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- W2005089141 abstract "In rod photoreceptors, signaling persists as long as rhodopsin remains catalytically active. Phosphorylation by rhodopsin kinase followed by arrestin-1 binding completely deactivates rhodopsin. Timely termination prevents excessive signaling and ensures rapid recovery. Mouse rods express arrestin-1 and rhodopsin at ∼0.8:1 ratio, making arrestin-1 the second most abundant protein in the rod. The biological significance of wild type arrestin-1 expression level remains unclear. Here we investigated the effects of varying arrestin-1 expression on its intracellular distribution in dark-adapted photoreceptors, rod functional performance, recovery kinetics, and morphology. We found that rod outer segments isolated from dark-adapted animals expressing arrestin-1 at wild type or higher level contain much greater fraction of arrestin-1 than previously estimated, 15–25% of the total. The fraction of arrestin-1 residing in the outer segments (OS) in animals with low expression (4–12% of wild type) is much lower, 5–7% of the total. Only 4% of wild type arrestin-1 level in the outer segments was sufficient to maintain near-normal retinal morphology, whereas rapid recovery required at least ∼12%. Supra-physiological arrestin-1 expression improved light sensitivity and facilitated photoresponse recovery, but was detrimental for photoreceptor health, particularly in the peripheral retina. Thus, physiological level of arrestin-1 expression in rods reflects the balance between short-term functional performance of photoreceptors and their long-term health." @default.
- W2005089141 created "2016-06-24" @default.
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- W2005089141 date "2011-02-01" @default.
- W2005089141 modified "2023-10-07" @default.
- W2005089141 title "Arrestin-1 expression level in rods: balancing functional performance and photoreceptor health" @default.
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- W2005089141 doi "https://doi.org/10.1016/j.neuroscience.2010.11.009" @default.
- W2005089141 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3020241" @default.
- W2005089141 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21075174" @default.
- W2005089141 hasPublicationYear "2011" @default.
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