ArticleAdvances in experimental medicine and biology2014
Photoreceptor pathology in the X-linked retinoschisis (XLRS) mouse results in delayed rod maturation and impaired light driven transducin translocation.
Article in Advances in experimental medicine and biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Investigating the Role of Zebrafish Retinoschisin Homologs Rs1a and Rs1b During Retinal Development.Developmental neurobiology · 2026Article
- Morphological and Molecular Defects in Human Three-Dimensional Retinal Organoid Model of X-Linked Juvenile Retinoschisis.Stem cell reports · 2019Article
- Translational Retinal Research and Therapies.Translational vision science & technology · 2018Article
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4 authors at 2 institutions in 2 countries.
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Abstract
Light-activated movement of transducin-α (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gαt1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3-10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gαt1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.
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