ArticleNeural regeneration research2018
The protocadherin alpha cluster is required for axon extension and myelination in the developing central nervous system.
Article in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Ternary Neurexin-T178-PTPR complexes represent a pre-synaptic core-module of neuronal synapse organization.Nature communications · 2026Article
- Characterization of lncRNA and mRNA profiles in the process of repairing peripheral nerve defects with cell-matrixed nerve grafts.BMC genomics · 2024Article
- Schizophrenia Genomics: Convergence on Synaptic Development, Adult Synaptic Plasticity, or Both?Biological psychiatry · 2022Review
- Review
- Clustered Protocadherins Emerge as Novel Susceptibility Loci for Mental Disorders.Frontiers in neuroscience · 2020Review
- Selection in Australian Thoroughbred horses acts on a locus associated with early two-year old speed.PloS one · 2020Article
- Protocadherins at the Crossroad of Signaling Pathways.Frontiers in molecular neuroscience · 2020Review
- Distal Axonal Proteins and Their Related MiRNAs in Cultured Cortical Neurons.Molecular neurobiology · 2019Article
- Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia.Nature neuroscience · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In adult mammals, axon regeneration after central nervous system injury is very poor, resulting in persistent functional loss. Enhancing the ability of axonal outgrowth may be a potential treatment strategy because mature neurons of the adult central nervous system may retain the intrinsic ability to regrow axons after injury. The protocadherin (Pcdh) clusters are thought to function in neuronal morphogenesis and in the assembly of neural circuitry in the brain. We cultured primary hippocampal neurons from E17.5 Pcdhα deletion (del-α) mouse embryos. After culture for 1 day, axon length was obviously shorter in del-α neurons compared with wild-type neurons. RNA sequencing of hippocampal E17.5 RNA showed that expression levels of BDNF, Fmod, Nrp2, OGN, and Sema3d, which are associated with axon extension, were significantly down-regulated in the absence of the Pcdhα gene cluster. Using transmission electron microscopy, the ratio of myelinated nerve fibers in the axons of del-α hippocampal neurons was significantly decreased; myelin sheaths of P21 Pcdhα-del mice showed lamellar disorder, discrete appearance, and vacuoles. These results indicate that the Pcdhα cluster can promote the growth and myelination of axons in the neurodevelopmental stage.
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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.