Maria Nagy, PhD
Associate Research Scientist in GeneticsCards
Appointments
Genetics
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Genetics
333 Cedar Street, SHM I323
New Haven, CT 06511
United States
About
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Titles
Associate Research Scientist in Genetics
Appointments
Education & Training
- PhD
- Kansas State University, Department of Biochemistry, Biochemistry (2008)
- MSc
- Babes-Bolyai University, Faculty of Physics, Quantum Condensed State and Field Theory (1998)
- BS
- Babes-Bolyai University, Faculty of Physics, Physics (1997)
Research
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Maria Nagy's published research.
Publications Timeline
A big-picture view of Maria Nagy's research output by year.
Arthur Horwich, MD
Weiming Ni, PhD
Francesc Lopez-Giraldez, PhD
Joan Steitz, PhD
Shervin S. Takyar, MD, PhD
15Publications
411Citations
Publications
2019
Hsp110 mitigates α-synuclein pathology in vivo
Taguchi YV, Gorenberg EL, Nagy M, Thrasher D, Fenton WA, Volpicelli-Daley L, Horwich AL, Chandra SS. Hsp110 mitigates α-synuclein pathology in vivo. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 24310-24316. PMID: 31685606, PMCID: PMC6883785, DOI: 10.1073/pnas.1903268116.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsΑ-synuclein pathologyOverexpression of Hsp110Α-synuclein aggregationPresynaptic protein α-synucleinΑ-synuclein seedsΑ-synuclein oligomersLewy bodiesMouse modelParkinson's diseaseCell culture modelSynaptic proteomeΑ-synucleinProtein α-synucleinPathologyCulture modelDiseaseMammalian cell culture modelsProtein changesOverexpressionVivoHsp110Molecular facilitatorsMiceUnbiased analysisBrain
2016
Reduced high-frequency motor neuron firing, EMG fractionation, and gait variability in awake walking ALS mice
Hadzipasic M, Ni W, Nagy M, Steenrod N, McGinley MJ, Kaushal A, Thomas E, McCormick DA, Horwich AL. Reduced high-frequency motor neuron firing, EMG fractionation, and gait variability in awake walking ALS mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: e7600-e7609. PMID: 27821773, PMCID: PMC5127366, DOI: 10.1073/pnas.1616832113.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsALS miceAmyotrophic lateral sclerosisAcute spinal cord slicesSingle-unit extracellular recordingsWhole-cell patch-clamp recordingsLoss of neuronsMotor neuron lossMotor neuron firingSpinal cord slicesPatch-clamp recordingsHigh-frequency firingStep variabilityLethal neurodegenerative diseaseNeuron lossCord slicesSpinal cordLeg flexorsLateral sclerosisGait variabilityVivo effectsClamp recordingsExtracellular recordingsEMG patternsMutant miceNeuron firingExtended survival of misfolded G85R SOD1-linked ALS mice by transgenic expression of chaperone Hsp110
Nagy M, Fenton WA, Li D, Furtak K, Horwich AL. Extended survival of misfolded G85R SOD1-linked ALS mice by transgenic expression of chaperone Hsp110. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 5424-5428. PMID: 27114530, PMCID: PMC4868459, DOI: 10.1073/pnas.1604885113.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDisaggregation machineryHsp110 proteinsOverexpression of Hsp110Mammalian cellsMutant versionNucleotide exchangeTransgenic expressionHsp110Cu/ZnFold overexpressionNeuronal cellsRate-limiting stepMotor neuronsNative formG85R-SOD1Transgenic overexpressionHsc70OverexpressionDismutase 1MachineryProteinTransgenic miceMouse strainsMaximum survivalRecent studies
2015
Proteomics and Transcriptomics of BJAB Cells Expressing the Epstein-Barr Virus Noncoding RNAs EBER1 and EBER2
Pimienta G, Fok V, Haslip M, Nagy M, Takyar S, Steitz JA. Proteomics and Transcriptomics of BJAB Cells Expressing the Epstein-Barr Virus Noncoding RNAs EBER1 and EBER2. PLOS ONE 2015, 10: e0124638. PMID: 26121143, PMCID: PMC4487896, DOI: 10.1371/journal.pone.0124638.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMRNA-seq dataHost cell nucleusBJAB cellsCell proliferationGene expression featuresPro-survival effectsProtein adaptersAlternative splicingMRNA transcriptomeUpregulated proteinsSILAC dataRich elementsAkt activationPI3K-AktBiochemical assaysCell nucleiEBV latencySwitch eventsProteinMaintenance of latencyCell linesVEGFA proteinMechanistic explanationUpregulated oncogenesPIK3AP1
2014
Selective degeneration of a physiological subtype of spinal motor neuron in mice with SOD1-linked ALS
Hadzipasic M, Tahvildari B, Nagy M, Bian M, Horwich AL, McCormick DA. Selective degeneration of a physiological subtype of spinal motor neuron in mice with SOD1-linked ALS. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 16883-16888. PMID: 25385594, PMCID: PMC4250117, DOI: 10.1073/pnas.1419497111.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMN cell bodiesMotor neuronsMo of ageCell bodiesSpinal cordSpinal cord tissue slicesWhole-cell patch-clamp recordingsCell patch-clamp recordingsAdult mouse spinal cordIntrinsic electrophysiologic propertiesTwitch muscleSpinal motor neuronsLower extremity musclesTransgenic mouse modelMouse motor neuronsPatch-clamp recordingsAmyotrophic lateral sclerosisMouse spinal cordSlow-twitch muscleSteady-state firing ratePhysiological subtypesRetrograde tracingAcute slicesExtremity musclesPathophysiologic eventsAbsence of lipofuscin in motor neurons of SOD1-linked ALS mice
Bandyopadhyay U, Nagy M, Fenton WA, Horwich AL. Absence of lipofuscin in motor neurons of SOD1-linked ALS mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 11055-11060. PMID: 25024188, PMCID: PMC4121794, DOI: 10.1073/pnas.1409314111.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdaptor Proteins, Signal TransducingAmino Acid SubstitutionAmyotrophic Lateral SclerosisAnimalsAutophagyAutophagy-Related Protein-1 HomologHeat-Shock ProteinsHumansLipofuscinLysosomesMechanistic Target of Rapamycin Complex 1MiceMice, TransgenicMicrotubule-Associated ProteinsMotor NeuronsMultiprotein ComplexesMutation, MissenseProtein Serine-Threonine KinasesSequestosome-1 ProteinSuperoxide DismutaseSuperoxide Dismutase-1TOR Serine-Threonine KinasesConceptsUnc-51-like kinase 1Autophagy/lysosome pathwayMotor neuron cell bodiesLight chain 3Neuron cell bodiesLysosome pathwayRapamycin complex 1 (mTORC1) pathwayMotor neuronsALS miceProtein 1 light chain 3Microtubule-associated protein 1 light chain 3Cell bodiesAbsence of lipofuscinPresymptomatic ALS miceMutant human Cu/ZnMarkers of autophagySequestosome 1Kinase 1Mammalian targetChain 3Cu/ZnG93A-SOD1Human Cu/ZnLysosomal hydrolysisRed autofluorescenceProduction of RNA for Transcriptomic Analysis from Mouse Spinal Cord Motor Neuron Cell Bodies by Laser Capture Microdissection
Bandyopadhyay U, Fenton WA, Horwich AL, Nagy M. Production of RNA for Transcriptomic Analysis from Mouse Spinal Cord Motor Neuron Cell Bodies by Laser Capture Microdissection. Journal Of Visualized Experiments 2014, 51168. PMID: 24457537, PMCID: PMC4089401, DOI: 10.3791/51168.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLaser capture microdissectionMotor neuronsSpinal cordMotor neuron cell bodiesCapture microdissectionMouse spinal cordNeuron cell bodiesTotal cell populationCell typesPharmacologic treatmentStained neuronsCell bodiesNeurodegenerative diseasesNeuronsExogenous RNasesQRT-PCRSame cell typeCell populationsCordRNA damageDiseaseTotal RNASuch preparationsMicrodissectionTranscriptional differences
2013
Molecular chaperone Hsp110 rescues a vesicle transport defect produced by an ALS-associated mutant SOD1 protein in squid axoplasm
Song Y, Nagy M, Ni W, Tyagi NK, Fenton WA, López-Giráldez F, Overton JD, Horwich AL, Brady ST. Molecular chaperone Hsp110 rescues a vesicle transport defect produced by an ALS-associated mutant SOD1 protein in squid axoplasm. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 5428-5433. PMID: 23509252, PMCID: PMC3619309, DOI: 10.1073/pnas.1303279110.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAxonal TransportBacterial ProteinsDecapodiformesGene Expression ProfilingHSP110 Heat-Shock ProteinsHumansLuminescent ProteinsMAP Kinase Kinase Kinase 5MiceMice, TransgenicMutation, Missensep38 Mitogen-Activated Protein KinasesPhosphorylationProtein FoldingProteomicsRecombinant Fusion ProteinsSpinal CordSuperoxide DismutaseSuperoxide Dismutase-1Transport VesiclesConceptsMutant SOD1 proteinTransport defectSOD1 proteinApoptosis signal-regulating kinase 1 inhibitorsPhosphorylation of kinesinNucleotide exchange factorsMolecular chaperone Hsc70Different oligomeric statesYellow fluorescent proteinTransgenic miceProtein disaggregationChaperone Hsc70Exchange factorMAPK cascadePhosphorylation of p38Oligomeric stateDiminished phosphorylationKinase 1 inhibitorFusion proteinFluorescent proteinP38 inhibitorP38 MAPKPhosphorylationHsp110Cu/ZnRNA-Seq Profiling of Spinal Cord Motor Neurons from a Presymptomatic SOD1 ALS Mouse
Bandyopadhyay U, Cotney J, Nagy M, Oh S, Leng J, Mahajan M, Mane S, Fenton WA, Noonan JP, Horwich AL. RNA-Seq Profiling of Spinal Cord Motor Neurons from a Presymptomatic SOD1 ALS Mouse. PLOS ONE 2013, 8: e53575. PMID: 23301088, PMCID: PMC3536741, DOI: 10.1371/journal.pone.0053575.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsRNA metabolismMutant proteinsMotor neuron cell bodiesPost-translational effectsRNA-seq profilingMotor neuronsNeuron cell bodiesWhole transcriptome profilingMonths of ageAltered expression levelsMutant human SOD1Transcriptome profilingLower motor neuron cell bodiesCell bodiesTransgenic strainsSpinal cord motor neuronsSymptoms of ALSMutant SOD1 miceSOD1-ALS miceAge-matched animalsHuman SOD1Amyotrophic lateral sclerosisProtein TDP43Expression levelsForms of ALS
2012
Flexible connection of the N-terminal domain in ClpB modulates substrate binding and the aggregate reactivation efficiency.
Zhang T, Ploetz EA, Nagy M, Doyle SM, Wickner S, Smith PE, Zolkiewski M. Flexible connection of the N-terminal domain in ClpB modulates substrate binding and the aggregate reactivation efficiency. Proteins 2012, 80: 2758-68. PMID: 22890624, DOI: 10.1002/prot.24159.Peer-Reviewed Original Research
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Genetics
333 Cedar Street, SHM I323
New Haven, CT 06511
United States