Search results for "Spectroscopy"

showing 10 items of 10293 documents

Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation

2017

IF 3.226; International audience; Ubiquitination is a post-translational modification that defines the cellular fate of intracellular proteins. It can modify their stability, their activity, their subcellular location, and even their interacting pattern. This modification is a reversible event whose implementation is easy and fast. It contributes to the rapid adaptation of the cells to physiological intracellular variations and to intracellular or environmental stresses. E2F1 (E2 promoter binding factor 1) transcription factor is a potent cell cycle regulator. It displays contradictory functions able to regulate both cell proliferation and cell death. Its expression and activity are tightly…

0301 basic medicineProgrammed cell deathReviewubiquitinationCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciencesUbiquitinAnimalsHumansE2F1Physical and Theoretical Chemistry[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologylcsh:QH301-705.5Molecular BiologyTranscription factorSpectroscopybiologyCell growthOrganic ChemistryE2F1 Transcription FactorGeneral MedicineCell cycleComputer Science ApplicationsCell biology030104 developmental biologyE2F1lcsh:Biology (General)lcsh:QD1-999biology.proteinDNA damagecell cycleE2F1 Transcription FactorIntracellularInternational Journal of Molecular Sciences
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Regulation of Autophagic Signaling by Mechanical Loading and Inflammation in Human PDL Fibroblasts

2020

Autophagy (cellular self-consumption) is a crucial adaptation mechanism during cellular stress conditions. This study aimed to examine how this important process is regulated in human periodontal ligament (PDL) fibroblasts by mechanical and inflammatory stress conditions and whether the mammalian target of rapamycin (mTOR) signaling pathway is involved. Autophagy was quantified by flow cytometry. Qualitative protein phosphorylation profiling of the mTOR pathway was carried out. Effects of mTOR regulation were assessed by quantification of important synthesis product collagen 1, cell proliferation and cell death with real-time PCR and flow cytometry. Autophagy as a response to mechanical or …

0301 basic medicineProgrammed cell deathautophagyInflammationCatalysisArticlelcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineinflammatory conditionsmedicineHumansProtein phosphorylationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyPI3K/AKT/mTOR pathwayCells CulturedInflammationCell DeathCell growthChemistryOrganic ChemistryAutophagymechanical stress030206 dentistryGeneral MedicineFibroblastsComputer Science ApplicationsCell biologyorthodontic tooth movement030104 developmental biologylcsh:Biology (General)lcsh:QD1-999mammalian target of rapamycin (mTOR) signaling pathwayPhosphorylationStress Mechanicalmedicine.symptomSignal transductionSignal TransductionInternational Journal of Molecular Sciences
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2017

Epidermal growth factor receptor (EGFR) and the mutant EGFRvIII are major focal points in current concepts of targeted cancer therapy for glioblastoma multiforme (GBM), the most malignant primary brain tumor. The receptors participate in the key processes of tumor cell invasion and tumor-related angiogenesis and their upregulation correlates with the poor prognosis of glioma patients. Glioma cell invasion and increased angiogenesis share mechanisms of the degradation of the extracellular matrix (ECM) through upregulation of ECM-degrading proteases as well as the activation of aberrant signaling pathways. This review describes the role of EGFR and EGFRvIII in those mechanisms which might off…

0301 basic medicineProteasesAngiogenesisBrain tumorCatalysisInorganic ChemistryExtracellular matrix03 medical and health sciences0302 clinical medicineDownregulation and upregulationGliomaMedicineEpidermal growth factor receptorPhysical and Theoretical ChemistryMolecular BiologySpectroscopybiologybusiness.industryOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science Applications030104 developmental biology030220 oncology & carcinogenesisImmunologyCancer researchbiology.proteinSignal transductionbusinessInternational Journal of Molecular Sciences
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Lunasin is a redox sensitive intrinsically disordered peptide with two transiently populated α-helical regions.

2016

Lunasin is a 43 amino acid peptide with anti-cancer, antioxidant, anti-inflammatory and cholesterol-lowering properties. Although the mechanism of action of lunasin has been characterized to some extent, its exact three-dimensional structure as well as the function of the N-terminal sequence remains unknown. We established a novel method for the production of recombinant lunasin that allows efficient isotope labeling for NMR studies. Initial studies showed that lunasin can exist in a reduced or oxidized state with an intramolecular disulfide bond depending on solution conditions. The structure of both forms of the peptide at pH 3.5 and 6.5 was characterized by CD spectroscopy and multidimen…

0301 basic medicineProtein Conformation alpha-HelicalCircular dichroismPhysiologyBeta sheetPeptideIntrinsically disordered proteinsBiochemistryLunasinAntioxidantsHistones03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineEndocrinologyNeoplasmsAnticarcinogenic AgentsHumansAmino Acid SequenceDisulfidesProtein secondary structureNuclear Magnetic Resonance BiomolecularPlant Proteinschemistry.chemical_classificationChemistryAcetylationNuclear magnetic resonance spectroscopyIntrinsically Disordered Proteins030104 developmental biologyBiochemistry030220 oncology & carcinogenesisBiophysicsSoybean ProteinsPeptidesOxidation-ReductionFunction (biology)Peptides
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Plasmin-Induced Activation of Human Platelets Is Modulated by Thrombospondin-1, Bona Fide Misfolded Proteins and Thiol Isomerases

2020

Inflammatory processes are triggered by the fibrinolytic enzyme plasmin. Tissue-type plasminogen activator, which cleaves plasminogen to plasmin, can be activated by the cross-&beta

0301 basic medicineProtein FoldingPlatelet AggregationPlasmin030204 cardiovascular system & hematologyProtein aggregationFibrinogenThrombospondin 10302 clinical medicinePlateletFibrinolysinprotein misfoldingIsomerasesSpectroscopyChemistryfood and beveragesGeneral Medicinethiol-isomerasesComputer Science ApplicationsCell biologyP-Selectinplateletsmedicine.drugcirculatory and respiratory physiologyBlood PlateletsCatalysisArticleInorganic Chemistry03 medical and health sciencesProtein AggregatesThrombospondin 1medicineHumansPlatelet activationSulfhydryl CompoundsPhysical and Theoretical Chemistrythrombospondin-1Molecular BiologyplasminInflammationOrganic ChemistryfungiFibrinogen bindingFibrinogenPlasminogenPlatelet Activation030104 developmental biologyProtein Conformation beta-StrandPeptidesPlasminogen activatorInternational Journal of Molecular Sciences
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2019

Traumatic brain injury (TBI) can lead to impaired cognition and memory consolidation. The acute phase (24–48 h) after TBI is often characterized by neural dysfunction in the vicinity of the lesion, but also in remote areas like the contralateral hemisphere. Protein homeostasis is crucial for synaptic long-term plasticity including the protein degradation systems, proteasome and autophagy. Still, little is known about the acute effects of TBI on synaptic long-term plasticity and protein degradation. Thus, we investigated TBI in a controlled cortical impact (CCI) model in the motor and somatosensory cortex of mice ex vivo-in vitro. Late long-term potentiation (l-LTP) was induced by theta-burs…

0301 basic medicineProtein degradationNeuroprotectionCatalysisInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCa2+/calmodulin-dependent protein kinaseMG132medicinePhysical and Theoretical ChemistryMolecular BiologySpectroscopybusiness.industryOrganic ChemistryLong-term potentiationGeneral MedicineComputer Science Applications030104 developmental biologychemistrySynaptic plasticityProteasome inhibitorMemory consolidationbusinessNeuroscience030217 neurology & neurosurgerymedicine.drugInternational Journal of Molecular Sciences
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Biomarkers in Anderson–Fabry Disease

2020

Fabry disease is a rare lysosomal storage disorder caused by a deficiency of α-galactosidase A, resulting in multisystemic involvement. Lyso-Gb3 (globotriaosylsphingosine), the deacylated form of Gb3, is currently measured in plasma as a biomarker of classic Fabry disease. Intensive research of biomarkers has been conducted over the years, in order to detect novel markers that may potentially be used in clinical practice as a screening tool, in the context of the diagnostic process and as an indicator of response to treatment. An interesting field of application of such biomarkers is the management of female heterozygotes who present difficulty in predictable clinical progression. This revi…

0301 basic medicineProteomeContext (language use)ReviewDisease030204 cardiovascular system & hematologylyso-Gb3BioinformaticsCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansPhysical and Theoretical Chemistryfabrylcsh:QH301-705.5Molecular BiologySpectroscopybusiness.industryMolecular pathologyOrganic ChemistryClinical coursebiomarkersBiomarkerGeneral Medicinemedicine.diseaseResponse to treatmentFabry diseaseComputer Science ApplicationsMicroRNAsAnderson-Fabry Disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999MetabolomeFabry DiseaseBiomarker (medicine)businessInternational Journal of Molecular Sciences
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Quantitative Proteomics Reveals Changes Induced by TIMP-3 on Cell Membrane Composition and Novel Metalloprotease Substrates

2021

Ectodomain shedding is a key mechanism of several biological processes, including cell-communication. Disintegrin and metalloproteinases (ADAMs), together with the membrane-type matrix metalloproteinases, play a pivotal role in shedding transmembrane proteins. Aberrant shedding is associated to several pathological conditions, including arthritis. Tissue inhibitor of metalloproteases 3 (TIMP-3), an endogenous inhibitor of ADAMs and matrix metalloproteases (MMPs), has been proven to be beneficial in such diseases. Thus, strategies to increase TIMP-3 bioavailability in the tissue have been sought for development of therapeutics. Nevertheless, high levels of TIMP-3 may lead to mechanism-based …

0301 basic medicineProteomicsADAM15ProteomeCellMatrix metalloproteinaseMass SpectrometryCell membranelcsh:Chemistryanalysis [Proteome]lcsh:QH301-705.5proteomicSpectroscopybiologyChemistrytissue inhibitor of metalloproteases 3 (TIMP-3)General MedicineTransmembrane proteinComputer Science ApplicationsCell biologymedicine.anatomical_structureEctodomainddc:540TIMP3 protein humanmetalloproteinaseectodomain sheddingmetabolism [Tissue Inhibitor of Metalloproteinase-3]Quantitative proteomicsADAM15 protein humanchemistry [Cell Membrane]Catalysismetabolism [Cell Membrane]ArticlemetalloproteinasesInorganic Chemistry03 medical and health sciencestissue inhibitor of metalloproteases 3 (TIMP-3).medicineDisintegrinHumansPhysical and Theoretical ChemistryMolecular BiologyTissue Inhibitor of Metalloproteinase-3030102 biochemistry & molecular biologyOrganic ChemistryCell MembraneMembrane Proteinsmetabolism [Proteome]ADAM Proteins030104 developmental biologyHEK293 Cellslcsh:Biology (General)lcsh:QD1-999metabolism [ADAM Proteins]biology.proteinmetabolism [Membrane Proteins]International Journal of Molecular Sciences
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The Small Heat Shock Protein α-Crystallin B Shows Neuroprotective Properties in a Glaucoma Animal Model

2017

Glaucoma is a neurodegenerative disease that leads to irreversible retinal ganglion cell (RGC) loss and is one of the main causes of blindness worldwide. The pathogenesis of glaucoma remains unclear, and novel approaches for neuroprotective treatments are urgently needed. Previous studies have revealed significant down-regulation of α-crystallin B as an initial reaction to elevated intraocular pressure (IOP), followed by a clear but delayed up-regulation, suggesting that this small heat-shock protein plays a pathophysiological role in the disease. This study analyzed the neuroprotective effect of α-crystallin B in an experimental animal model of glaucoma. Significant IOP elevation induced b…

0301 basic medicineProteomicsRetinal Ganglion Cellsgenetic structuresNerve fiber layerGlaucomaCell CountMass Spectrometrylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineexperimental glaucoma; α-crystallin B; neuroprotection; proteomicsProtein Interaction Mapslcsh:QH301-705.5Spectroscopyα-crystallin BGeneral MedicineComputer Science ApplicationsUp-Regulationmedicine.anatomical_structureNeuroprotective AgentsRetinal ganglion cellneuroprotectionRetinal Neuronsmedicine.medical_specialtyDown-RegulationBiologyNeuroprotectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCrystallinOphthalmologyHeat shock proteinmedicineElectroretinographyAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular Pressureexperimental glaucomaOrganic Chemistryalpha-Crystallin B ChainRetinalGlaucomamedicine.diseaseeye diseasesDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometrysense organsInternational Journal of Molecular Sciences; Volume 18; Issue 11; Pages: 2418
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Cytotoxic activity of the histone deacetylase 3-Selective inhibitor Pojamide on MDA-MB-231 triple-negative breast cancer cells

2019

We examined the effects of the ferrocene-based histone deacetylase-3 inhibitor Pojamide (N1-(2-aminophenyl)-N8-ferrocenyloctanediamide) and its two derivatives N1-(2-aminophenyl)-N6-ferrocenyladipamide and N1-(2-aminophenyl)-N8-ferroceniumoctanediamide tetrafluoroborate on triple-negative MDA-MB-231 breast cancer cells. Viability/growth assays indicated that only the first two compounds at 70 &mu

0301 basic medicineQD0901Triple Negative Breast Neoplasmslcsh:Chemistry0302 clinical medicinebreast cancer cellmitochondrial transmembrane potentialCytotoxic T cellQDSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyTriple-negative breast cancerreactive oxygen speciesCell DeathChemistryHistone deacetylase inhibitorQapoptosisGeneral MedicineCell cycle3. Good healthComputer Science Applications030220 oncology & carcinogenesisFemalecell cycleProgrammed cell deathautophagymedicine.drug_classCell SurvivalCatalysisArticleHistone DeacetylasesInorganic Chemistry03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumansViability assayPhysical and Theoretical ChemistryMolecular Biologyhistone deacetylase inhibitorcell viabilityOrganic ChemistryAutophagyapoptosiMatrix MetalloproteinasesHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer researchQD0146breast cancer cells
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