ArticleJournal of molecular neuroscience : MN2015
Regulation of rod photoreceptor differentiation by STAT3 is controlled by a tyrosine phosphatase.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Glia Regulate the Timing of Photoreceptor Differentiation in the Drosophila Visual System.Glia · 2026Article
- Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis.Aging and disease · 2024Review
- Somatostatin signalling promotes the differentiation of rod photoreceptors in human pluripotent stem cell-derived retinal organoid.Cell proliferation · 2022Article
- Investigation of Visual System Involvement in Spinocerebellar Ataxia Type 14.Cerebellum (London, England) · 2020Article
- Loss of Shp2 Rescues BDNF/TrkB Signaling and Contributes to Improved Retinal Ganglion Cell Neuroprotection.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- A comparative analysis of rod bipolar cell transcriptomes identifies novel genes implicated in night vision.Scientific reports · 2018Article
- The 3-Phosphoinositide-Dependent Protein Kinase 1 Inhibits Rod Photoreceptor Development.Frontiers in cell and developmental biology · 2018Article
- Glaucoma Pathogenesis and Neurotrophins: Focus on the Molecular and Genetic Basis for Therapeutic Prospects.Current neuropharmacology · 2018Review
- Regulation of Brain-Derived Neurotrophic Factor and Growth Factor Signaling Pathways by Tyrosine Phosphatase Shp2 in the Retina: A Brief Review.Frontiers in cellular neuroscience · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Signal pathways that reduce the levels of tyrosine-phosphorylated STAT3 (pSTAT3) allow late retinal progenitors to exit the cell cycle and enter a terminal differentiation pathway into rod photoreceptors. In the mouse retina, we previously identified PKC-β1 and PKC-γ isoforms as essential components of a key signal pathway and IGF-1 as a major extrinsic factor regulating rod formation. In this manuscript, we demonstrate that PKC decreases phosphotyrosine but not phosphoserine on STAT3 in neonatal mouse retinas. Neither IGF-1 nor PMA induced a significant change in the levels of STAT3 or in the levels of the key proteins regulating STAT3 degradation, SOCS3, and PIAS3. Treatment of neonatal mouse retinal explants with sodium orthovanadate inhibited the PKC-mediated reduction in pSTAT3, indicating a role for a phosphatase. Addition of the PTEN inhibitor bpV(phen) to explant cultures treated with IGF-1 or PMA had no effect on the reduction in pSTAT3 levels, but the effect of both IGF-1 and PMA was blocked by a concentration of the inhibitor NSC87877 that is selective for the phosphatases Shp1 and Shp2. Inhibition of Shp1/2 phosphatases was also sufficient to abolish the IGF1-mediated induction of rod photoreceptor differentiation in the retina explant cultures. We conclude that one or both of these phosphatases are key components regulating the formation of rod photoreceptors in mouse retina.
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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.