ArticleNeurobiology of disease2014
DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 93 citations in OpenAlex.
- Article
- Combinatorial chemistry identifies additional compounds that selectively inhibit DLK-dependent retrograde signaling while minimally affecting other axonal roles of DLK.Scientific reports · 2026Article
- MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury.Cell death discovery · 2025Article
- Deletion of murineScience translational medicine · 2025Article
- Evaluating the Optic Nerve Crush Model to Understand the Function of Microglia in Glaucoma Neuroprotection.Investigative ophthalmology & visual science · 2025Article
- Inhibiting acute, axonal DLK palmitoylation is neuroprotective and avoids deleterious effects of cell-wide DLK inhibition.Nature communications · 2025Article
- Functional optic tract rewiring via subtype- and target-specific axonal regeneration and presynaptic activity enhancement.Nature communications · 2025Article
- Preservation of Murine Whole Eyes With Supplemented UW Cold Storage Solution: Anatomical Considerations.Translational vision science & technology · 2024Article
- Microtubules, Membranes, and Movement: New Roles for Stathmin-2 in Axon Integrity.Journal of neuroscience research · 2024Review
- Recruitment, regulation, and release: Control of signaling enzyme localization and function by reversible S-acylation.The Journal of biological chemistry · 2024Review
- DLK signaling in axotomized neurons triggers complement activation and loss of upstream synapses.Cell reports · 2024Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023Review
- Protective effects of NAMPT or MAPK inhibitors and NaR on Wallerian degeneration of mammalian axons.Neurobiology of disease · 2022Article
- BclXCell death discovery · 2022Article
- Stress-induced vesicular assemblies of dual leucine zipper kinase are signaling hubs involved in kinase activation and neurodegeneration.The EMBO journal · 2022Article
- Vascular derived endothelin receptor A controls endothelin-induced retinal ganglion cell death.Cell death discovery · 2022Article
- Palmitoylation couples the kinases DLK and JNK3 to facilitate prodegenerative axon-to-soma signaling.Science signaling · 2022Article
- Bax Contributes to Retinal Ganglion Cell Dendritic Degeneration During Glaucoma.Molecular neurobiology · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Injury to retinal ganglion cell (RGC) axons triggers rapid activation of Jun N-terminal kinase (JNK) signaling, a major prodeath pathway in injured RGCs. Of the multiple kinases that can activate JNK, dual leucine kinase (Dlk) is known to regulate both apoptosis and Wallerian degeneration triggered by axonal insult. Here we tested the importance of Dlk in regulating somal and axonal degeneration of RGCs following axonal injury. Removal of DLK from the developing optic cup did not grossly affect developmental RGC death or inner plexiform layer organization. In the adult, Dlk deficiency significantly delayed axonal-injury induced RGC death. The activation of JUN was also attenuated in Dlk deficient retinas. Dlk deficiency attenuated the activation of the somal pool of JNK but did not prevent activation of the axonal pool of JNK after axonal injury, indicating that JNK activation in different cellular compartments of an RGC following axonal injury is regulated by distinct upstream kinases. In contrast to its robust influence on somal degeneration, Dlk deficiency did not alter RGC axonal degeneration after axonal injury as assessed using physiological readouts of optic nerve function.
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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.