Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

An RNAi strategy for treatment of amyotrophic lateral sclerosis caused by mutant Cu,Zn superoxide dismutase.

Journal of neurochemistry - 1 Jan 2005

Xia Xu Gang, Zhou Hongxia, Zhou Sili, Yu Yingping, Wu Rui, Xu Zuoshang

Abstract excerpt

Amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) is a neurodegenerative disease characterized by motor neuron degeneration, paralysis and death. One cause of this disease is mutations in the Cu,Zn superoxide dismutase (SOD1) gene. As mutant SOD1 acquires a toxic property that kills motor neurons, by reducing the mutant protein the disease progression may be slowed or prevented. While mutant SOD1 is...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis
Share to Gene Transfer Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genetic Therapy

Share to Kidney

Share to RNA Interference

Share to RNA, Small Interfering

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 15663483
DOI: 10.1111/j.1471-4159.2004.02860.x

Genes

SOD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An RNAi strategy for treatment of amyotrophic lateral sclerosis caused by mutant Cu,Zn superoxide dismutase.PMID 15663483Read ↗

Selective silencing by RNAi of a dominant allele that causes amyotrophic lateral sclerosis.Semantic proximity Read ↗

Therapeutic gene silencing delivered by a chemically modified small interfering RNA against mutant SOD1 slows amyotrophic lateral sclerosis progression.Semantic proximity Read ↗

RNA interference and amyotrophic lateral sclerosis.Semantic proximity Read ↗

Silence superoxide dismutase 1 (SOD1): a promising therapeutic target for amyotrophic lateral sclerosis (ALS).Semantic proximity Read ↗

Silencing strategies for therapy of SOD1-mediated ALS.Semantic proximity Read ↗

Transgenic small interfering RNA halts amyotrophic lateral sclerosis in a mouse model.Semantic proximity Read ↗

Silencing mutant SOD1 using RNAi protects against neurodegeneration and extends survival in an ALS model.Semantic proximity Read ↗

Allele-specific RNAi selectively silences mutant SOD1 and achieves significant therapeutic benefit in vivo.Semantic proximity Read ↗

Current developments in gene therapy for amyotrophic lateral sclerosisSemantic proximity Read ↗

RNA interference-mediated silencing of mutant superoxide dismutase rescues cyclosporin A-induced death in cultured neuroblastoma cellsSemantic proximity Read ↗

In vivo application of an RNAi strategy for the selective suppression of a mutant allele.Semantic proximity Read ↗

Copper Homeostasis as a Therapeutic Target in Amyotrophic Lateral Sclerosis with SOD1 Mutations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.