The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Integrin-linked kinase is required for laminin-2–induced oligodendrocyte cell spreading and CNS myelination
Open accessAbstract
Early steps in myelination in the central nervous system (CNS) include a specialized and extreme form of cell spreading in which oligodendrocytes extend large lamellae that spiral around axons to form myelin. Recent studies have demonstrated that laminin-2 (LN-2; α2β1γ1) stimulates oligodendrocytes to extend elaborate membrane sheets in vitro (cell spreading), mediated by integrin α6β1. Although a congenital LN-2 deficiency in humans is associated with CNS white matter changes, LN-2–deficient (dy/dy) mice have shown abnormalities primarily within the peripheral nervous system. Here, we demonstrate a critical role for LN-2 in CNS myelination by showing that dy/dy mice have quantitative and morphologic defects in CNS myelin. We have defined the molecular pathway through which LN-2 signals oligodendrocyte cell spreading by demonstrating requirements for phosphoinositide 3-kinase activity and integrin-linked kinase (ILK). Interaction of oligodendrocytes with LN-2 stimulates ILK activity. A dominant negative ILK inhibits LN-2–induced myelinlike membrane formation. A critical component of the myelination signaling cascade includes LN-2 and integrin signals through ILK.
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“There are many examples of regional differences in dysmyelination caused by genetic manipulation of mice between areas such as the optic nerve, spinal cord, cerebellum and corpus callosum.”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [11]
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“For example, laminin‐deficient dystrophia muscularis mice exhibit hypomyelination in the corpus callosum and optic nerve, but not the spinal cord (11)”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [11]
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LAMININ FUNCTIONS IN TISSUE MORPHOGENESIS
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Metadata
- Authors
- Chun, S. J., Rasband, M. N., Sidman, R. L., Habib, A. A., & Vartanian, T.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- UConn Health (US)
- Corresponding author
- Vartanian, Timothy
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2003-10-27
- Volume
- 163
- Issue
- 2
- Pages
- 397-408
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2173507
- OpenAlex
- W2120316837
- Cited by
- 170
- References
- 41
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 5 · 2019: 10 · 2018: 4 · 2017: 8 · 2016: 6 · 2015: 10 · 2014: 4 · 2013: 7 · 2012: 8
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k02ns002028-04)
- National Institute of Neurological Disorders and Stroke (K02 NS02028, P01 NS 38475, R01NS044916, P01NS038475, R01NS042317, R01 NS42317)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- integrin-linked kinase, laminin-2, CNS myelination, alpha6beta1 integrin, phosphatidylinositol 3-kinase, myelination, integrin signaling
- MeSH terms
- Scaffold Protein ILK, Adenoviridae, Animals, Axons, Cell Survival, Cells, Cultured, Central Nervous System, Cytoskeletal Proteins, Enzyme Activation, Homozygote, Laminin, Mice, Mutant Strains, Mutation, Myelin Sheath, Oligodendroglia, Optic Nerve, Phosphoproteins, Cell Adhesion Molecules, Rats, Sprague-Dawley, Protein Serine-Threonine Kinases, Phosphatidylinositol 3-Kinases, Mice, Rats, Paxillin
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