ArticleScience advances2025
Transcription factor activator protein 4 (AP4)-mediated intrinsic control of axon regeneration.
Article in Science advances, 2025. 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.
- Widespread AAV-mediated CSPG digestion impairs functional recovery after cervical spinal cord injury.bioRxiv : the preprint server for biology · 2026Article
- Disproportionality Analysis of Fluoroquinolone-Associated Peripheral Neuropathy in the FAERS Database (2007-2024).Clinical and translational science · 2026Article
- From Regeneration Failure to Functional Restoration: Unlocking the Neuronal-Intrinsic Regenerative Capacity as a Therapeutic Frontier for Optic Neuropathy and Glaucoma.CNS neuroscience & therapeutics · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activator protein 4 (AP4) is a basic helix-loop-helix leucine-zipper transcription factor, a direct transcriptional target of c-Myc and a key regulator of cell growth and apoptosis, abundantly expressed in cancer cells. Here, we reveal a role for the c-Myc-AP4 axis in axon regeneration and the intrinsic growth capacity of injured neurons. Through bioinformatic and functional analyses, we demonstrated that overexpression of AP4 in mice not only accelerated in vivo axon regeneration and functional recovery after peripheral nerve injury but also promoted robust axon regeneration and neuronal survival after optic nerve injury by activating mammalian target of rapamycin activity. Neuronal-specific knockdown of AP4 abolished the regenerative phenotype induced by c-Myc overexpression and phosphatase and tensin homolog (PTEN) deletion. AP4 overexpression rendered the intrinsic growth capacity of c-Myc silencing injured retinal ganglion cells unaffected. These findings unveil a distinct aspect of the c-Myc-AP4 axis and highlight a previously unrecognized intrinsic role of AP4 in axon regeneration, with potential therapeutic implications.
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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 Socratic graph.