Linked Life Data

7054282

Source:http://linkedlifedata.com/resource/pubmed/id/7054282

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-3-13
pubmed:abstractText
We report here the results of EAE induction in 1758 mice from 9 inbred strains, 5 H-2 congenic strains, and 6 F1 hybrids. EAE responsiveness is under the primary control of genes outside the H-2 complex. The F1 data do not show a unifactorial inheritance of EAE responsiveness. The F1 data do imply a maternal factor, sex hormone, or sex-linked gene(s) that modifies EAE responsiveness. The data suggest that the H-2 complex modifies the degree of EAE responsiveness. This modulatory effect by H-2 could account for the contradictory reports in the literature on the association of H-2 type and EAE responsiveness.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
421-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Experimental allergic encephalomyelitis (EAE) in mice: primary control of EAE susceptibility is outside the H-2 complex.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.