Immunodeficiency in protein kinase C beta-deficient mice

被引：394
作者：
Leitges, M
Schmedt, C
Guinamard, R
Davoust, J
Schaal, S
Stabel, S
Tarakhovsky, A
机构：
[1] MAX PLANCK GESELL, MAX DELBRUCK LAB, D-50829 COLOGNE, GERMANY
[2] UNIV COLOGNE, INST GENET, D-50931 COLOGNE, GERMANY
[3] CNRS, INSERM MARSEILLE LUMINY, CTR IMMUNOL, F-13288 MARSEILLE 9, FRANCE
来源：
SCIENCE | 1996年 / 273卷 / 5276期
关键词：
D O I：
10.1126/science.273.5276.788
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Cross-linking of the antigen receptor on lymphocytes by antigens or antibodies to the receptor results in activation of enzymes of the protein kinase C (PKC) family. Mice homozygous for a targeted disruption of the gene encoding the PKC-beta I and PKC-beta II isoforms develop an immunodeficiency characterized by impaired humoral immune responses and reduced cellular responses of B cells, which is similar to X-linked immunodeficiency in mice. Thus PKC-beta I and PKC-beta II play an important role in B cell activation and may be functionally linked to Bruton's tyrosine kinase in antigen receptor-mediated signal transduction.
引用
收藏
页码：788 / 791
页数：4
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