MAPKAP kinase 2 phosphorylates serum response factor in vitro and in vivo.

Heidenreich O, Neininger A, Schratt G, Zinck R, Cahill MA, Engel K, Kotlyarov A, Kraft R, Kostka S, Gaestel M, Nordheim A

J Biol Chem 1999 May 14;274(20):14434-14443

學生: 翁志鴻 (g874255)

摘要

SRE( serum response element ) 是一段與生長因子(熱感應蛋白質調控因子) stress -regulated promoter有關的序列,是c-tos與egr-1因子表現所必須的。而SRE須借由其轉譯 因子SRF( serum response factor )與其他如TCFs的共同合作而產生表現。於此,上游的磷 酸化顐狾p:SAPK、ERKs、 P38…就扮演了磷酸化SRF而且使其活化的角色。於此篇中,作者以二種不同的細胞及基因轉殖老鼠 (缺乏MK2(-/-) )來處理不同的重 金屬離子,以使其產生stress進而造成P38 / SAPK2以及相關的MAPKAP kinase 2(MK2)的活性,借以探討此條訊息傳導的路逕,作者成功的證明MK2於SRF ser-103的位置,進行磷酸化 P活化的功用,以幫助我們對於了解如何活化生長或保護基因提供重要的一個訊息。

References:

  1. Stress-induced stimulation of early growth response gene-1 by p38/stress-acti vated protein kinase 2 is mediated by a cAMP-responsive promoter element in a MA PKAP kinase 2-independent manner.J Biol Chem. 1999 Jul 9;274(28):19559-64.
  2. Regulation of actin filament dynamics by p38 map kinase-mediated phosphorylat ion of heat shock protein 27.J Cell Sci. 1997 Feb;110 ( Pt 3):357-68.
  3. Net, a negative Ras-switchable TCF, contains a second inhibition domain, the CID, that mediates repression through interactions with CtBP and de-acetylation. EMBO J. 1999 Jun 15;18(12):3392-403.

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