Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1991-10-3
pubmed:abstractText
We describe a murine autosomal recessive mutation claw paw (gene symbol clp), which in homozygous clp/clp mice produces striking abnormalities of limb posture within the first one or two postnatal days. Affected animals have delayed and abnormal myelination in the peripheral nervous system but not in the central nervous system, and also have persistently blocked myelination of small caliber axons that are myelinated in normal mice. Both abnormalities suggest that an important effect of the clp mutation is to impair the putative signaling mechanism by which an axon instructs a Schwann cell whether or not to myelinate it. The early onset of behavioral abnormalities in clp/clp mutant mice, as well as certain other features of the disorder, suggest that some effects of the clp gene are not accounted for by the pathological findings. The clp gene has been mapped to chromosome 7 near the Gpi-1 locus.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0022-1503
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
287-94
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:articleTitle
The mouse mutation claw paw: forelimb deformity and delayed myelination throughout the peripheral nervous system.
pubmed:affiliation
Department of Neuropathology, Harvard Medical School, Boston, MA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.