Search results for "factor"

showing 10 items of 17757 documents

p27Kip1 regulates alpha-synuclein expression

2018

Alpha-synuclein (α-SYN) is the main component of anomalous protein aggregates (Lewy bodies) that play a crucial role in several neurodegenerative diseases (synucleinopathies) like Parkinson’s disease and multiple system atrophy. However, the mechanisms involved in its transcriptional regulation are poorly understood. We investigated here the role of the cyclin-dependent kinase (Cdk) inhibitor and transcriptional regulator p27Kip1 (p27) in the regulation of α-SYN expression. We observed that selective deletion of p27 by CRISPR/Cas9 technology in neural cells resulted in increased levels of α-SYN. Knock-down of the member of the same family p21Cip1 (p21) also led to increased α-SYN levels, in…

0301 basic medicinep27Kip1[SDV]Life Sciences [q-bio]03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCyclin-dependent kinaseTranscriptional regulationalpha synucleinAlpha synucleinPsychological repressionE2F4Alpha-synucleinSynucleinopathiesbiologyPromoterEnzyme inhibitorsMolecular biologyExpressió gènica3. Good healthnervous system diseases030104 developmental biologyOncologychemistryInhibidors enzimàticsnervous systemE2F4biology.proteinGene expressionTranscription Factor E2F4transcriptionp21Cip1Transcription030217 neurology & neurosurgeryResearch Paper
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The MID1 protein is a central player during development and in disease.

2015

Loss-of-function mutations in the MID1 gene cause a rare monogenic disorder, Opitz BBB/G syndrome (OS), which is characterized by malformations of the ventral midline. The MID1 gene encodes the MID1 protein, which assembles a large microtubule-associated protein complex. Intensive research over the past several years has shed light on the function of the MID1 protein as a ubiquitin ligase and regulator of mTOR signalling and translational activator. As a central player in the cell MID1 has been implicated in the pathogenesis of various other disorders in addition to OS including cancer and neurodegenerative diseases. Influencing the activity of the MID1 protein complex is a promising new st…

0301 basic medicinephysiopathology [Huntington Disease]CarcinogenesisUbiquitin-Protein LigasesRegulatorDiseaseBiologyBioinformaticsmedicine.disease_causephysiopathology [Alzheimer Disease]Congenital AbnormalitiesPathogenesis03 medical and health sciencesMiceAlzheimer Diseasephysiology [Nuclear Proteins]medicineAnimalsHumansgenetics [Microtubule Proteins]ddc:610GenePI3K/AKT/mTOR pathwayActivator (genetics)Nuclear Proteinsgenetics [Nuclear Proteins]genetics [Transcription Factors]physiology [Transcription Factors]Ubiquitin ligase030104 developmental biologyHuntington DiseaseMutationbiology.proteinMicrotubule Proteinsphysiology [Microtubule Proteins]CarcinogenesisMid1 protein humanTranscription FactorsFrontiers in bioscience (Landmark edition)
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Role of Ocular Angiogenic Factors in the Development of Neovascular Age-Related Macular Degeneration

2020

Abstract Age-related macular degeneration (AMD) is a progressive degenerative eye disease. Neovascular age-related macular degeneration (nAMD) is the advanced form of AMD characterised by abnormal growth of newly formed blood vessels in chorioidea which typically involves fluid accumulation in the retina or retinal haemorrhage, retinal epithelial detachments, hard exudate or subretinal scars. The process of angiogenesis is controlled by ocular angiogenic factors, which have enabled the development of different treatment options aimed at these factors. This review aims to compile the available information about the most commonly identified ocular angiogenic factors, uncovering their role in …

0301 basic medicinepigment epithelium-derived factormedicine.medical_specialtyMultidisciplinaryvascular endothelial growth factorgenetic structuresGeneral interestScienceangiogenic factorsQbiomarkersMacular degenerationmedicine.diseaseeye diseases03 medical and health sciences030104 developmental biology0302 clinical medicineAge relatedOphthalmology030221 ophthalmology & optometrymedicinesense organsProceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.
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Regulation of Alpha-Secretase ADAM10 In vitro and In vivo: Genetic, Epigenetic, and Protein-Based Mechanisms

2017

ADAM10 (A Disintegrin and Metalloproteinase 10) has been identified as the major physiological alpha-secretase in neurons, responsible for cleaving APP in a non-amyloidogenic manner. This cleavage results in the production of a neuroprotective APP-derived fragment, APPs-alpha, and an attenuated production of neurotoxic A-beta peptides. An increase in ADAM10 activity shifts the balance of APP processing towards APPs-alpha and protects the brain from amyloid deposition and disease. Thus, increasing ADAM10 activity has been proposed an attractive target for the treatment of neurodegenerative diseases and it appears to be timely to investigate the physiological mechanisms regulating ADAM10 expr…

0301 basic medicinepromoterADAM10agingADAM10ReviewBiologyAlzheimer's diseaseNeuroprotectionspineProtein–protein interaction03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologyAlpha secretaseIn vivoalpha-secretasetranscription factorsmicroRNAmouse modelsEpigeneticsNeuroscienceTranscription factorMolecular BiologyNeuroscienceFrontiers in Molecular Neuroscience
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Enzyme replacement therapy with recombinant pro-CTSD (cathepsin D) corrects defective proteolysis and autophagy in neuronal ceroid lipofuscinosis

2019

CTSD (cathepsin D) is one of the major lysosomal proteases indispensable for the maintenance of cellular proteostasis by turning over substrates of endocytosis, phagocytosis and autophagy. Consequently, CTSD deficiency leads to a strong impairment of the lysosomal-autophagy machinery. In mice and humans CTSD dysfunction underlies the congenital variant (CLN10) of neuronal ceroid lipofuscinosis (NCL). NCLs are distinct lysosomal storage disorders (LSDs) sharing various hallmarks, namely accumulation of protein aggregates and ceroid lipofuscin leading to neurodegeneration and blindness. The most established and clinically approved approach to treat LSDs is enzyme replacement therapy (ERT) aim…

0301 basic medicineproteolysisCathepsin DCathepsin DCathepsin BstorageCathepsin L03 medical and health sciencesSequestosome 1Neuronal Ceroid-LipofuscinosesAutophagymedicineAnimalsHumansEnzyme Replacement TherapyeducationMolecular BiologyMice Knockouttherapyeducation.field_of_studyTripeptidyl-Peptidase 1030102 biochemistry & molecular biologybiologyAutophagy; cathepsin D; enzyme replacement therapy; lysosome; neuronal ceroid lipofuscinosis; proteolysis; storage; therapyBrainCell BiologyFibroblastsTripeptidyl peptidase Imedicine.diseaseLRP1Cell biologyDisease Models Animal030104 developmental biologylysosomebiology.proteinAllograft inflammatory factor 1Neuronal ceroid lipofuscinosisneuronal ceroid lipofuscinosisLysosomesResearch PaperAutophagy
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Modulating Neuronal Competition Dynamics in the Dentate Gyrus to Rejuvenate Aging Memory Circuits.

2015

The neural circuit mechanisms underlying the integration and functions of adult-born dentate granule cell (DGCs) are poorly understood. Adult-born DGCs are thought to compete with mature DGCs for inputs to integrate. Transient genetic overexpression of a negative regulator of dendritic spines, Kruppel-like factor 9 (Klf9), in mature DGCs enhanced integration of adult-born DGCs and increased NSC activation. Reversal of Klf9 overexpression in mature DGCs restored spines and activity and reset neuronal competition dynamics and NSC activation, leaving the DG modified by a functionally integrated, expanded cohort of age-matched adult-born DGCs. Spine elimination by inducible deletion of Rac1 in …

0301 basic medicinerac1 GTP-Binding ProteinAgingDendritic spineCell SurvivalDendritic SpinesNeurogenesisKruppel-Like Transcription FactorsRAC1BiologyNegative regulator03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationNeural Stem CellsMemorymedicineAnimalsCell ProliferationNeuronsMemory circuitsGeneral NeuroscienceDentate gyrusNeuropeptidesGranule cellUp-RegulationKLF9Adult Stem Cells030104 developmental biologymedicine.anatomical_structureDentate GyrusMutationNeuroscience030217 neurology & neurosurgeryNeuron
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European contribution to the study of ROS : A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

2017

WOS: 000410470000009

0301 basic medicinereactive oxygen species ; reactive nitrogen species ; redox signaling ; oxidative stress ; antioxidants ; redox therapeuticsRedox signalingInternational CooperationSMOOTH-MUSCLE-CELLS[SDV]Life Sciences [q-bio]Clinical BiochemistryISCHEMIA-REPERFUSION INJURYReviewddc:616.07Bioinformaticsmedicine.disease_causeBiochemistryAntioxidants0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCost actionlcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSmedia_commonlcsh:R5-920Redox therapeuticsReactive nitrogen species3. Good healthVariety (cybernetics)MANGANESE SUPEROXIDE-DISMUTASECHRONIC GRANULOMATOUS-DISEASERisk analysis (engineering)ddc:540lcsh:Medicine (General)Oxidation-ReductionSignal TransductionSocieties ScientificPULMONARY ARTERIAL-HYPERTENSIONMedicinaEstrès oxidatiuBiology03 medical and health sciencesAntioxidants ; Oxidative Stress ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Redox Signaling ; Redox TherapeuticsJournal Articlemedicinemedia_common.cataloged_instanceAnimalsHumans[CHIM]Chemical SciencesEuropean UnionEuropean unionNITRIC-OXIDE SYNTHASETANDEM MASS-SPECTROMETRYMolecular BiologyMITOCHONDRIAL OXIDATIVE STRESSGROWTH-FACTOR-BETAOrganic ChemistryDisease progressionBiology and Life SciencesOxidation reductionManganese Superoxide Dismutase030104 developmental biologylcsh:Biology (General)Oxidative stressReactive oxygen species030217 neurology & neurosurgeryOxidative stressRedox biology
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Effects of Infant Formula With Human Milk Oligosaccharides on Growth and Morbidity: A Randomized Multicenter Trial

2017

Objectives:The aim of the study was to evaluate the effects of infant formula supplemented with 2 human milk oligosaccharides (HMOs) on infant growth, tolerance, and morbidity. Methods:Healthy infants, 0 to 14 days old, were randomized to an intact-protein, cow's milk-based infant formula (control, n=87) or the same formula with 1.0g/L 2fucosyllactose (2FL) and 0.5g/L lacto-N-neotetraose (LNnT) (test, n=88) from enrollment to 6 months; all infants received standard follow-up formula without HMOs from 6 to 12 months. Primary endpoint was weight gain through 4 months. Secondary endpoints included additional anthropometric measures, gastrointestinal tolerance, behavioral patterns, and morbidit…

0301 basic medicinesafetyMalePediatricsmedicine.medical_specialtyMEDLINEOligosaccharidesWeight Gainlaw.inventionbronchitis03 medical and health scienceschemistry.chemical_compound2'-FucosyllactoseRandomized controlled trialDouble-Blind Method2fucosyllactose; bronchitis; lacto-N-neotetraose; safety; tolerancelawMulticenter trialmedicineAnimalsHumansLacto-N-neotetraoseRespiratory Tract Infectionslacto-N-neotetraose2′fucosyllactose030109 nutrition & dieteticstoleranceMilk Humanbusiness.industryGastroenterologyOriginal Articles: NutritionInfant Newbornfood and beveragesInfantProtective Factorsmedicine.diseaseInfant Formula030104 developmental biologyMilkchemistryInfant formulaPediatrics Perinatology and Child Health2'fucosyllactose bronchitis lacto-N-neotetraose safety toleranceBronchitisFemalemedicine.symptombusinessWeight gainFollow-Up Studies
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Biochemical Properties of Human D-Amino Acid Oxidase

2017

D-amino acid oxidase catalyzes the oxidative deamination of D-amino acids. In the brain, the NMDA receptor coagonist D-serine has been proposed as its physiological substrate. In order to shed light on the mechanisms regulating D-serine concentration at the cellular level, we biochemically characterized human DAAO (hDAAO) in greater depth. In addition to clarify the physical-chemical properties of the enzyme, we demonstrated that divalent ions and nucleotides do not affect flavoenzyme function. Moreover, the definition of hDAAO substrate specificity demonstrated that D-cysteine is the best substrate, which made it possible to propose it as a putative physiological substrate in selected tiss…

0301 basic medicinestructure-function relationshipssubstrate specificityD-amino acid oxidaseD-serineGenetics and Molecular Biology (miscellaneous)Flavin groupBiochemistry Genetics and Molecular Biology (miscellaneous)BiochemistryCofactor03 medical and health sciencesMolecular BiosciencesMolecular Biologylcsh:QH301-705.5D-cysteineOriginal Researchchemistry.chemical_classificationbiologyActive siteSubstrate (chemistry)Oxidative deaminationLigand (biochemistry)Amino acidD-amino acid oxidase; D-cysteine; D-serine; structure-function relationships; substrate specificity030104 developmental biologyBiochemistrychemistrylcsh:Biology (General)biology.proteinD-amino acid oxidase; D-cysteine; D-serine; Structure-function relationships; Substrate specificity; Molecular Biology; Biochemistry; Biochemistry Genetics and Molecular Biology (miscellaneous)D-amino acid oxidaseFrontiers in Molecular Biosciences
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Human D-Amino Acid Oxidase: Structure, Function, and Regulation

2018

D-Amino acid oxidase (DAAO) is an FAD-containing flavoenzyme that catalyzes with absolute stereoselectivity the oxidative deamination of all natural D-amino acids, the only exception being the acidic ones. This flavoenzyme plays different roles during evolution and in different tissues in humans. Its three-dimensional structure is well conserved during evolution: minute changes are responsible for the functional differences between enzymes from microorganism sources and those from humans. In recent years several investigations focused on human DAAO, mainly because of its role in degrading the neuromodulator D-serine in the central nervous system. D-Serine is the main coagonist of N-methyl D…

0301 basic medicinestructure-function relationshipssubstrate specificityD-amino acid oxidaseD-serineReviewFlavin groupBiochemistry Genetics and Molecular Biology (miscellaneous)BiochemistryCofactor03 medical and health sciences0302 clinical medicineMolecular BiosciencesReceptorlcsh:QH301-705.5Molecular Biologychemistry.chemical_classificationOxidase testbiologyOxidative deaminationNMDA receptorAmino acid030104 developmental biologyEnzymelcsh:Biology (General)chemistryBiochemistrybiology.proteinD-amino acid oxidase030217 neurology & neurosurgery
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