Novin Balafkan
Visiting Research ScientistCards
About
Research
Publications
2021
Distinct Mitochondrial Remodeling During Mesoderm Differentiation in a Human-Based Stem Cell Model
Mostafavi S, Balafkan N, Pettersen I, Nido G, Siller R, Tzoulis C, Sullivan G, Bindoff L. Distinct Mitochondrial Remodeling During Mesoderm Differentiation in a Human-Based Stem Cell Model. Frontiers In Cell And Developmental Biology 2021, 9: 744777. PMID: 34722525, PMCID: PMC8553110, DOI: 10.3389/fcell.2021.744777.Peer-Reviewed Original ResearchGlycolysis to oxidative phosphorylationMitochondrial remodelingOxidative phosphorylationMesoderm differentiationRemodeling of mitochondriaMitochondrial contentGerm layer specificationStem cell fateIncreased mitochondrial activityATP-linked respirationIncreased OXPHOS activityCell fateMitochondria remodelingOXPHOS activityRegulate self-renewalMitochondrial activityMultipotent stateMitochondrial adaptationsEctoderm commitmentMitochondriaStem cell modelNeuronal differentiationMesodermal derivativesEndodermal lineagesGlycolysis
2020
A method for differentiating human induced pluripotent stem cells toward functional cardiomyocytes in 96-well microplates
Balafkan N, Mostafavi S, Schubert M, Siller R, Liang K, Sullivan G, Bindoff L. A method for differentiating human induced pluripotent stem cells toward functional cardiomyocytes in 96-well microplates. Scientific Reports 2020, 10: 18498. PMID: 33116175, PMCID: PMC7595118, DOI: 10.1038/s41598-020-73656-2.Peer-Reviewed Original ResearchConceptsPluripotent stem cellsCapacity of pluripotent stem cellsFunctional cardiomyocytesStem cellsFunctional human cardiomyocytesHuman induced pluripotent stem cellsCardiac-specific markersSerum-free culture mediumElectrophysiological propertiesHuman cardiomyocytesSelf-renewalCardiomyocytesProtein levelsHuman diseasesSpecific markersDevelopmental biologyCell typesMicroplate formatEfficient differentiationCulture mediumCellsDiseaseDisease‐specific phenotypes in iPSC‐derived neural stem cells with POLG mutations
Liang K, Kristiansen C, Mostafavi S, Vatne G, Zantingh G, Kianian A, Tzoulis C, Høyland L, Ziegler M, Perez R, Furriol J, Zhang Z, Balafkan N, Hong Y, Siller R, Sullivan G, Bindoff L. Disease‐specific phenotypes in iPSC‐derived neural stem cells with POLG mutations. EMBO Molecular Medicine 2020, 12: emmm202012146. PMID: 32840960, PMCID: PMC7539330, DOI: 10.15252/emmm.202012146.Peer-Reviewed Original ResearchConceptsPOLG mutationsComplex ILoss of complex IHeterozygous POLG mutationsMitochondrial dysfunctionLoss of mtDNAFate determination processesHuman stem cell modelsNeural stem cellsMtDNA replicationIncreased UCP2 expressionStem cellsAssociated with POLG mutationsMtDNANAD+ metabolismActivating mitophagyPOLGNeurological phenotypePost-mortem brain tissueDisease-specific phenotypesPatient cellsStem cell modelMutationsBiochemical defectROS overproduction
2019
Mitochondrial DNA depletion in sporadic inclusion body myositis
Bhatt P, Tzoulis C, Balafkan N, Miletic H, Tran G, Sanaker P, Bindoff L. Mitochondrial DNA depletion in sporadic inclusion body myositis. Neuromuscular Disorders 2019, 29: 242-246. PMID: 30850168, DOI: 10.1016/j.nmd.2019.02.001.Peer-Reviewed Original ResearchConceptsMtDNA deletionsCopy numberMeasurement of mtDNA copy numberMitochondrial changesMitochondrial DNA depletionDeletions of mtDNAMtDNA copy numberLevels of mtDNASporadic inclusion body myositisMitochondrial DNAMtDNA abnormalitiesDNA depletionMtDNAMtDNA depletionNecrotising myopathyInclusion body myositisDeletionSporadic inclusion body myositis patientsHealthy controlsQualitative anlysisNo significant differenceInflammatory cellsDNAPatientsSignificant difference
2014
A large sample of Kohonen-selected SDSS quasars with weak emission lines: selection effects and statistical properties⋆
Meusinger H, Balafkan N. A large sample of Kohonen-selected SDSS quasars with weak emission lines: selection effects and statistical properties⋆. Astronomy & Astrophysics 2014, 568: a114. DOI: 10.1051/0004-6361/201423810.Peer-Reviewed Original ResearchWeak emission linesRadio-quiet quasarsSpectral energy distributionAccretion rateEmission linesEnergy distributionSloan Digital Sky Survey Data Release 7Radio-detected quasarsBlack hole massBroad line regionPower-law componentRedshift range zData Release 7Selection effectsBluer continuumEddington ratioHole massQuasar populationRadio quasarsRadio-loudQuasar activityRadio propertiesQuasar spectraRadio sourcesAccretion activityMolecular pathogenesis of polymerase gamma–related neurodegeneration
Tzoulis C, Tran G, Coxhead J, Bertelsen B, Lilleng P, Balafkan N, Payne B, Miletic H, Chinnery P, Bindoff L. Molecular pathogenesis of polymerase gamma–related neurodegeneration. Annals Of Neurology 2014, 76: 66-81. PMID: 24841123, PMCID: PMC4140551, DOI: 10.1002/ana.24185.Peer-Reviewed Original ResearchConceptsPolymerase gamma (POLGPOLG mutationsCause of mitochondrial diseaseAccumulation of mitochondrial DNA deletionsMitochondrial DNA depletionMitochondrial DNA deletionsMitochondrial genomeNeuronal lossDNA depletionDNA deletionsSomatic mutagenesisMicrodissected neuronsFocal neuronal necrosisMitochondrial diseaseEvidence of neuronal lossPoint mutationsCombination of histopathologyMassive neuronal lossStable depletionFrozen brain tissueBiological processesMitochondrial dysfunctionFocal cortical lesionsPOLGMolecular mechanisms
2013
Severe nigrostriatal degeneration without clinical parkinsonism in patients with POLG mutations
Tzoulis C, Tran G, Schwarzlmüller T, Specht K, Haugarvoll K, Balafkan N, Lilleng P, Miletic H, Martin B, Bindoff L. Severe nigrostriatal degeneration without clinical parkinsonism in patients with POLG mutations. Journal Of The Neurological Sciences 2013, 333: e101. DOI: 10.1016/j.jns.2013.07.621.Peer-Reviewed Original ResearchSevere nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations
Tzoulis C, Tran G, Schwarzlmüller T, Specht K, Haugarvoll K, Balafkan N, Lilleng P, Miletic H, Biermann M, Bindoff L. Severe nigrostriatal degeneration without clinical parkinsonism in patients with polymerase gamma mutations. Brain 2013, 136: 2393-2404. PMID: 23625061, DOI: 10.1093/brain/awt103.Peer-Reviewed Original ResearchConceptsMitochondrial DNA abnormalitiesPolymerase gamma-encephalopathyCatalytic subunit of polymerase gammaMitochondrial diseaseCopy number of mitochondrial DNAMitochondrial DNA homeostasisDNA abnormalitiesMitochondrial quality controlPolymerase gamma mutationDopamine transporter imagingComplex I deficiencyLevels of deletionIn vivo functional studiesPositron emission tomographyPathogenesis of neurodegenerationMitochondrial DNADNA homeostasisSubstantia nigraPolymerase gammaCatalytic subunitNeurons of patientsRespiratory chainCopy numberClinical parkinsonismGamma mutations
2012
Number of CAG repeats in POLG1 and its association with Parkinson disease in the Norwegian population
Balafkan N, Tzoulis C, Müller B, Haugarvoll K, Tysnes O, Larsen J, Bindoff L. Number of CAG repeats in POLG1 and its association with Parkinson disease in the Norwegian population. Mitochondrion 2012, 12: 640-643. PMID: 22963882, DOI: 10.1016/j.mito.2012.08.004.Peer-Reviewed Original ResearchConceptsCAG repeatsAssociated with Parkinson's diseaseMeta-analysisMitochondrial DNA polymerase gammaDNA polymerase gammaPOLG1 allelesLinkage disequilibriumCAG tractNorwegian populationAllelic variationParkinson's diseaseGenetic variantsPOLG1Multiple testingNorwegian patientsCAGRepeatsPathogenesis of PDPublished studiesAssociationPopulationPOLGAllelesDisequilibriumDisease
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