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丝裂原活化蛋白激酶信号转导通路对转录因子AP-1的调控

Transcription factor AP-1 regulation by mitogen-activated protein kinase signal transduction pathways.

作者信息

Whitmarsh A J, Davis R J

机构信息

Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester 01605, USA.

出版信息

J Mol Med (Berl). 1996 Oct;74(10):589-607. doi: 10.1007/s001090050063.

Abstract

Mitogen-activated protein (MAP) kinases are proline-directed serine/threonine kinases that are activated by dual phosphorylation on threonine and tyrosine residues in response to a wide array of extracellular stimuli. Three distinct groups of MAP kinases have been identified in mammalian cells [extracellular-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38]. These MAP kinases are mediators of signal transduction from the cell surface to the nucleus. One nuclear target of these MAP kinase signaling pathways is the transcription factor AP-1. MAP kinases regulate AP-1 transcriptional activity by multiple mechanisms. Here we review recent progress towards understanding AP-1 regulation by the ERK, JNK, and p38 MAP kinase signal transduction pathways.

摘要

丝裂原活化蛋白(MAP)激酶是脯氨酸导向的丝氨酸/苏氨酸激酶,可通过苏氨酸和酪氨酸残基上的双重磷酸化而被激活,以响应多种细胞外刺激。在哺乳动物细胞中已鉴定出三组不同的MAP激酶[细胞外调节激酶(ERK)、c-Jun氨基末端激酶(JNK)和p38]。这些MAP激酶是从细胞表面到细胞核的信号转导介质。这些MAP激酶信号通路的一个核靶点是转录因子AP-1。MAP激酶通过多种机制调节AP-1的转录活性。在这里,我们综述了在理解ERK、JNK和p38 MAP激酶信号转导途径对AP-1调节方面的最新进展。

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