ArticleCell death & disease2017
Damage-induced neuronal endopeptidase (DINE) enhances axonal regeneration potential of retinal ganglion cells after optic nerve injury.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Unraveling the Morphological and Functional Maturation Mechanisms Underlying Human Neural Development Using iPSCs-Derived Neuronal Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatiotemporal Immune Dynamics in Experimental Retinal Ganglion Cell Injury Models.Immunity, inflammation and disease · 2025Review
- Endothelin-Converting Enzyme-Like 1 Regulated by LIF Contributes to Chronic Constriction Injury-Induced Neuropathic Pain in Mice.CNS neuroscience & therapeutics · 2025Article
- Zebrafish optic nerve injury results in systemic retinal ganglion cell dedifferentiation.PLoS genetics · 2025Article
- SIRT1-based therapy targets a gene program involved in mitochondrial turnover in a model of retinal neurodegeneration.Scientific reports · 2025Article
- Cellular evolution of the hypothalamic preoptic area of behaviorally divergent deer mice.eLife · 2025Article
- Functional optic tract rewiring via subtype- and target-specific axonal regeneration and presynaptic activity enhancement.Nature communications · 2025Article
- Brachial Plexus Root Avulsion Injury-Induced Endothelin-Converting Enzyme-Like 1 Overexpression Is Associated with Injured Motor Neurons Survival.Molecular neurobiology · 2024Article
- Repeated cold stress, an animal model for fibromyalgia, elicits proprioceptor-induced chronic pain with microglial activation in mice.Journal of neuroinflammation · 2024Article
- Article
- Traumatic optic neuropathy: a review of current studies.Neurosurgical review · 2022Review
- ATF3 promotes ferroptosis in sorafenib-induced cardiotoxicity by suppressing Slc7a11 expression.Frontiers in pharmacology · 2022Article
- Differential Retinal Ganglion Cell Vulnerability, A Critical Clue for the Identification of Neuroprotective Genes in Glaucoma.Frontiers in ophthalmology · 2022Review
- Identification of long noncoding RNAs in injury-resilient and injury-susceptible mouse retinal ganglion cells.BMC genomics · 2021Article
- Commonalities of optic nerve injury and glaucoma-induced neurodegeneration: Insights from transcriptome-wide studies.Experimental eye research · 2021Review
- ATF3 Suppresses Growth and Metastasis of Clear Cell Renal Cell Carcinoma by Deactivating EGFR/AKT/GSK3β/β-Catenin Signaling Pathway.Frontiers in cell and developmental biology · 2021Article
- Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush.Investigative ophthalmology & visual science · 2020Article
- Neuro-protection and neuro-regeneration of the optic nerve: recent advances and future directions.Current opinion in neurology · 2020Review
- New Insights of a Neuronal Peptidase DINE/ECEL1: Nerve Development, Nerve Regeneration and Neurogenic Pathogenesis.Neurochemical research · 2019Review
- ATF3 inhibits the tumorigenesis and progression of hepatocellular carcinoma cells via upregulation of CYR61 expression.Journal of experimental & clinical cancer research : CR · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage-induced neuronal endopeptidase (DINE)/endothelin-converting enzyme-like 1 (ECEL1) is a membrane-bound metalloprotease that we identified as a nerve regeneration-associated molecule. The expression of DINE is upregulated in response to nerve injury in both the peripheral and central nervous systems, while its transcription is regulated by the activating transcription factor 3 (ATF3), a potent hub-transcription factor for nerve regeneration. Despite its unique hallmark of injury-induced upregulation, the physiological relevance of DINE in injured neurons has been unclear. In this study, we have demonstrated that the expression of DINE is upregulated in injured retinal ganglion cells (RGCs) in a coordinated manner with that of ATF3 after optic nerve injury, whereas DINE and ATF3 are not observed in any normal retinal cells. Recently, we have generated a mature DINE-deficient (KO
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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.