Search results for "peptide fragments"

showing 10 items of 353 documents

Factors associated with plasma antigen carbohydrate 125 and amino-terminal pro-B-type natriuretic peptide concentrations in acute heart failure

2020

Background: Plasma amino-terminal pro-B-type natriuretic peptide and antigen carbohydrate 125 levels are positively associated with a higher risk of adverse clinical outcomes in acute heart failure. As a proxy of congestion, antigen carbohydrate 125 has also been proposed as a right-sided heart failure marker. Thus, we aimed to determine in this population the main factors – including echocardiographic right-sided heart failure parameters – associated with antigen carbohydrate 125 and amino-terminal pro-B-type natriuretic peptide. Methods and results: We prospectively included 2949 patients admitted with acute heart failure. Amino-terminal pro-B-type natriuretic peptide and antigen carbohy…

Malemedicine.medical_specialtymedicine.drug_classacute heart failureAmino terminalCa 125 antigen030204 cardiovascular system & hematologyCritical Care and Intensive Care Medicine03 medical and health sciences0302 clinical medicineAntigenInternal medicineNatriuretic Peptide BrainNatriuretic peptidemedicineHumans030212 general & internal medicineProspective Studiesright-sided heart failureProtein PrecursorsAgedHeart Failurebusiness.industryGeneral MedicineCarbohydratemedicine.diseasePrognosisPeptide FragmentsEndocrinologyEchocardiographyNT-proBNPHeart failureCA-125 AntigenAcute DiseaseDisease ProgressionFemaleAntigen carbohydrate 125Cardiology and Cardiovascular MedicinebusinessRight-sided heart failureBiomarkersFollow-Up Studies
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N-Terminal Fragment of Pro B-type Natriuretic Peptide as a Marker of Contrast-Induced Nephropathy After Primary Percutaneous Coronary Intervention fo…

2015

Contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) is frequent and associated with long-term renal impairment and mortality. Early markers of CIN are needed to improve risk stratification. We aimed to assess whether N-terminal fragment of pro B-type natriuretic peptide (Nt-proBNP) could be associated with CIN. From the French regional RICO survey, all the consecutive patients who underwent primary PCI for STEMI, from January 1, 2001, to December 3, 2013, were included. Nt-proBNP circulating levels were assessed on admission. CIN was defined as an increase in serum creatinine26.5 μmol/L or50% within 48 to 7…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentPopulationContrast-induced nephropathyMyocardial InfarctionContrast MediaRisk AssessmentCohort StudiesPercutaneous Coronary InterventionRisk FactorsInternal medicineNatriuretic Peptide BrainNatriuretic peptidemedicineDiabetes MellitusHumanscardiovascular diseasesMyocardial infarctionProspective StudieseducationProspective cohort studyAgedAged 80 and overeducation.field_of_studybusiness.industryAge FactorsPercutaneous coronary interventionOdds ratioAcute Kidney InjuryMiddle Agedmedicine.diseasePrognosisPeptide Fragmentssurgical procedures operativeCase-Control StudiesConventional PCICardiologyFemaleCardiology and Cardiovascular MedicinebusinessBiomarkersThe American journal of cardiology
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Presepsin and Midregional Proadrenomedullin in Pediatric Oncologic Patients with Febrile Neutropenia

2020

Abstract Objective In this study, we investigated the roles of presepsin (PSP) and midregional proadrenomedullin (mr-proADM) in children with febrile neutropenia (FN) due to chemotherapy. Methods We assessed 36 FN episodes in 26 children. Patients were classified into bacteremia (B) and fever of unknown origin (FUO) groups. We evaluated PSP and mr-proADM at admission (T0), after 24/48 h (T1), and after 5 days (T2). Results PSP and mr-proADM levels were elevated at T0 and significantly decreased at T2. mr-proADM levels did not significantly differ between the B and FUO groups. PSP levels significantly differed between the B and FUO groups only at T1. Both PSP and mr-proADM levels at T0 were …

Malemedicine.medical_specialtymedicine.medical_treatmentpediatric.Clinical BiochemistryLipopolysaccharide ReceptorsNeutropeniaAdrenomedullinmr-proADMmalignancieNeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsHumansneutropeniaMedicineBlood cultureProtein PrecursorsFever of unknown originChildFebrile NeutropeniafeverChemotherapymedicine.diagnostic_testReceiver operating characteristicbusiness.industryPresepsinBiochemistry (medical)Age FactorsPrognosismedicine.diseasePeptide FragmentsAdrenomedullinROC CurveoncologicBacteremiaFemalebusinessBiomarkersFebrile neutropeniaLaboratory Medicine
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Processing and MHC class I presentation of human cytomegalovirus pp65-derived peptides persist despite gpUS2–11-mediated immune evasion

2007

Immune control of human cytomegalovirus (HCMV) infection can be mediated by CD8+cytolytic T lymphocytes (CTL). Adoptive transfer of antiviral CTL confers protection against HCMV reactivation and disease. The tegument protein pp65 and the immediate-early 1 protein (IE1) are recognized to be major CTL targets, even though during productive infection the viral immunoevasion proteins gpUS2–11 act to suppress major histocompatibility complex (MHC) class I-restricted antigen presentation. Thus it was not clear how infected cells could be labelled with antigenic peptides in the face of immunoevasion. We show here that the immunodominant peptide pp65NLVwas presented by MHC class I in cells infected…

MalevirusesForeskinAntigen presentationCytomegalovirusMice TransgenicBiologyMajor histocompatibility complexCell LineViral Matrix ProteinsMiceImmune systemVirologyHLA-A2 AntigenMHC class IAnimalsHumansAntigen processingHistocompatibility Antigens Class Ivirus diseasesMHC restrictionPhosphoproteinsVirologyPeptide FragmentsCTL*Gene Expression RegulationCytomegalovirus InfectionsImmunologybiology.proteinCD8T-Lymphocytes CytotoxicJournal of General Virology
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Active Fragments from Pro- and Antiapoptotic BCL-2 Proteins Have Distinct Membrane Behavior Reflecting Their Functional Divergence

2010

International audience; BACKGROUND:The BCL-2 family of proteins includes pro- and antiapoptotic members acting by controlling the permeabilization of mitochondria. Although the association of these proteins with the outer mitochondrial membrane is crucial for their function, little is known about the characteristics of this interaction.METHODOLOGY/PRINCIPAL FINDINGS:Here, we followed a reductionist approach to clarify to what extent membrane-active regions of homologous BCL-2 family proteins contribute to their functional divergence. Using isolated mitochondria as well as model lipid Langmuir monolayers coupled with Brewster Angle Microscopy, we explored systematically and comparatively the…

Membrane lipidsLipid BilayersMolecular Sequence Databcl-X Proteinlcsh:MedicineApoptosisBiologyCell LineProtein–protein interactionMembrane LipidsMice03 medical and health sciences0302 clinical medicineProtein structureMembrane activityAnimalsHumansAmino Acid Sequence[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]lcsh:ScienceLipid bilayerInner mitochondrial membranebcl-2-Associated X Protein030304 developmental biologyMice KnockoutMicroscopy0303 health sciencesMultidisciplinarySequence Homology Amino Acidlcsh:RCytochromes cCell Biology/Cellular Death and Stress ResponsesFibroblastsPeptide FragmentsMitochondriaCell biologyBiochemistry/Molecular EvolutionMembrane proteinBiophysics/Membrane Proteins and Energy Transductionlcsh:QHydrophobic and Hydrophilic Interactions030217 neurology & neurosurgeryFunctional divergenceResearch ArticleBH3 Interacting Domain Death Agonist ProteinProtein BindingPLoS ONE
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MT5-MMP regulates adult neural stem cell functional quiescence through the cleavage of N-cadherin.

2014

The identification of mechanisms that maintain stem cell niche architecture and homeostasis is fundamental to our understanding of tissue renewal and repair. Cell adhesion is a well-characterized mechanism for developmental morphogenetic processes, but its contribution to the dynamic regulation of adult mammalian stem cell niches is still poorly defined. We show that N-cadherin-mediated anchorage of neural stem cells (NSCs) to ependymocytes in the adult murine subependymal zone modulates their quiescence. We further identify MT5-MMP as a membrane-type metalloproteinase responsible for the shedding of the N-cadherin ectodomain in this niche. MT5-MMP is co-expressed with N-cadherin in adult N…

MetalloproteinaseB-LymphocytesMatrix Metalloproteinases Membrane-AssociatedCadherinNicheCell BiologyBiologyMatrix metalloproteinaseCleavage (embryo)CadherinsImmunohistochemistryNeural stem cellPeptide Fragmentsnervous system diseasesCell biologyMicenervous systemEctodomainNeural Stem CellsCell AdhesionAnimalsbiological phenomena cell phenomena and immunityreproductive and urinary physiologyCells CulturedCell Proliferation
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Peptides corresponding to helices 5 and 6 of Bax can independently form large lipid pores

2006

Proteins of the B-cell lymphoma protein 2 (Bcl2) family are key regulators of the apoptotic cascade, controlling the release of apoptotic factors from the mitochondrial intermembrane space. A helical hairpin found in the core of water-soluble folds of these proteins has been reported to be the pore- forming domain. Here we show that peptides including any of the two a-helix fragments of the hairpin of Bcl2 associated protein X (Bax) can independently induce release of large labelled dextrans from synthetic lipid vesicles. The permeability promoted by these peptides is influenced by intrinsic monolayer curvature and accompanied by fast transbilayer redis- tribution of lipids, supporting a to…

Mitochondrial intermembrane spaceLipid BilayersMolecular Sequence DataIn Vitro TechniquesBiologyBiochemistryPermeabilityProtein Structure SecondaryMiceMonolayerAnimalsAmino Acid SequenceMolecular Biologybcl-2-Associated X ProteinCircular DichroismProtein xProteïnes de membranaCell BiologyPeptide FragmentsMitochondriaCell biologyMembrane proteinApoptosisLiposomesLipid vesiclePèptids
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Astrocytes Protect Neurons from Aβ1-42 Peptide-Induced Neurotoxicity Increasing TFAM and PGC-1 and Decreasing PPAR-γ and SIRT-1

2015

One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated re…

MnSODProgrammed cell deathPPAR-γPeroxisome proliferator-activated receptorMitochondrionBiologyBioinformaticsmedicine.disease_causeAlzheimer's DiseaseNeurologiaPGC-1Sirtuin 1medicineAnimalsTFAMCells Culturedchemistry.chemical_classificationNeuronsAmyloid beta-PeptidesCell DeathSirtuin 1Caspase 3Superoxide DismutaseNeurotoxicityTranscription Factor RelAGeneral MedicineTFAMmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCoculture TechniquesPeptide FragmentsCell biologyMitochondriaPeroxidesRatsPPAR gammachemistryMitochondrial biogenesisNF-κB.Astrocytesbiology.proteinFisiologia humanaLipid PeroxidationOxidative stressResearch PaperTranscription FactorsInternational Journal of Medical Sciences
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Pores Formed by Baxα5 Relax to a Smaller Size and Keep at Equilibrium

2010

AbstractPores made by amphipathic cationic peptides (e.g., antimicrobials and fragments of pore-forming proteins) are typically studied by examining the kinetics of vesicle leakage after peptide addition or obtaining structural measurements in reconstituted peptide-lipid systems. In the first case, the pores have been considered transient phenomena that allow the relaxation of the peptide-membrane system. In the second, they correspond to equilibrium structures at minimum free energy. Here we reconcile both approaches by investigating the pore activity of the α5 fragment from the proapoptotic protein Bax (Baxα5) before and after equilibrium of peptide/vesicle complexes. Quenching assays on …

Models MolecularCardiolipinsMacromolecular SubstancesKineticsMolecular Sequence DataBiophysicsPeptideIn Vitro TechniquesBiophysical PhenomenaAmphiphileAnimalsHumansAmino Acid SequencePeptide sequenceUnilamellar LiposomesFluorescent Dyesbcl-2-Associated X Proteinchemistry.chemical_classificationMicroscopy ConfocalChemistryBilayerVesicleMacromolecular SubstancesCationic polymerizationMembranePeptide FragmentsCrystallographyKineticsBiophysicsPhosphatidylcholinesThermodynamicsCattle
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Conformational control of Bax localization and apoptotic activity by Pro168.

2004

In healthy cells, Bax resides inactive in the cytosol because its COOH-terminal transmembrane region (TMB) is tucked into a hydrophobic pocket. During apoptosis, Bax undergoes a conformational change involving NH2-terminal exposure and translocates to mitochondria to release apoptogenic factors. How this process is regulated remains unknown. We show that the TMB of Bax is both necessary and sufficient for mitochondrial targeting. However, its availability for targeting depends on Pro168 located within the preceding loop region. Pro168 mutants of Bax lack apoptotic activity, cannot rescue the apoptosis-resistant phenotype of Bax/Bak double knockout cells, and are retained in the cytosol even…

Models MolecularConformational changeProlineCell SurvivalProtein ConformationMutantMolecular Sequence DataApoptosisMitochondrionMitochondrial apoptosis-induced channelArticleCell Line03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsAnimalsHumansAmino Acid Sequence030304 developmental biologybcl-2-Associated X Proteinapoptosis; Bcl-2 family; NH2-terminal exposure; mitochondria; targeting0303 health sciencesbiologyMembrane ProteinsCell BiologyPeptide FragmentsCell biologyTransport proteinMitochondriaCytosolProtein Transportbcl-2 Homologous Antagonist-Killer ProteinProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisbiology.proteinBcl-2 Homologous Antagonist-Killer ProteinHeLa CellsThe Journal of cell biology
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