ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Mutant superoxide dismutase-1-linked familial amyotrophic lateral sclerosis: molecular mechanisms of neuronal death and protection.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 197 citations in OpenAlex.
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- SOD1 gains pro-oxidant activity upon aberrant oligomerization: change in enzymatic activity by intramolecular disulfide bond cleavage.Scientific reports · 2022Article
- Pro-Oxidant Activity of an ALS-Linked SOD1 Mutant in Zn-Deficient Form.Molecules (Basel, Switzerland) · 2020Article
- Is Modulation of Oxidative Stress an Answer? The State of the Art of Redox Therapeutic Actions in Neurodegenerative Diseases.Oxidative medicine and cellular longevity · 2016Review
- Systemic inflammation and the brain: novel roles of genetic, molecular, and environmental cues as drivers of neurodegeneration.Frontiers in cellular neuroscience · 2015Review
- New insight into neurodegeneration: the role of proteomics.Molecular neurobiology · 2014Review
- A role for copper in the toxicity of zinc-deficient superoxide dismutase to motor neurons in amyotrophic lateral sclerosis.Antioxidants & redox signaling · 2009Review
- The mitochondrial death pathway: a promising therapeutic target in diseases.Journal of cellular and molecular medicine · 2009Review
- Superoxide dismutases: a physiopharmacological update.Journal of physiology and biochemistry · 2009Review
- Novel toxicity of the unedited GluR2 AMPA receptor subunit dependent on surface trafficking and increased Ca2+-permeability.Molecular and cellular neurosciences · 2007Article
- Direct imaging shows that insulin granule exocytosis occurs by complete vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Glutamate carboxypeptidase II inhibition protects motor neurons from death in familial amyotrophic lateral sclerosis models.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Misfolded CuZnSOD and amyotrophic lateral sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2003Review
- Recent advances in amyotrophic lateral sclerosis research.Current neurology and neuroscience reports · 2003Review
- Programmed cell death in amyotrophic lateral sclerosis.The Journal of clinical investigation · 2003Review
- The role of iron and copper in the aetiology of neurodegenerative disorders: therapeutic implications.CNS drugs · 2002Review
- Bcl-2 expression by retrograde transport of adenoviral vectors with Cre-loxP recombination system in motor neurons of mutant SOD1 transgenic mice.Gene therapy · 2001Article
- Prion infection impairs the cellular response to oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in human Cu/Zn superoxide dismutase-1 (SOD) cause approximately 20% of cases of familial amyotrophic lateral sclerosis (FALS). We investigated the mechanism of mutant SOD-induced neuronal degeneration by expressing wild-type and mutant SODs in neuronal cells by means of infection with replication-deficient recombinant adenoviruses. Expression of two FALS-related mutant SODs (A4V and V148G) caused death of differentiated PC12 cells, superior cervical ganglion neurons, and hippocampal pyramidal neurons. Cell death included many features typical of apoptosis. Death could be prevented by copper (Cu2+) chelators, Bcl-2, glutathione, vitamin E, and inhibitors of caspases. Mutant SOD-expressing PC12 cells had higher rates of superoxide (O2-) production under a variety of conditions. The results support the hypothesis that mutant SOD induced-neurodegeneration is associated with disturbances of neuronal free radical homeostasis.
Indexed as
Identifiers
9348345PMC6573090W2123413118What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.