA RepairDNA damageArtesunateCell Cycle ProteinsArticlegrowth inhibition03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumormedicineHumansddc:610Medicine Chinese Traditionalskin and connective tissue diseaseslcsh:QH301-705.5Cell ProliferationCisplatinartesunate (ART)Cell growthAutophagyapoptosisGeneral MedicineCell cycleG1 Phase Cell Cycle Checkpoints030104 developmental biologychemistrylcsh:Biology (General)Urinary Bladder NeoplasmsApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchbladder cancer (BCa)Growth inhibitioncisplatin resistanceMicrotubule-Associated Proteinsmedicine.drug
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Exome Sequencing Reveals VCP Mutations as a Cause of Familial ALS

2010

Summary Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein ( VCP ) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS). Mutations in VCP have previously been identified in families with Inclusion Body Myopathy, Paget disease, and Frontotemporal Dementia (IBMPFD). Screening of VCP in a cohort of 210 familial ALS cases and 78 autopsy-proven ALS cases identified four additional mutations including a p.R155H mutation in a pathologically proven case of ALS. VCP protein is essential for maturation of ubiquitin-containing autophagosomes, and mutant VCP toxicity is partially mediated through its effect on…

Adenosine TriphosphataseMaleCell Cycle ProteinsUBQLN2Cohort Studies0302 clinical medicineReference ValuesValosin Containing ProteinCell Cycle ProteinReference ValueAmyotrophic lateral sclerosisExome sequencingAdenosine TriphosphatasesGenetics0303 health sciencesGeneral NeuroscienceExonsMiddle AgedPedigree3. Good healthMultisystem proteinopathyFemaleSettore MED/26 - NeurologiaCase-Control StudieChromosomes Human Pair 9HumanFrontotemporal dementiaNeuroscience(all)Valosin-containing proteinExonBiologyProtein degradationTARDBPArticle03 medical and health sciencesmedicineHumansAged030304 developmental biologyAmyotrophic lateral sclerosis familial ALS exome sequencingNeuroscience (all)business.industryAmyotrophic Lateral Sclerosismedicine.diseaseAmino Acid SubstitutionCase-Control StudiesMutationbiology.proteinCohort Studiebusiness030217 neurology & neurosurgeryAmyotrophic Lateral SclerosiNeuron
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Erratum: By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy

2019

Basal-like breast cancer is an aggressive tumor subtype with a poor response to conventional therapies. Tumor formation and relapse are sustained by a cell subset of Breast Cancer Stem Cells (BrCSCs). Here we show that miR-100 inhibits maintenance and expansion of BrCSCs in basal-like cancer through Polo-like kinase1 (Plk1) down-regulation. Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal. It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. The key role played by miR-100 in breast cancer free-survival is confirmed by the analysis of a cohort of patients' tumors, which sho…

AdultAntineoplastic Agents HormonalTransplantation HeterologousBreast cancer basal-like differentiation miR-100Breast NeoplasmsCell Cycle ProteinsKaplan-Meier EstimateMice SCIDProtein Serine-Threonine KinasesMice Inbred NODCell Line TumorProto-Oncogene ProteinsAnimalsHumansAgedAged 80 and overReverse Transcriptase Polymerase Chain ReactionCorrectionCell DifferentiationMiddle AgedPrognosisImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAsTamoxifenOncologyReceptors EstrogenMCF-7 CellsNeoplastic Stem CellsFemale
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Frequent Alteration of the Yin Yang 1/Raf-1 Kinase Inhibitory Protein Ratio in Hepatocellular Carcinoma

2011

The transcription factor Yin Yang 1 (YY1) can favor several aspects of tumorigenesis. In turn, Raf-1 Kinase Inhibitor Protein (RKIP) inhibits the oncogenic activities of MAPK and NF-κB pathways and promotes drug-induced apoptosis. Mutual influences between YY1 and RKIP may exist, and there are already separate evidences that relevant increases in YY1 and reductions in RKIP occur in hepatocellular carcinoma (HCC). However, the levels of the two factors have never been concomitantly examined in HCC. We evaluated by RT-PCR the mRNA levels of YY1, YY1AP, RKIP, and survivin in 35 clinical HCCs (91% HCV-related), in their adjacent cirrhotic tissues and in 6 healthy livers. Immunohistochemical ana…

AdultLiver CirrhosisMaleMAPK/ERK pathwayCarcinoma HepatocellularSettore MED/09 - Medicina InternaSurvivinCell Cycle ProteinsPhosphatidylethanolamine Binding ProteinSettore MED/08 - Anatomia PatologicaBiologymedicine.disease_causeBiochemistryInhibitor of Apoptosis ProteinsSurvivinGeneticsmedicineHumansRNA MessengerHepatocellular carcinomaYY1RKIPMolecular BiologyTranscription factorYY1 Transcription FactorAgedAged 80 and overSettore MED/12 - GastroenterologiaHepatocellular carcinoma Yin Yang 1 Raf-1 Kinase Inhibitor Protein Yin Yang 1-associated proteinKinaseYY1Liver NeoplasmsNuclear ProteinsMiddle AgedHCCSmedicine.diseaseGene Expression Regulation NeoplasticLiverHepatocellular carcinomaembryonic structuresSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineFemaleSettore SECS-S/01 - StatisticaCarcinogenesisTranscription FactorsBiotechnologyOMICS: A Journal of Integrative Biology
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Phenotype and natural history of inherited neuropathies caused byHSJ1c.352+1G>A mutation

2015

Mutations in the HSJ1 ( Heat-Shock Protein J1 ) gene, also called DNAJB2 (DnaJ (Hsp40) homologue, subfamily B, member 2), have been recently described as a cause of hereditary neuropathies. The HSJ1 c.352+1G>A mutation in homozygote state has been reported as the causative mutation in a single family with autosomal recessive distal hereditary motor neuropathy (dHMN).1 Since then, two other families with different HSJ1 mutations have been described: one with a dHMN phenotype and the other with a Charcot-Marie-Tooth disease type 2 (CMT2) phenotype.2 We identified the HSJ1 c.352+1G>A mutation in 10 patients who underwent long-lasting follow-up. We describe their phenotype and clinical evolutio…

AdultMale0301 basic medicineNeural ConductionCell Cycle ProteinsNeurological examinationDisease03 medical and health sciencessymbols.namesake0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumansGeneHeat-Shock ProteinsExome sequencingAdaptor Proteins Signal TransducingGenetic testingGeneticsSanger sequencingmedicine.diagnostic_testbusiness.industryNuclear ProteinsMiddle AgedPhenotypePsychiatry and Mental healthPhenotype030104 developmental biologySpainMutationMutation (genetic algorithm)symbolsFemaleSurgeryNeurology (clinical)Hereditary Sensory and Motor Neuropathybusiness030217 neurology & neurosurgeryJournal of Neurology, Neurosurgery & Psychiatry
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Lymph node metastasis in lower lip squamous cell carcinoma in relation to tumour size, histologic variables and p27Kip1 protein expression.

2003

We studied a consecutive series of 95 patients undergoing radical surgical resection of lower lip squamous cell carcinoma (LLSCC) to assess the correlation between lymph node status and several prognostic variables, such as sex and age, tumour size, histologic grading, maximal microscopic tumour thickness, perineural infiltration and p27Kip1 protein status, to see which of these might be predictive of the development of lymph node metastases. Statistical analysis demonstrated a significant association between node status and tumour size, histological grading, maximal thickness, perineural invasion and p27Kip1 protein expression; additionally to node metastasis, low p27Kip1 protein expressio…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyPrognostic variablePerineural invasionCell Cycle ProteinsMetastasisCarcinomamedicineHumansNeoplasm InvasivenessLymph nodeGrading (tumors)Agedbusiness.industryTumor Suppressor ProteinsHistologyMiddle AgedLymph node metastasis Sqamous cell Carcinoma Lower lip p27 tumour thcikness.medicine.diseasePrognosisImmunohistochemistrymedicine.anatomical_structureOncologyEpidermoid carcinomaLymphatic MetastasisLip NeoplasmsCarcinoma Squamous CellFemaleOral SurgerybusinessCyclin-Dependent Kinase Inhibitor p27Oral oncology
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