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- W55009720 endingPage "116" @default.
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- W55009720 abstract "The retinal rod cell is an exquisitely sensitive single-photon detector that primarily functions in dim light (e.g., moonlight). However, rod cells must routinely survive light intensities more than a billion times greater (e.g., bright daylight). One serious challenge to rod cell survival in daylight is the massive amount of all-trans-retinal that is released by Meta II, the light-activated form of the photoreceptor rhodopsin. All-trans-retinal is toxic, and its condensation products have been implicated in disease. Our recent work has developed the concept that rod arrestin (arrestin-1), which terminates Meta II signaling, has an additional role in protecting rod cells from the consequences of bright light by limiting free all-trans-retinal. In this chapter we will elaborate upon the molecular mechanisms by which arrestin-1 serves as both a single-photon response quencher as well as an instrument of rod cell survival in bright light. This discussion will take place within the framework of three distinct functional modules of vision: signal transduction, the retinoid cycle, and protein translocation." @default.
- W55009720 created "2016-06-24" @default.
- W55009720 creator A5000618696 @default.
- W55009720 creator A5021314496 @default.
- W55009720 creator A5064368106 @default.
- W55009720 date "2013-11-05" @default.
- W55009720 modified "2023-10-04" @default.
- W55009720 title "Not Just Signal Shutoff: The Protective Role of Arrestin-1 in Rod Cells" @default.
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- W55009720 doi "https://doi.org/10.1007/978-3-642-41199-1_5" @default.
- W55009720 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24292826" @default.
- W55009720 hasPublicationYear "2013" @default.
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