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rdf:type |
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lifeskim:mentions |
umls-concept:C0002131,
umls-concept:C0003250,
umls-concept:C0204727,
umls-concept:C0205409,
umls-concept:C0439849,
umls-concept:C0439851,
umls-concept:C0445223,
umls-concept:C0591833,
umls-concept:C0949787,
umls-concept:C1419986,
umls-concept:C1420192,
umls-concept:C1552596,
umls-concept:C1552599,
umls-concept:C1704787,
umls-concept:C1880022,
umls-concept:C1947931,
umls-concept:C1953353
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pubmed:issue |
1
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pubmed:dateCreated |
1999-6-9
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pubmed:abstractText |
Nineteen mAb directed against murine fusion regulatory protein-1 (mFRP-1)/4F2/CD98 were isolated and their biological properties were analysed. Intriguingly, mFRP-1 was found to be an alloantigen, namely, FRP-1.1 (DBA/2 and CBA mice type) and FRP-1.2 (BALB/c, C57BL/6 and C3H/He mice type). The nucleotide sequences of FRP-1.1 and FRP-1.2 were determined, demonstrating that amino acid change at 129 (P<-->R) is related to the alloantigenicity. mFRP-1 is expressed on thymocytes, on spleen cells, on peripheral lymphocytes and on blood monocytes, suggesting that the physiological role in vivo of murine FRP-1 is different from that of human FRP-1. The biological activities of antimFRP-1 mAbs showed by the present study are: (i) enhancement of Newcastle disease virus-induced cell fusion; (ii) suppression of HIVgp160-mediated cell fusion; and (iii) induction of aggregation and multinucleated giant cells of monocytes/macrophages.
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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 |
Feb
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pubmed:issn |
0818-9641
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pubmed:author |
pubmed-author:ItoYY,
pubmed-author:KawanoMM,
pubmed-author:KomadaHH,
pubmed-author:KozukaYY,
pubmed-author:KusagawaSS,
pubmed-author:KusauraTT,
pubmed-author:NishioMM,
pubmed-author:ShimuraKK,
pubmed-author:TajimaMM,
pubmed-author:TsumuraHH,
pubmed-author:TsurudomeMM,
pubmed-author:YoshimuraSS
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pubmed:issnType |
Print
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pubmed:volume |
77
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
19-27
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10101682-Amino Acid Sequence,
pubmed-meshheading:10101682-Amino Acid Substitution,
pubmed-meshheading:10101682-Animals,
pubmed-meshheading:10101682-Antibodies, Monoclonal,
pubmed-meshheading:10101682-Antigens, CD,
pubmed-meshheading:10101682-Antigens, CD98,
pubmed-meshheading:10101682-Base Sequence,
pubmed-meshheading:10101682-Carrier Proteins,
pubmed-meshheading:10101682-Cell Aggregation,
pubmed-meshheading:10101682-Cell Fusion,
pubmed-meshheading:10101682-Cell Line,
pubmed-meshheading:10101682-DNA Primers,
pubmed-meshheading:10101682-Giant Cells,
pubmed-meshheading:10101682-HIV Envelope Protein gp160,
pubmed-meshheading:10101682-Humans,
pubmed-meshheading:10101682-Isoantigens,
pubmed-meshheading:10101682-Mice,
pubmed-meshheading:10101682-Mice, Inbred BALB C,
pubmed-meshheading:10101682-Mice, Inbred C3H,
pubmed-meshheading:10101682-Mice, Inbred C57BL,
pubmed-meshheading:10101682-Mice, Inbred CBA,
pubmed-meshheading:10101682-Mice, Inbred DBA,
pubmed-meshheading:10101682-Molecular Sequence Data,
pubmed-meshheading:10101682-Newcastle disease virus,
pubmed-meshheading:10101682-Sequence Homology, Amino Acid
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pubmed:year |
1999
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pubmed:articleTitle |
Isolation and characterization of monoclonal antibodies directed against murine FRP-1/CD98/4F2 heavy chain: murine FRP-1 is an alloantigen and amino acid change at 129 (P<-->R) is related to the alloantigenicity.
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pubmed:affiliation |
Department of Microbiology, Mie University School of Medicine, Mie-ken, Japan. tsumura@doc.medic.mie-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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