Lethal toxicity caused by expression of shRNA in the mouse striatum: implications for therapeutic design. - Wikidata - awgldk - TriplyDB

Lethal toxicity caused by expression of shRNA in the mouse striatum: implications for therapeutic design.

Lethal toxicity caused by expression of shRNA in the mouse striatum: implications for therapeutic design.

http://www.wikidata.org/entity/Q41983597

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Manufacturing of recombinant adeno-associated viral vectors for clinical trials Synthetic biology and therapeutic strategies for the degenerating brain: Synthetic biology approaches can transform classical cell and gene therapies, to provide new cures for neurodegenerative diseases Preclinical Evaluation of a Lentiviral Vector for Huntingtin Silencing.Early lethality of shRNA-transgenic pigs due to saturation of microRNA pathways Adeno-associated virus-delivered polycistronic microRNA-clusters for knockdown of vascular endothelial growth factor in vivo.DYT1 knock-in mice are not sensitized against mitochondrial complex-II inhibition.siSPOTR: a tool for designing highly specific and potent siRNAs for human and mouse.The Drosophila ETV5 Homologue Ets96B: Molecular Link between Obesity and Bipolar Disorder.Molecular dissection of human Argonaute proteins by DNA shuffling.RNA interference-based therapy for spinocerebellar ataxia type 7 retinal degeneration.Development of gene therapy for treatment of age-related macular degeneration.Repair of rhodopsin mRNA by spliceosome-mediated RNA trans-splicing: a new approach for autosomal dominant retinitis pigmentosa.Viral delivery of shRNA to amygdala neurons leads to neurotoxicity and deficits in Pavlovian fear conditioning Aberrant Purkinje cell activity is the cause of dystonia in a shRNA-based mouse model of Rapid Onset Dystonia-Parkinsonism.The ubiquitin ligase F-box/G-domain protein 1 promotes the degradation of the disease-linked protein torsinA through the ubiquitin-proteasome pathway and macroautophagy.Therapeutic rAAVrh10 Mediated SOD1 Silencing in Adult SOD1(G93A) Mice and Nonhuman Primates.Targeted disruption of influenza A virus hemagglutinin in genetically modified mice reduces viral replication and improves disease outcome.miRNA-embedded shRNAs for Lineage-specific BCL11A Knockdown and Hemoglobin F Induction Recent advances in RNA interference therapeutics for CNS diseases.Studies of efficacy and liver toxicity related to adeno-associated virus-mediated RNA interference.Disruption of Protein Processing in the Endoplasmic Reticulum of DYT1 Knock-in Mice Implicates Novel Pathways in Dystonia Pathogenesis.Robust RNAi enhancement via human Argonaute-2 overexpression from plasmids, viral vectors and cell lines.Lineage-specific BCL11A knockdown circumvents toxicities and reverses sickle phenotype.Recombinant AAV as a platform for translating the therapeutic potential of RNA interference.Prospect of induced pluripotent stem cell genetic repair to cure genetic diseases.α-Synuclein elevation in human neurodegenerative diseases: experimental, pathogenetic, and therapeutic implications.Gene therapy in animal models of autosomal dominant retinitis pigmentosa Lentiviral vector-mediated RNA silencing in the central nervous system.Lentiviral vectors encoding short hairpin RNAs efficiently transduce and knockdown LINGO-1 but induce an interferon response and cytotoxicity in central nervous system neurones.RNAi therapeutics for brain cancer: current advancements in RNAi delivery strategies.Dissecting microRNA dysregulation in age-related macular degeneration: new targets for eye gene therapy.The dose can make the poison: lessons learned from adverse in vivo toxicities caused by RNAi overexpression.Caspase-3 and GFAP as early markers for apoptosis and astrogliosis in shRNA-induced hippocampal cytotoxicity.Sodium Chloride Enhances Recombinant Adeno-Associated Virus Production in a Serum-Free Suspension Manufacturing Platform Using the Herpes Simplex Virus System.Multigenic lentiviral vectors for combined and tissue-specific expression of miRNA- and protein-based antiangiogenic factors Sustained miRNA-mediated knockdown of mutant AAT with simultaneous augmentation of wild-type AAT has minimal effect on global liver miRNA profiles.shRNA-induced saturation of the microRNA pathway in the rat brain.Safe and Efficient Silencing with a Pol II, but Not a Pol lII, Promoter Expressing an Artificial miRNA Targeting Human Huntingtin.GHS-R1a signaling in the DMH and VMH contributes to food anticipatory activity.Gene suppression approaches to neurodegeneration.

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Lethal toxicity caused by expression of shRNA in the mouse striatum: implications for therapeutic design.

http://www.wikidata.org/entity/Q41983597

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2011 nî lūn-bûn

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J N Martin

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M E Ehrlich

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N Wolken

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P Gonzalez-Alegre

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T Brown

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P2860

Effect of torsinA on membrane proteins reveals a loss of function and a dominant-negative phenotype of the dystonia-associated DeltaE-torsinA mutant

Loss of the dystonia-associated protein torsinA selectively disrupts the neuronal nuclear envelope

Argonaute proteins are key determinants of RNAi efficacy, toxicity, and persistence in the adult mouse liver

Cellular toxicity following application of adeno-associated viral vector-mediated RNA interference in the nervous system

Artificial microRNAs as siRNA shuttles: improved safety as compared to shRNAs in vitro and in vivo.

MicroRNA-21 is upregulated during the proliferative phase of liver regeneration, targets Pellino-1, and inhibits NF-kappaB signaling.

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

The early-onset torsion dystonia gene (DYT1) encodes an ATP-binding protein.

Fatality in mice due to oversaturation of cellular microRNA/short hairpin RNA pathways.

DNA constructs designed to produce short hairpin, interfering RNAs in transgenic mice sometimes show early lethality and an interferon response.

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10.1038/GT.2011.10

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7

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18

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William T Dauer

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corpus striatum

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3131434

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