ArticleCell death and differentiation2015
REDD2-mediated inhibition of mTOR promotes dendrite retraction induced by axonal injury.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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
39 citing papers in PubMed, 60 citations in OpenAlex.
- Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration in adult zebrafish.iScience · 2026Article
- GSK3β promotes p53/Nrf2-dependent expression of the stress response protein REDD2 in retinal Müller glia exposed to hyperlipidemic conditions.Experimental eye research · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Identifying transcriptomic signatures that mediate the causal effect of genotype on Alzheimer's disease.Frontiers in neuroscience · 2026Article
- Rapid proteasomal degradation of the stress response protein REDD2 is mediated by the E3 ligase HUWE1.Biochemical and biophysical research communications · 2025Article
- Retinal Ganglion Cell Subtypes and Their Vulnerability in Glaucoma.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Membrane-anchored intracellular insulin receptor or insulin-like growth factor-1 receptor elicits ligand-independent downstream signaling.Biochemistry and biophysics reports · 2024Article
- Insulin restores retinal ganglion cell functional connectivity and promotes visual recovery in glaucoma.Science advances · 2024Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- Structure, Function, and Molecular Landscapes of the Aging Retina.Annual review of vision science · 2023Review
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Analysis of Axonal Regrowth and Dendritic Remodeling After Optic Nerve Crush in Adult Zebrafish.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Development of a machine learning framework for radiation biomarker discovery and absorbed dose prediction.Frontiers in oncology · 2023Article
- Article
- Pericyte dysfunction and loss of interpericyte tunneling nanotubes promote neurovascular deficits in glaucoma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- AMPK hyperactivation promotes dendrite retraction, synaptic loss, and neuronal dysfunction in glaucoma.Molecular neurodegeneration · 2021Article
- Retinal Ganglion Cell Transplantation: Approaches for Overcoming Challenges to Functional Integration.Cells · 2021Review
- A Fair Assessment of Evaluation Tools for the Murine Microbead Occlusion Model of Glaucoma.International journal of molecular sciences · 2021Article
- Putative dendritic correlates of chronic traumatic encephalopathy: A preliminary quantitative Golgi exploration.The Journal of comparative neurology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Dendritic defects occur in neurodegenerative diseases accompanied by axonopathy, yet the mechanisms that regulate these pathologic changes are poorly understood. Using Thy1-YFPH mice subjected to optic nerve axotomy, we demonstrate early retraction of retinal ganglion cell (RGC) dendrites and selective loss of mammalian target of rapamycin (mTOR) activity, which precede soma loss. Axonal injury triggered rapid upregulation of the stress-induced protein REDD2 (regulated in development and DNA damage response 2), a potent inhibitor of mTOR. Short interfering RNA-mediated REDD2 knockdown restored mTOR activity and rescued dendritic length, area and branch complexity in a rapamycin-dependent manner. Whole-cell recordings demonstrated that REDD2 depletion leading to mTOR activation in RGCs restored their light response properties. Lastly, we show that REDD2-dependent mTOR activity extended RGC survival following axonal damage. These results indicate that injury-induced stress leads to REDD2 upregulation, mTOR inhibition and dendrite pathology causing neuronal dysfunction and subsequent cell death.
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Registered trials
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.