Six-month partial suppression of Huntingtin is well tolerated in the adult rhesus striatum. - Wikidata - wikimedia - TriplyDB

Six-month partial suppression of Huntingtin is well tolerated in the adult rhesus striatum.

Six-month partial suppression of Huntingtin is well tolerated in the adult rhesus striatum.

http://www.wikidata.org/entity/Q35888618

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Huntington's disease: the past, present, and future search for disease modifiers.Characterization of HTT inclusion size, location, and timing in the zQ175 mouse model of Huntington's disease: an in vivo high-content imaging study Huntingtin is required for normal excitatory synapse development in cortical and striatal circuits A fully humanized transgenic mouse model of Huntington disease.Allele-Selective Suppression of Mutant Huntingtin in Primary Human Blood Cells.Preclinical Evaluation of a Lentiviral Vector for Huntingtin Silencing.Oligonucleotide-based strategies to combat polyglutamine diseases.Targets for future clinical trials in Huntington's disease: what's in the pipeline?Phosphorodiamidate morpholino oligomers suppress mutant huntingtin expression and attenuate neurotoxicity.Broad distribution of ataxin 1 silencing in rhesus cerebella for spinocerebellar ataxia type 1 therapy.Gene suppression strategies for dominantly inherited neurodegenerative diseases: lessons from Huntington's disease and spinocerebellar ataxia.Transcription, epigenetics and ameliorative strategies in Huntington's Disease: a genome-wide perspective A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity Onset Time and Durability of Huntingtin Suppression in Rhesus Putamen After Direct Infusion of Antihuntingtin siRNA.Synthetic zinc finger repressors reduce mutant huntingtin expression in the brain of R6/2 mice.Mechanism of allele-selective inhibition of huntingtin expression by duplex RNAs that target CAG repeats: function through the RNAi pathway Translational research in Huntington's disease: opening up for disease modifying treatment Recent advances in RNA interference therapeutics for CNS diseases.Bidirectional control of postsynaptic density-95 (PSD-95) clustering by Huntingtin.Novel siRNA delivery strategy: a new "strand" in CNS translational medicine?Pharmacological protein targets in polyglutamine diseases: mutant polypeptides and their interactors.Use of genetically modified mesenchymal stem cells to treat neurodegenerative diseases.Promising Targets for the Treatment of Neurodegenerative Diseases.AAV5-miHTT gene therapy demonstrates suppression of mutant huntingtin aggregation and neuronal dysfunction in a rat model of Huntington's disease.Stacking up CRISPR against RNAi for therapeutic gene inhibition.Huntington's Disease: Mechanisms of Pathogenesis and Therapeutic Strategies.Identification of NUB1 as a suppressor of mutant Huntington toxicity via enhanced protein clearance.Silencing mutant huntingtin by adeno-associated virus-mediated RNA interference ameliorates disease manifestations in the YAC128 mouse model of Huntington's disease.Design, Characterization, and Lead Selection of Therapeutic miRNAs Targeting Huntingtin for Development of Gene Therapy for Huntington's Disease.In vivo evaluation of candidate allele-specific mutant huntingtin gene silencing antisense oligonucleotides.Elimination of huntingtin in the adult mouse leads to progressive behavioral deficits, bilateral thalamic calcification, and altered brain iron homeostasis.Knockdown and replacement therapy mediated by artificial mirtrons in spinocerebellar ataxia 7.CTG repeat-targeting oligonucleotides for down-regulating Huntingtin expression.Gene suppression approaches to neurodegeneration.Stereotaxic Surgical Targeting of the Nonhuman Primate Caudate and Putamen: Gene Therapy for Huntington's Disease.Therapies targeting DNA and RNA in Huntington's disease.Suppression of MAPK11 or HIPK3 reduces mutant Huntingtin levels in Huntington's disease models.Emerging Diagnostic and Therapeutic Strategies for Tauopathies.Effect of early embryonic deletion of huntingtin from pyramidal neurons on the development and long-term survival of neurons in cerebral cortex and striatum.Translation of MicroRNA-Based Huntingtin-Lowering Therapies from Preclinical Studies to the Clinic.

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P2860

Six-month partial suppression of Huntingtin is well tolerated in the adult rhesus striatum.

http://www.wikidata.org/entity/Q35888618

description

2012 nî lūn-bûn

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2012年論文

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2012年论文

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Six-month partial suppression ...... in the adult rhesus striatum.

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Deepak R Thakker

http://www.w3.org/2001/XMLSchema#string

Eric N Burright

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Janelle L Blum

http://www.w3.org/2001/XMLSchema#string

Jennifer Heisel

http://www.w3.org/2001/XMLSchema#string

Marcy R Weatherspoon

http://www.w3.org/2001/XMLSchema#string

Michael D Kaytor

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Peter T Nelson

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Richard Grondin

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William F Kaemmerer

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Yi Ai

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P2860

Oligonucleotide therapeutic approaches for Huntington disease

Huntingtin is required for mitotic spindle orientation and mammalian neurogenesis

Huntingtin phosphorylation acts as a molecular switch for anterograde/retrograde transport in neurons

Inactivation of the mouse Huntington's disease gene homolog Hdh

Inactivation of Hdh in the brain and testis results in progressive neurodegeneration and sterility in mice

Biological and clinical manifestations of Huntington's disease in the longitudinal TRACK-HD study: cross-sectional analysis of baseline data.

Nonallele-specific silencing of mutant and wild-type huntingtin demonstrates therapeutic efficacy in Huntington's disease mice.

RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse model.

Artificial miRNAs mitigate shRNA-mediated toxicity in the brain: implications for the therapeutic development of RNAi.

Recombinant AAV-mediated gene delivery to the central nervous system.

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1197-1209

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scholarly article

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10.1093/BRAIN/AWR333

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Pt 4

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135

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2012-01-16T00:00:00Z

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221754928

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22252996

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corpus striatum

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3326247

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