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丝裂原活化蛋白激酶的抑制作用可阻断胰岛素介导的血管平滑肌细胞中 Elk-1 对 c-fos 的 DNA 合成及转录激活。

Inhibition of MAP kinase blocks insulin-mediated DNA synthesis and transcriptional activation of c-fos by Elk-1 in vascular smooth muscle cells.

作者信息

Xi X P, Graf K, Goetze S, Hsueh W A, Law R E

机构信息

University of California, Los Angeles, School of Medicine 90024, USA.

出版信息

FEBS Lett. 1997 Nov 17;417(3):283-6. doi: 10.1016/s0014-5793(97)01303-3.

DOI:10.1016/s0014-5793(97)01303-3
PMID:9409734
Abstract

Insulin-stimulated DNA synthesis, MAP kinase (MAPK) activity and c-fos expression in vascular smooth muscle cells (VSMCs) was blocked by the MAPK inhibitor PD 98059. Regulation of c-fos expression by the transcription factor Elk-1 at the serum response element (SRE) is dependent on its phosphorylation by MAPK. PD 98059 also suppressed insulin-induced Elk-1 transcriptional activity through the SRE. These data show that MAPK plays a critical role in both insulin-mediated growth and Elk-1-dependent induction of c-fos in VSMCs.

摘要

丝裂原活化蛋白激酶(MAPK)抑制剂PD 98059可阻断胰岛素刺激的血管平滑肌细胞(VSMC)中的DNA合成、MAP激酶(MAPK)活性及c-fos表达。转录因子Elk-1在血清反应元件(SRE)处对c-fos表达的调控依赖于其被MAPK磷酸化。PD 98059还通过SRE抑制胰岛素诱导的Elk-1转录活性。这些数据表明,MAPK在VSMC中胰岛素介导的生长及Elk-1依赖的c-fos诱导过程中均起关键作用。

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