ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Identification of CRMP4 as a convergent regulator of axon outgrowth inhibition.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 104 citations in OpenAlex.
- Microtubules in Spinal Cord Injury: From Cytoskeletal Dysregulation to Therapeutic Regeneration.Journal of neurochemistry · 2026Review
- Research on the mechanism of CRMP4-mediated cytoskeletal actin polymerization in promoting invasive migration of stromal cells in endometriosis.Journal of translational medicine · 2026Article
- [Research advances in the inhibitory effect of chondroitin sulfate proteoglycans on axon growth after premature white matter injury and its underlying mechanisms].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- ROCK2 Downregulation in Pediatric Medulloblastoma Increases Migration and Predicts the Involvement of SHH Non-canonical Signaling.The Yale journal of biology and medicine · 2025Article
- Upregulation of dihydropyrimidinase-like 3 (DPYSL3) protein predicts poor prognosis in urothelial carcinoma.BMC cancer · 2023Article
- Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury.Neural regeneration research · 2023Review
- Article
- Beyond Neuronal Microtubule Stabilization: MAP6 and CRMPS, Two Converging Stories.Frontiers in molecular neuroscience · 2021Article
- Loss of Collapsin Response Mediator Protein 4 Attenuates 6-Hydroxydopamine-Induced Impairments in a Mouse Model of Parkinson's Disease.Neurochemical research · 2020Article
- Intra-Amniotic Delivery of CRMP4 siRNA Improves Mesenchymal Stem Cell Therapy in a Rat Spina Bifida Model.Molecular therapy. Nucleic acids · 2020Article
- Collapsin Response Mediator Proteins: Their Biological Functions and Pathophysiology in Neuronal Development and Regeneration.Frontiers in cellular neuroscience · 2020Article
- The CRISPR-Cas9 crADSL HeLa transcriptome: A first step in establishing a model for ADSL deficiency and SAICAR accumulation.Molecular genetics and metabolism reports · 2019Article
- Review
- DPYSL3 modulates mitosis, migration, and epithelial-to-mesenchymal transition in claudin-low breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Control of Growth Cone Polarity, Microtubule Accumulation, and Protrusion by UNC-6/Netrin and Its Receptors inGenetics · 2018Article
- CRMP2 and CRMP4 Are Differentially Required for Axon Guidance and Growth in Zebrafish Retinal Neurons.Neural plasticity · 2018Article
- CRMP4a suppresses cell motility by sequestering RhoA activity in prostate cancer cells.Cancer biology & therapy · 2018Article
- Human CRMP4 mutation and disrupted Crmp4 expression in mice are associated with ASD characteristics and sexual dimorphism.Scientific reports · 2017Article
- CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury.Molecular neurobiology · 2017Review
- In vitro models of axon regeneration.Experimental neurology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin-associated inhibitors (MAIs) and chondroitin sulfate proteoglycans (CSPGs) contribute to failed regeneration after neuronal injury. MAIs and CSPGs stimulate intracellular signals including the activation of RhoA and Rho kinase to block axonal extension through targeted modifications to the cytoskeleton. RhoA and ROCK are promising targets for therapeutic intervention to promote CNS repair; however, their ubiquitous expression will limit the specificity of drugs targeted to these molecules. We have identified the cytosolic phosphoprotein CRMP4b (collapsin-response mediator protein 4b) as a protein that physically and functionally interacts with RhoA to mediate neurite outgrowth inhibition. Short interfering RNA-mediated knockdown of CRMP4 promotes neurite outgrowth on myelin substrates, indicating a critical role for CRMP4 in neurite outgrowth inhibition. Disruption of CRMP4b-RhoA binding with a competitive inhibitor attenuates neurite outgrowth inhibition on myelin and aggrecan substrates. Stimulation of neuronal growth cones with Nogo leads to colocalization of CRMP4b and RhoA at discrete regions within the actin-rich central and peripheral domains of the growth cone, indicative of a potential function in cytoskeletal rearrangements during neurite outgrowth inhibition. Together, these data indicate that a RhoA-CRMP4b complex forms in response to inhibitory challenges in the growth cone environment and regulates cytoskeletal dynamics at distinct sites necessary for axon outgrowth inhibition. Competitive inhibition of CRMP4b-RhoA binding suggests a novel, highly specific therapeutic avenue for promoting regeneration after CNS injury.
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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.