THE NOVEL VARIANTS OF MB-1 AND B29 TRANSCRIPTS GENERATED BY ALTERNATIVE MESSENGER-RNA SPLICING

被引:21
作者
KOYAMA, M
NAKAMURA, T
HIGASHIHARA, M
HERREN, B
KUWATA, S
SHIBATA, Y
OKUMURA, K
KUROKAWA, KY
机构
[1] UNIV TOKYO,FAC MED,DEPT INTERNAL MED 1,BUNKYO KU,TOKYO 113,JAPAN
[2] UNIV TOKYO,FAC MED,DEPT TRANSFUS MED & IMMUNOHEMATOL,BUNKYO KU,TOKYO 113,JAPAN
[3] UNIV ALABAMA,DEPT MICROBIOL,DIV DEV & CLIN IMMUNOL,BIRMINGHAM,AL 35294
[4] JUNTENDO UNIV,SCH MED,DEPT IMMUNOL,BUNKYO KU,TOKYO 113,JAPAN
关键词
B-CELL RECEPTOR; IG-ALPHA; IG-BETA; ALTERNATIVE SPLICING; B-CELL ACTIVATION;
D O I
10.1016/0165-2478(95)00071-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The Ig-alpha/Ig-beta heterodimers encoded by mb-1 and B29 genes, respectively, are crucial for the constitution of the B-cell receptor (BCR). We report here novel variants of mb-1 and B29 transcripts produced by alternative mRNA splicing, The proteins encoded by these variants are predicted to conserve transmembrane and cytoplasmic portions of Ig-alpha and Ig-beta but lack a part of the extracellular portions containing cysteine residues which are required for intramolecular and intermolecular S-S bonds, Transfection studies revealed that the variant mb-1 and B29 did not contribute to the BCR expression on cell surfaces, Although peripheral B cells contain small amounts of the variant mb-1 and B29 transcripts, treatment with an anti-IgM antibody, LPS or IL-4 induces a significant increase in amounts of the variant transcripts, These observations suggest that B-cell activation induces alternative splicing of mb-1 and B29 transcripts which encode proteins unable to constitute the BCR.
引用
收藏
页码:151 / 156
页数:6
相关论文
共 29 条