ArticleGenesis (New York, N.Y. : 2000)2009
A new mouse model for temporal- and tissue-specific control of extracellular superoxide dismutase.
Article in Genesis (New York, N.Y. : 2000), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Forebrain Shh overexpression improves cognitive function and locomotor hyperactivity in an aneuploid mouse model of Down syndrome and its euploid littermates.Acta neuropathologica communications · 2021Article
- Redox regulation of T-cell function: from molecular mechanisms to significance in human health and disease.Antioxidants & redox signaling · 2013Review
- Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Oxidative stress and adult neurogenesis--effects of radiation and superoxide dismutase deficiency.Seminars in cell & developmental biology · 2012Review
- Irradiation enhances hippocampus-dependent cognition in mice deficient in extracellular superoxide dismutase.Hippocampus · 2011Article
- Enhanced expression of mitochondrial superoxide dismutase leads to prolonged in vivo cell cycle progression and up-regulation of mitochondrial thioredoxin.Free radical biology & medicine · 2010Article
- Radiation-induced reductions in neurogenesis are ameliorated in mice deficient in CuZnSOD or MnSOD.Free radical biology & medicine · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The extracellular isoform of superoxide dismutase (EC-SOD, Sod3) plays a protective role against various diseases and injuries mediated by oxidative stress. To investigate the pathophysiological roles of EC-SOD, we generated tetracycline-inducible Sod3 transgenic mice and directed the tissue-specific expression of transgenes by crossing Sod3 transgenic mice with tissue-specific transactivator transgenics. Double transgenic mice with liver-specific expression of Sod3 showed increased EC-SOD levels predominantly in the plasma as the circulating form, whereas double transgenic mice with neuronal-specific expression expressed higher levels of EC-SOD in hippocampus and cortex with intact EC-SOD as the dominant form. EC-SOD protein levels also correlated well with increased SOD activities in double transgenic mice. In addition to enabling tissue-specific expression, the transgene expression can be quickly turned on and off by doxycycline supplementation in the mouse chow. This mouse model, thus, provides the flexibility for on-off control of transgene expression in multiple target tissues.
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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.