Neha Gogia, PhD
About
Titles
Postdoctoral Associate
Biography
Presently my research is related to understanding the molecular basis of cellular pathology and disease mechanisms in polyglutamine (polyQ) related human neurodegenerative diseases such as, Spinocerebellar ataxia type 1 (SCA1) and Spinal-bulbar muscular atrophy (SBMA).
Keywords: Neuroscience; neurodegeneration; neurodegenerative disorders; polyglutamine repeat expansion; polyglutamine (polyQ) diseases; protein misfolding; proteinopathies; protein aggregation; protein quality control; neuromuscular; Spinal-bulbar muscular atrophy (SBMA); motor neuron disease; Spinocerebellar ataxia type 1 (SCA1); cell death; therapeutics.
Education & Training
- PhD
- Biological Sciences, The University of Dayton, Ohio, USA, Biology (2019)
- Student Exchange Program
- College of Agriculture and Life Sciences (CALS), Cornell University, Ithaca, New York, USA (2012)
- MS
- Biotechnology, Sardar Vallabhbhai Patel University of Agriculture and Technology, India (2012)
- BS
- Biotechnology, Sardar Vallabhbhai Patel University of Agriculture and Technology, India (2010)
Research
Publications
Dysregulation of alternative splicing in spinocerebellar ataxia type 1 (SCA 1)
Olmos* V, Thompson* E, Gogia N, Luttik K, Veeranki V, Ni L, Sim S, Chen K, Krause D, Lim J. Dysregulation of alternative splicing in spinocerebellar ataxia type 1. 2023. Human Molecular Genetics. PMID: 37802886 DOI: 10.1093/hmg/ddad170.Peer-Reviewed Original ResearchThe extra-cerebellar effects of spinocerebellar ataxia type 1 (SCA1): looking beyond the cerebellum
Olmos V, Gogia N, Luttik K, Haidery F, Lim J. The extra-cerebellar effects of spinocerebellar ataxia type 1 (SCA1): looking beyond the cerebellum. Cellular And Molecular Life Sciences 2022, 79: 404. PMID: 35802260, PMCID: PMC9993484, DOI: 10.1007/s00018-022-04419-7.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsSpinocerebellar ataxia type 1Type 1Ataxia type 1Cerebellar Purkinje cell lossProgressive motor deficitsSCA1 patientsPurkinje cell lossMouse model studiesMotor deficitsLimb incoordinationNumber of CAGMouse modelRespiratory problemsMemory impairmentCell lossCerebellar regionsCognitive defectsNeurodegenerative diseasesPatientsAtaxin-1 proteinDiverse pathologiesATXN1 expressionCerebellumDiseaseFurther investigationChapter 8 Exploring the role of protein quality control in aging and age-associated neurodegenerative diseases
Gogia N, Olmos V, Haidery F, Luttik K, Tejwani L, Lim J. Chapter 8 Exploring the role of protein quality control in aging and age-associated neurodegenerative diseases. 2022, 139-171. DOI: 10.1016/b978-0-323-90235-9.00012-4.ChaptersPQC systemAge-associated neurodegenerative diseasesAge-related neurodegenerative diseasesProtein quality control systemCell deathNeurodegenerative diseasesProtein quality controlHallmark of agingAlters cellular functionCellular proteomeCellular functionsProtein misfoldingQuality control systemCellular agingBiological processesPostmitotic natureNeuronal cell deathProteinDisease symptomsEfficient clearanceTherapeutic targetCellsDisease conditionsNervous system tissueEffective therapeuticsExploring the Role of Posttranslational Modifications in Spinal and Bulbar Muscular Atrophy
Gogia N, Ni L, Olmos V, Haidery F, Luttik K, Lim J. Exploring the Role of Posttranslational Modifications in Spinal and Bulbar Muscular Atrophy. Frontiers In Molecular Neuroscience 2022, 15: 931301. PMID: 35726299, PMCID: PMC9206542, DOI: 10.3389/fnmol.2022.931301.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsBulbar muscular atrophyAR proteinMuscular atrophyBulbar motor neuronsPolymorphic CAG trinucleotide repeatProgressive neuromuscular diseaseMain genetic causeMutant ARMotor neuronsTherapeutic approachesAR functionNeuromuscular diseaseProtective roleDisease pathophysiologyGenetic causeSkeletal muscleDiseaseCAG trinucleotide repeatAtrophySBMACell deathPolyQ tract expansionTractPolyQ disordersPolyglutamine expansionChapter 11 Role of AMP-activated protein kinase and sirtuins as antiaging proteins
Ramu M, Vishal S, Gogia N. Chapter 11 Role of AMP-activated protein kinase and sirtuins as antiaging proteins. 2022, 241-278. DOI: 10.1016/b978-0-323-90235-9.00015-x.ChaptersProtein kinaseAMP/ATP ratioDifferent cellular compartmentsCommon cellular targetActivity of AMPKFuel-sensing enzymeAge-associated disordersChapter 11 RoleSirtuin isoformsCellular compartmentsAge-related disordersSirtuin modulatorsSirtuin activityDifferent speciesAMPKCellular targetsAMPK pathwayContext of agingMitochondrial functionMitochondrial disordersPotential therapeutic targetATP ratioAge-related processesKinaseSIRT1Unbiased automated quantitation of ROS signals in live retinal neurons of Drosophila using Fiji/ImageJ
Deshpande P, Gogia N, Chimata AV, Singh A. Unbiased automated quantitation of ROS signals in live retinal neurons of Drosophila using Fiji/ImageJ. BioTechniques 2021, 71: 416-424. PMID: 34350780, PMCID: PMC10288391, DOI: 10.2144/btn-2021-0006.Peer-Reviewed Original ResearchHippo signaling: bridging the gap between cancer and neurodegenerative disorders
Gogia N, Chimata AV, Deshpande P, Singh A, Singh A. Hippo signaling: bridging the gap between cancer and neurodegenerative disorders. Neural Regeneration Research 2020, 16: 643-652. PMID: 33063715, PMCID: PMC8067938, DOI: 10.4103/1673-5374.295273.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCell deathHippo pathwayGrowth regulationAberrant cell deathRole of HippoNeurodegenerative disordersCell proliferationCell death mechanismsCell death resultsOrgan sizeDeath mechanismsNeuronal cell populationsChemical inhibitorsHippoNormal developmentVariety of mechanismsFundamental processesCell proliferation resultsCell populationsPathwayVariety of diseasesNeurodegenerative diseasesRegulationDeath resultsProliferation resultsAn E3 ubiquitin ligase, cullin‐4 regulates retinal differentiation in Drosophila eye
Tare M, Chimata AV, Gogia N, Narwal S, Deshpande P, Singh A. An E3 ubiquitin ligase, cullin‐4 regulates retinal differentiation in Drosophila eye. Genesis 2020, 58: e23395. PMID: 32990387, PMCID: PMC9277906, DOI: 10.1002/dvg.23395.Peer-Reviewed Original ResearchConceptsCUL-4E3 ubiquitin ligaseEye developmentCullin 4Morphogenetic furrowRetinal differentiationUbiquitin ligaseCell deathForward genetic screenDrosophila eye modelEarly eye developmentSpecific cell typesGenetic screenDrosophila eyeGenomic stabilityEye phenotypeProcess of differentiationProtein degradationNegative regulatorGene expressionDevelopmental defectsFunction backgroundCell cycleMolecular mechanismsCell typesGeneration of Third Dimension: Axial Patterning in the Developing Drosophila Eye
Gogia N, Puli O, Raj A, Singh A. Generation of Third Dimension: Axial Patterning in the Developing Drosophila Eye. 2020, 53-95. DOI: 10.1007/978-3-030-42246-2_2.ChaptersAxial patterningDrosophila eyeDrosophila eye imaginal discVentral cell populationsMulti-cellular organismsDrosophila eye modelEye imaginal discFundamental processesOnset of expressionDorsal eye marginActivation of NotchProximo-distal axesN signalingOrgan primordiaImaginal discsGrowth defectDorsal fateThree-dimensional organsFly retinaOrganogenesis resultsPD axisEye primordiumGroups of cellsAP axisCell proliferationInactivation of Hippo and cJun-N-terminal Kinase (JNK) signaling mitigate FUS mediated neurodegeneration in vivo
Gogia N, Sarkar A, Mehta A, Ramesh N, Deshpande P, Kango-Singh M, Pandey UB, Singh A. Inactivation of Hippo and cJun-N-terminal Kinase (JNK) signaling mitigate FUS mediated neurodegeneration in vivo. Neurobiology Of Disease 2020, 140: 104837. PMID: 32199908, PMCID: PMC9277911, DOI: 10.1016/j.nbd.2020.104837.Peer-Reviewed Original ResearchMeSH KeywordsAmyotrophic Lateral SclerosisAnimalsAxonsCytoplasmDisease Models, AnimalDrosophilaDrosophila ProteinsIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase 4Motor NeuronsMutationNerve DegenerationNeuromuscular JunctionPhenotypeProtein Serine-Threonine KinasesProtein TransportRNA-Binding Protein FUSSignal TransductionConceptsDrosophila eyeHippo signalingJNK signalingAmyotrophic lateral sclerosisCell deathC-Jun amino-terminal kinaseGenetic modifiersInactivation of HippoCJun N-terminal kinaseTrigger cell deathAmino-terminal kinaseGrowth regulatory pathwaysLate-onset neurodegenerative disorderTargeted misexpressionRNA metabolismPromotes Cell ProliferationHippo pathwayInteresting phenotypesDrosophila modelGenetic mechanismsHuman FUSFUS accumulationRegulatory pathwaysAxonal targetingCytoplasmic mislocalization