ArticleProceedings of the National Academy of Sciences of the United States of America2010
Allelic variation in the Tyk2 and EGF genes as potential genetic determinants of CNS repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Epidermal Growth Factor in the CNS: A Beguiling Journey from Integrated Cell Biology to Multiple Sclerosis. An Extensive Translational Overview.Cellular and molecular neurobiology · 2022Review
- Resilience in Long-Term Viral Infection: Genetic Determinants and Interactions.International journal of molecular sciences · 2021Article
- New Epidermal-Growth-Factor-Related Insights Into the Pathogenesis of Multiple Sclerosis: Is It Also Epistemology?Frontiers in neurology · 2021Review
- Genetic control of alphavirus pathogenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Quantitative genetics in the study of virus-induced disease.Advances in virus research · 2014Review
- Simian immunodeficiency virus infection in the brain and lung leads to differential type I IFN signaling during acute infection.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The potential for endogenous remyelination and axonal protection can be an important factor in determining disease outcome in demyelinating diseases like multiple sclerosis. In many multiple sclerosis (MS) patients CNS repair fails or is incomplete whereas in others the disease is accompanied by extensive repair of demyelinated lesions. We have described significant differences in the ability of two strains of mice to repair CNS damage following Theiler's virus-induced demyelination: FVB/NJ (FVB) mice repair damaged myelin spontaneously and completely, whereas B10.D1-H2(q)/SgJ (B10.Q) mice are deficient in the repair process. A QTL analysis was performed to identify genetic loci that differentially regulate CNS repair following chronic demyelination in these strains and two QTL were detected: one on chromosome 3 with a LOD score of 9.3 and a second on chromosome 9 with a LOD score of 14.0. The mouse genes for epidermal growth factor (EGF) and Tyk2 are encoded within the QTL on chromosomes 3 and 9, respectively. Sequence polymorphisms between the FVB and B10.Q strains at both the EGF and Tyk2 loci define functional variations consistent with roles for these genes in regulating myelin repair. EGF is a key regulator of cell growth and development and we show a sevenfold increase in EGF expression in FVB compared to B10.Q mice. Tyk2 is a Janus kinase that plays a central role in controlling the T(H)1 immune response and we show that attenuation of Tyk2 function correlates with enhanced CNS repair.
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