ArticleJournal of biomedicine & biotechnology2008
Characterization of phototransduction gene knockouts revealed important signaling networks in the light-induced retinal degeneration.
Article in Journal of biomedicine & biotechnology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Inhibition of polyisoprenylated methylated protein methyl esterase by synthetic musks induces cell degeneration.Environmental toxicology · 2014Article
- Gene expression profiling of light-induced retinal degeneration in phototransduction gene knockout mice.Experimental & molecular medicine · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Understanding the molecular pathways mediating neuronal function in retinas can be greatly facilitated by the identification of genes regulated in the retinas of different mutants under various light conditions. We attempted to conduct a gene chip analysis study on the genes regulated during rhodopsin kinase (Rhok-/-) and arrestin (Sag-/-) knockout and double knockouts in mice retina. Hence, mice were exposed to constant illumination of 450 lux or 6,000 lux on dilated pupils for indicated periods. The retinas were removed after the exposure and processed for microarray analysis. Double knockout was associated with immense changes in gene expression regulating a number of apoptosis inducing transcription factors. Subsequently, network analysis revealed that during early exposure the transcription factors, p53, c-MYC, c-FOS, JUN, and, in late phase, NFkappaB, appeared to be essential for the initiation of light-induced retinal rod loss, and some other classical pro- and antipoptotic genes appeared to be significantly important as well.
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