Oligodendrocyte development and CNS myelination are unaffected in a mouse model of severe spinal muscular atrophy

No abstract is available for this paper.

• Publication year

  2017

• Venue

  Human Molecular Genetics

• Publication date

  2017-01-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1093/hmg/ddw385PMID 28069797
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Molecular, Cellular and Developmental Biology Program – Specialization 2018/2019

  2017cited by this paper
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  2012influential reference
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• Integrin-linked kinase is required for laminin-2–induced oligodendrocyte cell spreading and CNS myelination

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• The human centromeric survival motor neuron gene (SMN2) rescues embryonic lethality in Smn(-/-) mice and results in a mouse with spinal muscular atrophy.

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• A single nucleotide in the SMN gene regulates splicing and is responsible for spinal muscular atrophy.

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• Incidence, prevalence, and gene frequency studies of chronic childhood spinal muscular atrophy.

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