Linked Life Data

6543920

Source:http://linkedlifedata.com/resource/pubmed/id/6543920

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1985-11-13
pubmed:abstractText
Acetylcholine receptor (AChR) metabolism was studied in muscle from juvenile and adult dogs with congenital myasthenia gravis (CMG) and their unaffected littermates. Although the amount of AChR in the junctional region of innervated CMG muscle fibers was 25% of normal, or less, denervation of CMG fibers resulted in the appearance of AChR in extrajunctional membranes at as high a concentration as in denervated normal fibers. The rate of degradation of junctional AChR in CMG fibers explanted to organ culture did not differ significantly from normal. In monolayer cultures derived from enzyme-dissociated CMG muscle, myotubes of normal morphology developed, and the synthesis and degradation of AChR did not differ from normal. Addition of sera from dogs with the acquired autoimmune form of MG accelerated the degradation of AChR on cultured myotubes, but CMG dog sera were without effect. These data suggest that the low junctional membrane density of AChR in CMG does not reflect a primary inability of muscle to synthesize AChR, nor an accelerated degradation of AChR in the postsynaptic membrane, but rather a low insertion rate of AChR in the postsynaptic membrane.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0148-639X
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
717-24
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Congenital canine myasthenia gravis: II. Acetylcholine receptor metabolism.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't