ArticleNeuroscience bulletin2018
AATYK is a Novel Regulator of Oligodendrocyte Differentiation and Myelination.
Article in Neuroscience bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- MRI signatures of cortical microstructure in human development align with oligodendrocyte cell-type expression.Nature communications · 2025Article
- The lemur tail kinase family in neuronal function and disfunction in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Illuminating the dark kinome: utilizing multiplex peptide activity arrays to functionally annotate understudied kinases.Cell communication and signaling : CCS · 2024Article
- ADAMTS4 Enhances Oligodendrocyte Differentiation and Remyelination by Cleaving NG2 Proteoglycan and AttenuatingThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Oligodendroglial GABAergic Signaling: More Than Inhibition!Neuroscience bulletin · 2021Review
- Genetic Evidence that Dorsal Spinal Oligodendrocyte Progenitor Cells are Capable of Myelinating Ventral Axons Effectively in Mice.Neuroscience bulletin · 2020Article
- Hyperactive and impulsive behaviors of LMTK1 knockout mice.Scientific reports · 2020Article
- LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons.Frontiers in molecular neuroscience · 2020Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendrocytes (OLs) are myelinating glial cells that form myelin sheaths around axons to ensure rapid and focal conduction of action potentials. Here, we found that an axonal outgrowth regulatory molecule, AATYK (apoptosis-associated tyrosine kinase), was up-regulated with OL differentiation and remyelination. We therefore studied its role in OL differentiation. The results showed that AATYK knockdown inhibited OL differentiation and the expression of myelin genes in vitro. Moreover, AATYK-deficiency maintained the proliferation status of OLs but did not affect their survival. Thus, AATYK is essential for the differentiation of OLs.
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