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c-Jun氨基末端激酶(JNK)介导的信号转导——从炎症到发育

Signal transduction by the c-Jun N-terminal kinase (JNK)--from inflammation to development.

作者信息

Ip Y T, Davis R J

机构信息

Department of Cell Biology, University of Massachusetts Medical School, Worcester 01605, USA.

出版信息

Curr Opin Cell Biol. 1998 Apr;10(2):205-19. doi: 10.1016/s0955-0674(98)80143-9.

Abstract

The c-Jun amino-terminal kinase (JNK) group of MAP kinases has been identified in mammals and insects. JNK is activated by exposure of cells to cytokines or environmental stress, indicating that this signaling pathway may contribute to inflammatory responses. Genetic and biochemical studies demonstrate that this signaling pathway also regulates cellular proliferation, apoptosis, and tissue morphogenesis. A functional role for JNK is therefore established in both the cellular response to stress and in many normal physiological processes.

摘要

丝裂原活化蛋白激酶(MAP激酶)中的c-Jun氨基末端激酶(JNK)组已在哺乳动物和昆虫中得到鉴定。JNK通过细胞暴露于细胞因子或环境应激而被激活,这表明该信号通路可能参与炎症反应。遗传学和生物化学研究表明,该信号通路还调节细胞增殖、凋亡和组织形态发生。因此,JNK在细胞应激反应和许多正常生理过程中都具有功能性作用。

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