ArticleProceedings of the National Academy of Sciences of the United States of America2009
Induction of corticospinal regeneration by lentiviral trkB-induced Erk activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 138 citations in OpenAlex.
- Beyond Scar Removal: Reprogramming the Glial Scar for Neural Repair.International journal of molecular sciences · 2026Review
- Molecular mechanism of ischemic postconditioning in promoting diabetic ischemic brain injury repair via the microRNA-34a-BDNF-SIX3 signaling axis.Animal models and experimental medicine · 2026Article
- Hyperactive delta isoform of PI3 kinase enables long-distance regeneration of adult rat corticospinal tract.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.Molecular neurobiology · 2025Review
- Neuronal maturation and axon regeneration: unfixing circuitry to enable repair.Nature reviews. Neuroscience · 2024Review
- Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis.Aging and disease · 2024Review
- Interleukin-4 protects retinal ganglion cells and promotes axon regeneration.Cell communication and signaling : CCS · 2024Article
- A bibliometric analysis of the top 100 most cited articles on corticospinal tract regeneration from 2004 to 2024.Frontiers in neuroscience · 2024Review
- Regulation of axonal regeneration after mammalian spinal cord injury.Nature reviews. Molecular cell biology · 2023Review
- Gliotransmission and adenosine signaling promote axon regeneration.Developmental cell · 2023Article
- Liver Kinase B1 Functions as a Regulator for Neural Development and a Therapeutic Target for Neural Repair.Cells · 2022Review
- Article
- Promoting axon regeneration in the central nervous system by increasing PI3-kinase signaling.Neural regeneration research · 2022Review
- Review
- Co-Delivery of Docosahexaenoic Acid and Brain-Derived Neurotropic Factor from Electrospun Aligned Core-Shell Fibrous Membranes in Treatment of Spinal Cord Injury.Pharmaceutics · 2022Article
- MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022Review
- Receptor-ligand supplementation via a self-cleaving 2A peptide-based gene therapy promotes CNS axonal transport with functional recovery.Science advances · 2021Article
- Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS.Nature communications · 2020Article
- ARF6 and Rab11 as intrinsic regulators of axon regeneration.Small GTPases · 2020Review
- PI 3-kinase delta enhances axonal PIPEMBO molecular medicine · 2020Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Several experimental manipulations of the CNS environment successfully elicit regeneration of sensory and bulbospinal motor axons but fail to elicit regeneration of corticospinal axons, suggesting that cell-intrinsic mechanisms limit the regeneration of this critical class of motor neurons. We hypothesized that enhancement of intrinsic neuronal growth mechanisms would enable adult corticospinal motor axon regeneration. Lentiviral vectors were used to overexpress the BDNF receptor trkB in layer V corticospinal motor neurons. After subcortical axotomy, trkB transduction induced corticospinal axon regeneration into subcortical lesion sites expressing BDNF. In the absence of trkB overexpression, no regeneration occurred. Selective deletion of canonical, trkB-mediated neurite outgrowth signaling by mutation of the Shc/FRS-2 activation domain prohibited Erk activation and eliminated regeneration. These findings support the hypothesis that the refractory regenerative state of adult corticospinal axons can be attributed at least in part to neuron-intrinsic mechanisms, and that activation of ERK signaling can elicit corticospinal tract regeneration.
Indexed as
Identifiers
What OpenQuestion holds
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.