Search results for "BM"

showing 10 items of 1459 documents

Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

2014

Objective Growing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas. Methods EZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879…

MESH: Cell DeathAdenosine[SDV]Life Sciences [q-bio]Cancer Treatmentlcsh:MedicineMESH: Flow CytometryApoptosischemistry.chemical_compoundSpectrum Analysis Techniques0302 clinical medicineCell MovementMolecular Cell BiologyMedicine and Health Sciences3-Deazaneplanocin AMESH: Epigenesis GeneticEnzyme Inhibitorslcsh:Science0303 health sciencesMultidisciplinaryCell DeathbiologyReverse Transcriptase Polymerase Chain ReactionEZH2Polycomb Repressive Complex 2DrugsCell migrationMESH: ChondrosarcomaFlow Cytometry3. Good healthHistone[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemOncologyConnective TissueCell ProcessesSpectrophotometry030220 oncology & carcinogenesisHistone methyltransferaseHistone MethyltransferasesMESH: 3-deazaneplanocinCytophotometryAnatomyMESH: Polycomb Repressive Complex 2Epigenetic therapyMESH: Histone methyltransferaseResearch ArticleProgrammed cell deathHistologyChondrosarcoma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesResearch and Analysis MethodsCell GrowthEpigenetic Therapy03 medical and health sciencesRheumatologyCell Line TumorMESH: Blotting WesternHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEZH2Tumors030304 developmental biologyMESH: Apoptosislcsh:RMESH: Histone-Lysine N-MethyltransferaseBiology and Life SciencesMESH: ImmunohistochemistryHistone-Lysine N-MethyltransferaseCell BiologyBiological TissueCartilageHistone methyltransferasechemistryApoptosisbiology.proteinCancer researchMESH: EZH2 protein humanlcsh:QCytometry
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Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion

2011

Article Open access plus; International audience; The use of TRAIL/APO2L and monoclonal antibodies targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature review aims to present and highlight recent findings of the deadly discussion that determines tumor cell fate upon TRAIL engagement.

MESH: Cell DeathMESH: Signal TransductionCancer ResearchApoptosisTRAILMESH : Models BiologicalscaffoldCell membrane0302 clinical medicineDrug DiscoveryMESH: AnimalsPharmacology (medical)Receptordeath effector domain0303 health sciencesCell DeathGeneral MedicineTRAIL-R4.3. Good healthCell biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSignal transductionMESH : Apoptosis Regulatory ProteinsSignal TransductionProgrammed cell deathc-FLIPdeath domainmedicine.drug_classMESH : Cell MembraneCancer therapyBiologyMonoclonal antibodyModels BiologicalArticle03 medical and health sciencesmedicineAnimalsHumansChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionMESH: HumansMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell MembraneMESH: Models BiologicalDISCReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMESH : Cell DeathFADDCancer cellMESH : AnimalsApoptosis Regulatory ProteinsMESH : ApoptosisMESH: Cell MembraneRecent Patents on Anti-Cancer Drug Discovery
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

2009

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guid…

MESH: Cell DeathcytofluorometryMESH : Microscopy Fluorescenceved/biology.organism_classification_rank.speciesCellMESH: Flow CytometryMESH: Microscopy FluorescenceApoptosisfluorescence microscopyMESH: Eukaryotic CellsAnnexin Vnecrosis0302 clinical medicineEukaryotic Cells/cytologyMitochondrial membrane permeabilizationScanningMESH : ImmunoblottingGeneticsApoptosis; Cell Death; Eukaryotic Cells/cytology; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence0303 health sciencesMicroscopyMESH : Spectrometry FluorescenceMESH: ImmunoblottingCell DeathMESH: Guidelines as Topic//purl.org/becyt/ford/3.1 [https]Bioquímica y Biología MolecularFlow Cytometry3. Good healthTunelMedicina Básicamedicine.anatomical_structureEukaryotic Cellscaspases030220 oncology & carcinogenesis//purl.org/becyt/ford/3 [https]MESH: Spectrometry FluorescenceMESH : Microscopy Electron ScanningProgrammed cell deathautophagyCIENCIAS MÉDICAS Y DE LA SALUDMESH: Microscopy Electron ScanningMESH : Flow CytometrycaspaseImmunoblottingGuidelines as TopicComputational biologyBiologyElectronFluorescenceArticle03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyModel organismddc:612mitotic catastropheMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Guidelines as Topic030304 developmental biologycell death; Apoptosis; caspase; autophagy; Oxidative stress; fluorescence microscopyMESH: Humansved/biologySpectrometryInterpretation (philosophy)MESH: ApoptosisMESH : Eukaryotic CellsMESH : HumansApoptosis; Eukaryotic Cells; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence; Cell Death; Molecular Biology; Cell Biologyimmunofluorescence microscopyCell BiologySpectrometry FluorescenceMicroscopy FluorescenceOxidative stressMESH : Cell DeathCancer cellMicroscopy Electron ScanningMESH : Apoptosis
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Involvement of complement pathways in patients with bacterial septicemia.

2007

The complement system is a major humoral portion of the innate immune system, playing a significant role in host defence against microorganisms. The biological importance of this system is underlined by the fact that at least three different pathways for its activation exist, the classical, the MBL and the alternative pathway. To elucidate the involvement of the classical and/or the MBL pathway during bacterial septicemia, 32 patients with gram-positive and 30 patients with gram-negative bacterial infections were investigated. In patients with gram-positive bacteria, a significant consumption of C1q (p=0.005) but not of mannose-binding lectin (MBL) (p=0.2) was found during the acute phase o…

MESH: Complement Pathway Mannose-Binding LectinLipopolysaccharidesSalmonellaMESH: Complement C1qLipopolysaccharideImmunologychemical and pharmacologic phenomenaBacteremiamedicine.disease_causeGram-Positive BacteriaMannose-Binding LectinMicrobiologyMESH: Gram-Positive Bacteria03 medical and health scienceschemistry.chemical_compoundClassical complement pathway0302 clinical medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyComplement Pathway ClassicalMESH: BacteremiaMolecular Biology030304 developmental biology0303 health sciencesInnate immune systemMESH: HumansbiologyComplement C1qLectinSalmonella entericaComplement Pathway Mannose-Binding LectinMESH: Complement Pathway Classicalbiology.organism_classificationbacterial infections and mycoses3. Good healthComplement systemMESH: Mannose-Binding LectinchemistryMESH: Salmonella entericaImmunologyAlternative complement pathwaybiology.proteinMESH: LipopolysaccharidesBacteria030215 immunologyMolecular immunology
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PED in 2021: a major update of the protein ensemble database for intrinsically disordered proteins

2020

Abstract The Protein Ensemble Database (PED) (https://proteinensemble.org), which holds structural ensembles of intrinsically disordered proteins (IDPs), has been significantly updated and upgraded since its last release in 2016. The new version, PED 4.0, has been completely redesigned and reimplemented with cutting-edge technology and now holds about six times more data (162 versus 24 entries and 242 versus 60 structural ensembles) and a broader representation of state of the art ensemble generation methods than the previous version. The database has a completely renewed graphical interface with an interactive feature viewer for region-based annotations, and provides a series of descriptor…

MESH: Databases ProteinMESH: Search EngineAcademicSubjects/SCI00010[SDV.BBM.BS] Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM][SDV]Life Sciences [q-bio]media_common.quotation_subjectBiologycomputer.software_genreIntrinsically disordered proteins03 medical and health sciencesDatabases0302 clinical medicineInformation and Computing SciencesGeneticsFeature (machine learning)Database IssueHumansDatabases ProteinRepresentation (mathematics)Function (engineering)MESH: Tumor Suppressor Protein p53ComputingMilieux_MISCELLANEOUS030304 developmental biologymedia_commonGraphical user interfaceStructure (mathematical logic)MESH: Intrinsically Disordered Proteins0303 health sciencesMESH: HumansDatabase[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]business.industryProteinBiological Sciences[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM]MetadataSearch EngineIntrinsically Disordered ProteinsState (computer science)Generic health relevanceTumor Suppressor Protein p53businesscomputer030217 neurology & neurosurgeryEnvironmental SciencesDevelopmental Biology
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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Changes in the proton-motive force in Escherichia coli in response to external oxidoreduction potential.

1999

International audience; The pH homeostasis and proton-motive force (Deltap) of Escherichia coli are dependent on the surrounding oxidoreduction potential (ORP). Only the internal pH value and, thus, the membrane pH gradient (DeltapH) component of the Deltap is modified, while the membrane potential (DeltaPsi) does not change in a significant way. Under reducing conditions (Eh < 50 mV at pH 7.0), E. coli decreases its Deltap especially in acidic media (21% decrease at pH 7.0 and 48% at pH 5.0 for a 850-mV ORP decrease). Measurements of ATPase activity and membrane proton conductance (CH+m) depending on ORP and pH have shown that the internal pH decrease is due to an increase in membrane prot…

MESH: Oxidation-ReductionMESH : Escherichia coliMESH: Hydrogen-Ion ConcentrationMembrane permeabilitymedicine.disease_causeBiochemistryMembrane Potentials03 medical and health sciencesMESH : Hydrogen-Ion Concentration[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineEscherichia coliMESH: Adenosine TriphosphatasesMESH : Membrane PotentialsMESH : ProtonsMESH: Membrane Potentials[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[INFO.INFO-BT]Computer Science [cs]/Biotechnology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyEscherichia coliComputingMilieux_MISCELLANEOUS030304 developmental biologyMESH : Oxidation-ReductionMembrane potentialchemistry.chemical_classificationAdenosine Triphosphatases0303 health sciencesChromatographyMESH : Adenosine Triphosphatases030306 microbiologyChemiosmosisChemistryMESH: Escherichia coliConductanceHydrogen-Ion Concentration[INFO.INFO-BT] Computer Science [cs]/BiotechnologyMembranePermeability (electromagnetism)BiophysicsThiolMESH: ProtonsProtonsOxidation-Reduction[ INFO.INFO-BT ] Computer Science [cs]/Biotechnology
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Peroxisomal beta-oxidation activities and gamma-decalactone production by the yeast Yarrowia lipolytica.

1998

International audience; gamma-Decalactone is a peachy aroma compound resulting from the peroxisomal beta-oxidation of ricinoleic acid by yeasts. The expression levels of acyl-CoA oxidase (gene deletion) and 3-ketoacyl-CoA thiolase activities (gene amplification on replicative plasmids) were modified in the yeast Yarrowia lipolytica. The effects of these modifications on beta-oxidation were measured. Overexpression of thiolase activity did not have any effect on the overall beta-oxidation activity. The disruption of one of the acyl-CoA oxidase genes resulted in an enhanced activity. The enhancement led to an increase of overall beta-oxidation activity but reduced the gamma-decalactone produc…

MESH: Oxidation-ReductionRicinoleic acidMESH: MicrobodiesMicrobodiesApplied Microbiology and BiotechnologyAROME DE PECHELactoneschemistry.chemical_compoundMESH : BiotransformationYeastsMESH : Microbodies[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAcyl-CoA oxidaseMESH: Blotting NorthernNorthern[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[INFO.INFO-BT]Computer Science [cs]/Biotechnology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBiotransformationMESH : Oxidation-ReductionMESH: BiotransformationMESH : YeastsOxidase testbiologyBlottingCatabolismThiolaseMESH: YeastsMESH : Blotting NorthernYarrowiaGeneral MedicinePeroxisomeBlotting Northernbiology.organism_classificationYeastMESH : LactonesMESH: Ricinoleic Acids[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology[INFO.INFO-BT] Computer Science [cs]/BiotechnologyBiochemistrychemistryMESH : Ricinoleic AcidsACYL COA OXYDASERicinoleic AcidsOxidation-Reduction[ INFO.INFO-BT ] Computer Science [cs]/BiotechnologyMESH: LactonesBiotechnology
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