2020
Nemo-like kinase reduces mutant huntingtin levels and mitigates Huntington’s disease
Jiang M, Zhang X, Liu H, LeBron J, Alexandris A, Peng Q, Gu H, Yang F, Li Y, Wang R, Hou Z, Arbez N, Ren Q, Dong JL, Whela E, Wang R, Ratovitski T, Troncoso JC, Mori S, Ross CA, Lim J, Duan W. Nemo-like kinase reduces mutant huntingtin levels and mitigates Huntington’s disease. Human Molecular Genetics 2020, 29: 1340-1352. PMID: 32242231, PMCID: PMC7254850, DOI: 10.1093/hmg/ddaa061.Peer-Reviewed Original ResearchConceptsBrain atrophyHD miceNemo-like kinaseMHTT levelsHD mouse modelsNew molecular targetsHD human brainHuntingtin proteinEffect of NLKMouse striatal cellsFurther mechanistic studiesActivity-dependent mannerHTT protein levelsMouse modelAdult brainStriatal cellsProtective roleMutant Htt aggregationAmino acids 120Huntington's diseaseMutant huntingtin levelsMolecular targetsHuntingtin levelsProtein levelsBrain
2015
Antidepressants for neuroprotection in Huntington's disease: A review
Jamwal S, Kumar P. Antidepressants for neuroprotection in Huntington's disease: A review. European Journal Of Pharmacology 2015, 769: 33-42. PMID: 26511378, DOI: 10.1016/j.ejphar.2015.10.033.Peer-Reviewed Original ResearchConceptsHuntingtin proteinHuntington's diseaseMAPK/ERK signalingBrain-derived neurotrophic factor (BDNF) productionBDNF/TrkB pathwayProgression of HDDifferent neuroprotective mechanismsPrincipal neuropathological hallmarksUse of antidepressantsNeurotrophic factor productionCortical projection neuronsMutant huntingtin proteinCellular functionsPolyglutamine stretchMolecular mechanismsNH2 terminusERK signalingTrkB pathwayPreclinical evidenceNeuroprotective effectsNeuroprotective mechanismsCommon symptomsProjection neuronsAvailable treatmentsDisease progressionDetecting mutant huntingtin protein in HD patients
Brennand K. Detecting mutant huntingtin protein in HD patients. Science Translational Medicine 2015, 7 DOI: 10.1126/scitranslmed.aac8559.Commentaries, Editorials and Letters
2012
Calpain and STriatal-Enriched protein tyrosine Phosphatase (STEP) activation contribute to extrasynaptic NMDA receptor localization in a Huntington's disease mouse model
Gladding CM, Sepers MD, Xu J, Zhang LY, Milnerwood AJ, Lombroso PJ, Raymond LA. Calpain and STriatal-Enriched protein tyrosine Phosphatase (STEP) activation contribute to extrasynaptic NMDA receptor localization in a Huntington's disease mouse model. Human Molecular Genetics 2012, 21: 3739-3752. PMID: 22523092, PMCID: PMC3412376, DOI: 10.1093/hmg/dds154.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalpainCoculture TechniquesDisease Models, AnimalEnzyme ActivationEnzyme InhibitorsHuntington DiseaseIon Channel GatingMiceModels, BiologicalNeostriatumNeuronsPhosphorylationPhosphotyrosineProtein TransportProtein Tyrosine Phosphatases, Non-ReceptorReceptors, N-Methyl-D-AspartateSynapsesConceptsYAC128 striatumProtein tyrosine phosphatase activationNMDAR localizationCalpain cleavageProtein tyrosine phosphataseTyrosine phosphatase activationEarly synaptic defectsWhole-cell NMDAR currentsDisease mouse modelGluN2B expressionNMDA receptor traffickingMutant huntingtin proteinCalpain inhibitionTyrosine phosphataseHuntington's diseaseFull-length mhttPlasma membranePhosphatase activationC-terminusReceptor traffickingNMDAR traffickingPolyglutamine repeatsMouse modelHuntingtin proteinNMDA receptor localization
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