Lentiviral-mediated silencing of SOD1 through RNA interference retards disease onset and progression in a mouse model of ALS. (Q48146867)

9 February 2018

title

Lentiviral-mediated silencing of SOD1 through RNA interference retards disease onset and progression in a mouse model of ALS. (English)

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9 February 2018

amyotrophic lateral sclerosis

main subject

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Christopher E. Henderson

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object named as

Christopher E Henderson

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9 February 2018

author name string

Cédric Raoul

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9 February 2018

Toufik Abbas-Terki

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9 February 2018

Jean-Charles Bensadoun

3

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Sandrine Guillot

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9 February 2018

Georg Haase

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Jolanta Szulc

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9 February 2018

Patrick Aebischer

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language of work or name

English

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publication date

13 March 2005

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9 February 2018

published in

Nature Medicine

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volume

11

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issue

4

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9 February 2018

page(s)

423-428

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9 February 2018

https://scigraph.springernature.com/pub.10.1038/nm1207

exact match

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cites work

Unraveling the mechanisms involved in motor neuron degeneration in ALS

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Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS).

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Of mice, men and motor neurons

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Killing the messenger: short RNAs that silence gene expression

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Lentiviral-mediated RNA interference

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Selective silencing by RNAi of a dominant allele that causes amyotrophic lateral sclerosis

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Functional anatomy of siRNAs for mediating efficient RNAi in Drosophila melanogaster embryo lysate

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Motoneuron death triggered by a specific pathway downstream of Fas. potentiation by ALS-linked SOD1 mutations.

21 January 2018

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Wild-Type Nonneuronal Cells Extend Survival of SOD1 Mutant Motor Neurons in ALS Mice

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Local GDNF expression mediated by lentiviral vector protects facial nerve motoneurons but not spinal motoneurons in SOD1(G93A) transgenic mice

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Increased motoneuron survival and improved neuromuscular function in transgenic ALS mice after intraspinal injection of an adeno-associated virus encoding Bcl-2.

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VEGF delivery with retrogradely transported lentivector prolongs survival in a mouse ALS model

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Copper chaperone for superoxide dismutase is essential to activate mammalian Cu/Zn superoxide dismutase

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Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury

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Increased apoptosis and early embryonic lethality in mice nullizygous for the Huntington's disease gene homologue

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Analysis of gene function in somatic mammalian cells using small interfering RNAs

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Functional siRNAs and miRNAs Exhibit Strand Bias

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Self-inactivating lentiviral vectors with enhanced transgene expression as potential gene transfer system in Parkinson's disease

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Rats expressing human cytosolic copper-zinc superoxide dismutase transgenes with amyotrophic lateral sclerosis: associated mutations develop motor neuron disease

21 January 2018

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7 January 2021

Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

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7 January 2021

Restricted expression of G86R Cu/Zn superoxide dismutase in astrocytes results in astrocytosis but does not cause motoneuron degeneration

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Characterization of progressive motor deficits in mice transgenic for the human Huntington's disease mutation.

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Accumulation of SOD1 mutants in postnatal motoneurons does not cause motoneuron pathology or motoneuron disease

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Recessive amyotrophic lateral sclerosis families with the D90A SOD1 mutation share a common founder: evidence for a linked protective factor

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A third-generation lentivirus vector with a conditional packaging system

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Identifiers

DOI

10.1038/NM1207

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9 February 2018

PubMed ID

15768028

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9 February 2018