ReviewDevelopmental neurobiology2014
Altered expression of atypical PKC and Ryk in the spinal cord of a mouse model of amyotrophic lateral sclerosis.
Review in Developmental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Neurodegenerative Disease: From Molecular Basis to Therapy.International journal of molecular sciences · 2024Article
- Wnt signaling pathway in spinal cord injury: from mechanisms to potential applications.Frontiers in molecular neuroscience · 2024Review
- The ε-Isozyme of Protein Kinase C (PKCε) Is Impaired in ALS Motor Cortex and Its Pulse Activation by Bryostatin-1 Produces Long Term Survival in Degenerating SOD1-G93A Motor Neuron-like Cells.International journal of molecular sciences · 2023Article
- Membrane lipid raft homeostasis is directly linked to neurodegeneration.Essays in biochemistry · 2021Review
- Putative role of natural products as Protein Kinase C modulator in different disease conditions.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2021Review
- Planar cell polarity signaling components are a direct target of β-amyloid-associated degeneration of glutamatergic synapses.Science advances · 2021Article
- Neuroprotective Effects of Testosterone in Male Wobbler Mouse, a Model of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2021Article
- Review
- New insights into Wnt signaling alterations in amyotrophic lateral sclerosis: a potential therapeutic target?Neural regeneration research · 2020Review
- The roles of atypical protein kinase Cs (aPKCs) in the nervous system: targets for neuroregeneration?Neural regeneration research · 2020Article
- Cellular and Molecular Mechanisms of Spinal Cord Vascularization.Frontiers in physiology · 2020Review
- Wnt Signaling Alterations in the Human Spinal Cord of Amyotrophic Lateral Sclerosis Cases: Spotlight on Fz2 and Wnt5a.Molecular neurobiology · 2019Article
- aPKC in neuronal differentiation, maturation and function.Neuronal signaling · 2019Review
- Distinct Roles of Wnt/Mediators of inflammation · 2017Review
- Review
- Article
- Emerging Role and Therapeutic Implication of Wnt Signaling Pathways in Autoimmune Diseases.Journal of immunology research · 2016Review
- Wnt and extraocular muscle sparing in amyotrophic lateral sclerosis.Investigative ophthalmology & visual science · 2014Article
- Axon guidance and injury-lessons from Wnts and Wnt signaling.Current opinion in neurobiology · 2014Review
- Early gene expression changes in skeletal muscle from SOD1(G93A) amyotrophic lateral sclerosis animal model.Cellular and molecular neurobiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive paralysis due to the selective death of motor neurons of unknown causes. Increasing evidence indicates that Wnt signaling is altered in ALS. In this study, we focused on two non-canonical Wnt signaling components, atypical PKC (aPKC) and a Wnt receptor, Ryk, in a mouse model of ALS, SOD1 (G93A). aPKC mediates Wnt signaling to regulate growth cone guidance, axon differentiation and cell survival. Ryk is a Wnt repulsive receptor that regulates axon guidance and inhibits regeneration after spinal cord injury. aPKC expression was increased in motor neurons of the lumbar spinal cord in SOD1 (G93A) mice at both early and late stages. Interestingly, aPKC was co-localized with SOD1 in motor neuron cell bodies and extracellular aggregates, and aPKC-containing extracellular aggregates increased with disease progression. Biochemical fractionation showed that aPKC protein level was increased in the detergent-insoluble protein fraction in SOD1 (G93A) mice at late stage but decreased in the detergent-soluble fraction at symptomatic stage. These results suggest that aPKC may be sequestered in SOD1 aggregates, impairing its ability to protect motor neurons from death. Ryk expression was also increased in the motor neurons and the white matter in the ventral lumbar spinal cord of mutant SOD1 mice with a peak at early stage. These observations indicate that Wnt/aPKC and Wnt/Ryk signaling are altered in SOD1 (G93A) mice, suggesting that changed Wnt signaling may contribute to neurodegeneration in ALS.
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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 OpenQuestion graph.