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

页码：788 / 791

页数：4

共 51 条

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