Search results for "lipid"

showing 10 items of 3879 documents

The Effect of Resveratrol on the Composition and State of Lipids and the Activity of Phospholipase A2 During the Excitation and Regeneration of Somat…

2019

It has been shown that in the somatic nerve's lipids, both during excitation and transection, changes occur with the composition of individual phospholipids and in phospholipids fatty acids, which changes the phase state of the myelin and nerve fiber axolemma lipid bilayer. A main contribution in the nerve degenerative processes is dependent on the composition phospholipid's fatty acid changes during the activation of both Ca2+-dependent and Ca2+-independent phospholipase A2 forms. At the same time, we studded changes in phosphoinisitol (PI) and diacylglycerol (DAG), which depend on the phosphoinositide cycle function during nerve excitation and degeneration processes. It was found that mye…

0301 basic medicineRhythmic excitationMyelinated nerve fiberPhysiologyPhospholipidNerve fiberresveratrollcsh:Physiology03 medical and health sciencesMyelinchemistry.chemical_compound0302 clinical medicinePhospholipase A2Physiology (medical)medicineskin and connective tissue diseasesphospholipidsDiacylglycerol kinasebiologylcsh:QP1-981Chemistrynerve intersectionmyelinated nerve fibersrhythmic excitation030104 developmental biologymedicine.anatomical_structurenervous system030220 oncology & carcinogenesisBiophysicsbiology.proteinlipids (amino acids peptides and proteins)Sciatic nervesense organsFrontiers in Physiology
researchProduct

The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
researchProduct

Activity of the α-glucoside transporter Agt1 in Saccharomyces cerevisiae cells during dehydration-rehydration events

2018

Microbial cells can enter a state of anhydrobiosis under desiccating conditions. One of the main determinants of viability during dehydration-rehydration cycles is structural integrity of the plasma membrane. Whereas much is known about phase transitions of the lipid bilayer, there is a paucity of information on changes in activity of plasma membrane proteins during dehydration-rehydration events. We selected the α-glucoside transporter Agt1 to gain insights into stress mechanisms/responses and ecophysiology during anhydrobiosis. As intracellular water content of S. cerevisiae strain 14 (a strain with moderate tolerance to dehydration-rehydration) was reduced to 1.5 g water/g dry weight, th…

0301 basic medicineSaccharomyces cerevisiae ProteinsMonosaccharide Transport ProteinsEvolution030106 microbiologySaccharomyces cerevisiaeSaccharomyces cerevisiaeDehydration-rehydration03 medical and health sciencesGlucosidesBehavior and Systematicsα-Glucoside transporterMembrane proteinsGeneticsViability assayDesiccationLipid bilayerEcology Evolution Behavior and SystematicsMicrobial ViabilitySymportersbiologyStrain (chemistry)EcologyCell MembraneBiological TransportTransporterbiology.organism_classificationAnhydrobiosisYeastYeast030104 developmental biologyInfectious DiseasesBiochemistryMembrane proteinAnhydrobiosis; Dehydration-rehydration; Membrane proteins; Yeast; α-Glucoside transporter; Ecology Evolution Behavior and Systematics; Genetics; Infectious DiseasesIntracellular
researchProduct

The sphingosine kinase 1 activator, K6PC-5, attenuates Ebola virus infection

2021

Summary Ebola virus (EBOV) is responsible for outbreaks with case fatality rates of up to 90% and for an epidemic in West Africa with more than ten thousand deaths. EBOV glycoprotein (EBOV-GP) is the only viral surface protein and is responsible for viral entry into cells. Here, by employing pseudotyped EBOV-GP viral particles, we uncover a critical role for sphingolipids in inhibiting viral entry. Sphingosine kinase 1 (SphK1) catalyzes the phosphorylation of sphingosine to sphingosine 1-phosphate (S1P). The administration of the SphK1 activator, K6PC-5, or S1P, or the overexpression of SphK1 consistently exhibited striking inhibitory effects in EBOV-GP-driven entry in diverse cell lines. F…

0301 basic medicineScienceviruses02 engineering and technologymedicine.disease_causeArticle03 medical and health scienceschemistry.chemical_compoundViral entryVirologymedicinechemistry.chemical_classificationMultidisciplinaryEbola virusSphingosinebiologyActivator (genetics)QMolecular MicrobiologyCell Biology021001 nanoscience & nanotechnologyVirologySphingolipid030104 developmental biologychemistrySphingosine kinase 1Cell culturebiology.protein0210 nano-technologyGlycoproteiniScience
researchProduct

Anti-PCSK9 treatment: is ultra-low low-density lipoprotein cholesterol always good?

2018

Anti-PCSK9 (proprotein convertase subtilisin kexin 9) monoclonal antibodies (Mab) are novel, potent lipid-lowering drugs. They demonstrated to improve the lipid profile in high cardiovascular risk patients. Anti-PCSK9 Mab inhibit the targeted low-density lipoprotein (LDL)-receptor degradation induced by PCSK9 protein and are able to reduce LDL cholesterol (LDL-C) levels on top of conventional lipid-lowering therapy. Though these drugs proved to be very safe in the short-term, little is known about the possible long-term effects, due to the short period of their marketing. The genetic low cholesterol syndromes (LCS) represent the natural models of the lipid-lowering anti-PCSK9 therapy, and a…

0301 basic medicineSerine Proteinase InhibitorsTime FactorsPhysiologymedicine.drug_class030204 cardiovascular system & hematologyPharmacologyMonoclonal antibodyRisk Assessment03 medical and health sciencesPCSK9 Genechemistry.chemical_compound0302 clinical medicineRisk FactorsPhysiology (medical)Diabetes mellitusmedicineAnimalsHumansDyslipidemiasmedicine.diagnostic_testbusiness.industryCholesterolPCSK9Anticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalCholesterol LDLmedicine.diseaseFatty LiverHypocholesterolemia030104 developmental biologyTreatment OutcomechemistryDiabetes Mellitus Type 2lipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineLipid profilebusinessCognition DisordersBiomarkersLipoproteinCardiovascular research
researchProduct

The O-antigen of Plesiomonas shigelloides serotype O36 containing pseudaminic acid

2016

The structure of the repeating unit of O-antigen of Plesiomonas shigelloides serotype O36 has been investigated by 1H and 13C NMR spectroscopy, matrix-assisted laser-desorption/ionization time-of-flight mass spectrometry and chemical methods. The new structure of trisaccharide has been established: →4)-β-Pse5Ac7(R3Hb)-(2 → 4)-β-D-Galp-(1 → 3)-β-D-GlcpNAc-(1→ These trisaccharide O-antigen units substitute the core undecasaccharide at C-4 of the β-D-GlcpNAc residue. The core oligosaccharide and lipid A are identical with these of the serotype O17 (PCM 2231) (Maciejewska, A., Lukasiewicz, J., Kaszowska, M., Jachymek, W., Man-Kupisinska, A.; Lugowski, C. Mar. Drugs.2013, 11 (2), 440–454; Lukasi…

0301 basic medicineSerotypeMagnetic Resonance SpectroscopyStereochemistryMass spectrometrySerogroupBiochemistryAnalytical ChemistryLipid A03 medical and health sciencesResidue (chemistry)AntigenMALDI-TOF MSTrisaccharidechemistry.chemical_classification030102 biochemistry & molecular biologybiologyChemistryOrganic ChemistryO AntigensGeneral MedicineO-antigenbiology.organism_classificationPlesiomonas shigelloidesNMRMatrix-assisted laser desorption/ionization030104 developmental biologyBiochemistryCarbohydrate SequencePlesiomonas shigelloidesPlesiomonasCarbohydrate Research
researchProduct

Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
researchProduct

Trichomonicidal and parasite membrane damaging activity of bidesmosic saponins from Manilkara rufula.

2017

The infection caused by Trichomonas vaginalis is the most common but overlooked non-viral sexually transmitted disease worldwide. Treatment relies on one class of drugs, the 5-nitroimidazoles, but resistance is widespread. New drugs are urgently needed. We reported the effect of crude and purified saponin fractions of Manilkara rufula against Trichomonas vaginalis. The compound responsible for antitrichomonal activity was isolated and identified as an uncommon bidesmosic saponin, Mi-saponin C. This saponin eliminated parasite viability without toxicity against the human vaginal epithelial line (HMVII). In addition, the isolated saponin fraction improved the metronidazole effect against a me…

0301 basic medicineSexually transmitted diseaseNeutrophilsCell MembranesSaponinlcsh:Medicinemedicine.disease_causePathology and Laboratory MedicineBiochemistryMass SpectrometryAnalytical ChemistryWhite Blood CellsOxidative DamageSpectrum Analysis TechniquesAnimal CellsMedicine and Health SciencesParasite hostingElectron Microscopylcsh:Sciencechemistry.chemical_classificationSexually transmitted diseasesTrichomonas VaginalisMicroscopyMultidisciplinaryEukaryotaProtistsMatrix-Assisted Laser Desorption Ionization Mass Spectrometrymusculoskeletal systemChemistryFlagellaToxicityPhysical SciencesVaginaTrichomonasFemaleCellular TypesCellular Structures and OrganellesPathogensMalalties de transmissió sexualIntracellularmedicine.drugResearch ArticlePathogen MotilityEfecte dels medicaments sobre els microorganismesVirulence FactorsImmune CellsImmunologyBiologyResearch and Analysis Methodscomplex mixturesMicrobiologyCell Line03 medical and health sciencesParasite Groupsparasitic diseasesmedicineTrichomonas vaginalisSaponinasHumansTrophozoitesResistència als medicamentsManilkaraBlood CellsCell Membranelcsh:ROrganismsBiology and Life SciencesCell BiologyIntracellular MembranesSaponinsbiology.organism_classificationCell membranescarbohydrates (lipids)MetronidazoleMicroscopy Electron030104 developmental biologychemistryManilkara rufulaDrug resistanceEffect of drugs on microorganismsTrichomonas vaginalisParasitologyTransmission Electron Microscopylcsh:QReactive Oxygen SpeciesApicomplexaMembranes cel·lularsChromatography LiquidPRODUTOS NATURAISPLoS ONE
researchProduct

ERK1/2 activation in human taste bud cells regulates fatty acid signaling and gustatory perception of fat in mice and humans

2016

Obesity is a major public health problem. An in-depth knowledge of the molecular mechanisms of oro-sensory detection of dietary lipids may help fight it. Humans and rodents can detect fatty acids via lipido-receptors, such as CD36 and GPR120. We studied the implication of the MAPK pathways, in particular, ERK1/2, in the gustatory detection of fatty acids. Linoleic acid, a dietary fatty acid, induced via CD36 the phosphorylation of MEK1/2-ERK1/2-ETS-like transcription factor-1 cascade, which requires Fyn-Src kinase and lipid rafts in human taste bud cells (TBCs). ERK1/2 cascade was activated by Ca2+ signaling via opening of the calcium-homeostasis modulator-1 (CALHM1) channel. Furthermore, f…

0301 basic medicineSmall interfering RNAMouseCD36BiochemistryMapkObesechemistry.chemical_compound0302 clinical medicinegpr120Cd36Mice Knockoutchemistry.chemical_classificationGene knockdownbiologyKinaseFatty AcidsTaste PerceptionGPR120Taste BudsLipidsProtein-tyrosine kinases3. Good healthTasteBenzamidesBiotechnologymedicine.medical_specialtyMAP Kinase Signaling SystemLinoleic acid[SDV.BC]Life Sciences [q-bio]/Cellular BiologyPreferenceFood Preferences03 medical and health sciencesCalhm1Internal medicineDietary-fatGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCalcium SignalingObesityMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyResearchDiphenylamineFatty acidDietary FatsMicroRNAs030104 developmental biologyEndocrinologychemistrybiology.proteinIon-channelCALHM1Src kinase030217 neurology & neurosurgery
researchProduct

PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
researchProduct