ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Collapsin response mediator protein 4a (CRMP4a) is upregulated in motoneurons of mutant SOD1 mice and can trigger motoneuron axonal degeneration and cell death.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 60 citations in OpenAlex.
- Gene therapy breakthroughs in ALS: a beacon of hope for 20% of ALS patients.Translational neurodegeneration · 2025Review
- Using ALS to understand profilin 1's diverse roles in cellular physiology.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024Article
- Article
- A CRMP4-dependent retrograde axon-to-soma death signal in amyotrophic lateral sclerosis.The EMBO journal · 2021Article
- Review
- Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021Review
- Intra-Amniotic Delivery of CRMP4 siRNA Improves Mesenchymal Stem Cell Therapy in a Rat Spina Bifida Model.Molecular therapy. Nucleic acids · 2020Article
- Dysregulation of CRMP2 Post-Translational Modifications Drive Its Pathological Functions.Molecular neurobiology · 2019Review
- Proteomics Approaches for Biomarker and Drug Target Discovery in ALS and FTD.Frontiers in neuroscience · 2019Review
- Multi-Study Proteomic and Bioinformatic Identification of Molecular Overlap between Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA).Brain sciences · 2018Article
- CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury.Molecular neurobiology · 2017Review
- Article
- Deletion of collapsin response mediator protein 4 results in abnormal layer thickness and elongation of mitral cell apical dendrites in the neonatal olfactory bulb.Journal of anatomy · 2016Article
- Degeneration of proprioceptive sensory nerve endings in mice harboring amyotrophic lateral sclerosis-causing mutations.The Journal of comparative neurology · 2015Article
- Crmp4 deletion promotes recovery from spinal cord injury by neuroprotection and limited scar formation.Scientific reports · 2015Article
- CRMP4 and CRMP2 Interact to Coordinate Cytoskeleton Dynamics, Regulating Growth Cone Development and Axon Elongation.Neural plasticity · 2015Article
- Semaphorin 3A signaling through neuropilin-1 is an early trigger for distal axonopathy in the SOD1G93A mouse model of amyotrophic lateral sclerosis.Journal of neuropathology and experimental neurology · 2014Article
- Advances in cellular models to explore the pathophysiology of amyotrophic lateral sclerosis.Molecular neurobiology · 2014Review
- The emerging role of class-3 semaphorins and their neuropilin receptors in oncology.OncoTargets and therapy · 2014Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Embryonic motoneurons from mutant SOD1 (mSOD1) mouse models of amyotrophic lateral sclerosis (ALS), but not wild-type motoneurons, can be triggered to die by exposure to nitric oxide (NO), leading to activation of a motoneuron-specific signaling pathway downstream of the death receptor Fas/CD95. To identify effectors of mSOD1-dependent cell death, we performed a proteomic analysis. Treatment of cultured mSOD1 motoneurons with NO led to a 2.5-fold increase in levels of collapsin response mediator protein 4a (CRMP4a). In vivo, the percentage of mSOD1 lumbar motoneurons expressing CRMP4 in mSOD1 mice increased progressively from presymptomatic to early-onset stages, reaching a maximum of 25%. Forced adeno-associated virus (AAV)-mediated expression of CRMP4a in wild-type motoneurons in vitro triggered a process of axonal degeneration and cell death affecting 60% of motoneurons, whereas silencing of CRMP4a in mSOD1 motoneurons protected them from NO-induced death. In vivo, AAV-mediated overexpression of CRMP4a but not CRMP2 led to the death of 30% of the lumbar motoneurons and an 18% increase in denervation of neuromuscular junctions in the gastrocnemius muscle. Our data identify CRMP4a as a potential early effector in the neurodegenerative process in ALS.
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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.