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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1989-4-6
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pubmed:abstractText |
A quantitative model is developed to explore the effects of prezygotic and postzygotic incompatibility on the origin and maintenance of associations between the major histocompatibility complex (MHC) and the t-complex in the mouse. Incompatibility is represented by a reduction in the rate of conception or gestation of offspring derived from sperm bearing MHC antigens in common with the mother. Incompatibility encourages the evolution of associations from a state of complete independence between the two complexes by promoting the invasion of all novel antigens, including those that exhibit associations with the t-complex. Incompatibility can modify the relative numbers of antigens associated with each haplotype by actively promoting the exclusion or invasion of recombinants that bear formerly +-specific or t-specific antigens on the alternative haplotype. The results of the analysis indicate that the state of complete independence between the MHC and the t-complex is not preserved over evolutionary time in the presence of incompatibility. Further, the expression of incompatibility maintains fully associated states that include a single antigen associated with the t-haplotype and up to three to five antigens associated with the +-haplotype within a single population.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-1172603,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-1196352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-134129,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-14171459,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-16589989,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-16589990,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-17246937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-17247957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-2897062,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-2897063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-2917712,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-3396863,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-3623083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-3753900,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-3770466,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-3968429,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-4407212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-4881822,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-4926899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-5245622,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-5518513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-5728745,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-6007869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-6053776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-6201441,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-6295638,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-7030925,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-7141223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-7151178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2917711-7203013
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0016-6731
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
121
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
139-51
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:2917711-Animals,
pubmed-meshheading:2917711-Antigens, Differentiation,
pubmed-meshheading:2917711-Biological Evolution,
pubmed-meshheading:2917711-Genes,
pubmed-meshheading:2917711-Haplotypes,
pubmed-meshheading:2917711-Heterozygote,
pubmed-meshheading:2917711-Histocompatibility Antigens,
pubmed-meshheading:2917711-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:2917711-Major Histocompatibility Complex,
pubmed-meshheading:2917711-Mathematics,
pubmed-meshheading:2917711-Mice,
pubmed-meshheading:2917711-Microtubule-Associated Proteins,
pubmed-meshheading:2917711-Models, Genetic,
pubmed-meshheading:2917711-Nuclear Proteins,
pubmed-meshheading:2917711-Selection, Genetic,
pubmed-meshheading:2917711-Zygote,
pubmed-meshheading:2917711-t-Complex Genome Region
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pubmed:year |
1989
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pubmed:articleTitle |
Coevolution of the major histocompatibility complex and the t-complex in the mouse. I. Generation and maintenance of high complementarity associations.
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pubmed:affiliation |
Department of Zoology, Duke University, Durham, North Carolina 27706.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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