Featured Publications
The 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 investigationInactivation 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 mislocalizationA soy protein Lunasin can ameliorate amyloid-beta 42 mediated neurodegeneration in Drosophila eye
Sarkar A, Gogia N, Glenn N, Singh A, Jones G, Powers N, Srivastava A, Kango-Singh M, Singh A. A soy protein Lunasin can ameliorate amyloid-beta 42 mediated neurodegeneration in Drosophila eye. Scientific Reports 2018, 8: 13545. PMID: 30202077, PMCID: PMC6131139, DOI: 10.1038/s41598-018-31787-7.Peer-Reviewed Original ResearchConceptsRetinal neuronsNeuroprotective roleAlzheimer's diseaseHuman Aβ42Fatal progressive neurodegenerative disorderNovel neuroprotective roleProgressive neurodegenerative disorderAnti-cancer effectsPotential therapeutic agentJNK signalingAβ42 plaquesNeuronal deathNeuroprotective functionMortality rateTransgenic modelAxonal targetingNeurodegenerative disordersTherapeutic agentsCJun N-terminal kinaseNeurodegenerationOxidative stressAβ42NeuronsAbnormal signalingLunasin
2015
Drosophila Eye Model to Study Neuroprotective Role of CREB Binding Protein (CBP) in Alzheimer’s Disease
Cutler T, Sarkar A, Moran M, Steffensmeier A, Puli OR, Mancini G, Tare M, Gogia N, Singh A. Drosophila Eye Model to Study Neuroprotective Role of CREB Binding Protein (CBP) in Alzheimer’s Disease. PLOS ONE 2015, 10: e0137691. PMID: 26367392, PMCID: PMC4569556, DOI: 10.1371/journal.pone.0137691.Peer-Reviewed Original ResearchConceptsCREB Binding ProteinTargeted misexpressionCBP proteinGAL4/UAS systemBinding proteinGenetic modifiersDrosophila eye modelNormal cellular processesTargeting of axonsFruit fly modelStructure-function analysisAmyloid precursor proteinProgressive neurodegenerative phenotypeTransgenic fliesCellular processesPolyglutamine domainHistone acetylaseNeuroprotective functionPhotoreceptor neuronsFly modelGenetic basisUAS systemAmyloid plaquesMisexpressionDifferent proteins