Both E12 and E47 allow commitment to the B cell lineage

被引：174

作者：

Bain, G

Maandag, ECR

Riele, HPJT

Feeney, AJ

Sheehy, A

Schlissel, M

Shinton, SA

Hardy, RR

Murre, C

机构：

[1] NETHERLANDS CANC INST, DEPT MOL GENET, NL-1066 CX AMSTERDAM, NETHERLANDS

[2] Scripps Res Inst, DEPT IMMUNOL, LA JOLLA, CA 92037 USA

[3] FOX CHASE CANC CTR, INST CANC RES, PHILADELPHIA, PA 19111 USA

[4] JOHNS HOPKINS UNIV, SCH MED, DEPT MED, BALTIMORE, MD 21205 USA

[5] JOHNS HOPKINS UNIV, SCH MED, DEPT MOL BIOL & GENET, BALTIMORE, MD 21205 USA

来源：

IMMUNITY | 1997年 / 6卷 / 02期

关键词：

D O I：

10.1016/S1074-7613(00)80421-5

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

The E2A gene products, E12 and E47, are required for proper B cell development. Mice lacking the E2A gene products generate only a very small number of 8220(+) cells, which lack immunoglobulin DJ(H) rearrangements. We have now generated mice expressing either E12 or E47. B cell development in mice expressing E12 but lacking E47 is perturbed at the pro-B cell stage, and these mice lack IgM(+)B220(+) B cells in both bone marrow and spleen. IgM(+)B220(+) B cells can be detected, albeit at significantly reduced levels, in the bone marrow and spleen of mice lacking E12. Ectopic expression of both E12 and E47 in a null mutant background shows that E12 and E47 act in concert to promote B lineage development. Taken together, the data indicate that both E12 and E47 allow commitment to the B cell lineage and act synergistically to promote B lymphocyte maturation.

引用

页码：145 / 154

页数：10

共 43 条

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TRANSFORMATION OF AXIAL SKELETON DUE TO OVEREXPRESSION OF BMI-1 IN TRANSGENIC MICE [J].