Université catholique de Louvain, Brussels, Belgium.
Biochem J. 2012 Mar 15;442(3):681-92. doi: 10.1042/BJ20111530.
eEF2K [eEF2 (eukaryotic elongation factor 2) kinase] phosphorylates and inactivates the translation elongation factor eEF2. eEF2K is not a member of the main eukaryotic protein kinase superfamily, but instead belongs to a small group of so-called α-kinases. The activity of eEF2K is normally dependent upon Ca(2+) and calmodulin. eEF2K has previously been shown to undergo autophosphorylation, the stoichiometry of which suggested the existence of multiple sites. In the present study we have identified several autophosphorylation sites, including Thr(348), Thr(353), Ser(366) and Ser(445), all of which are highly conserved among vertebrate eEF2Ks. We also identified a number of other sites, including Ser(78), a known site of phosphorylation, and others, some of which are less well conserved. None of the sites lies in the catalytic domain, but three affect eEF2K activity. Mutation of Ser(78), Thr(348) and Ser(366) to a non-phosphorylatable alanine residue decreased eEF2K activity. Phosphorylation of Thr(348) was detected by immunoblotting after transfecting wild-type eEF2K into HEK (human embryonic kidney)-293 cells, but not after transfection with a kinase-inactive construct, confirming that this is indeed a site of autophosphorylation. Thr(348) appears to be constitutively autophosphorylated in vitro. Interestingly, other recent data suggest that the corresponding residue in other α-kinases is also autophosphorylated and contributes to the activation of these enzymes [Crawley, Gharaei, Ye, Yang, Raveh, London, Schueler-Furman, Jia and Cote (2011) J. Biol. Chem. 286, 2607-2616]. Ser(366) phosphorylation was also detected in intact cells, but was still observed in the kinase-inactive construct, demonstrating that this site is phosphorylated not only autocatalytically but also in trans by other kinases.
真核延伸因子 2 激酶(eEF2K)使翻译延伸因子 eEF2 磷酸化并使其失活。eEF2K 不属于主要的真核蛋白激酶超家族的成员,而是属于所谓的α-激酶小类。eEF2K 的活性通常依赖于 Ca2+和钙调蛋白。eEF2K 先前已被证明可进行自身磷酸化,其化学计量表明存在多个位点。在本研究中,我们鉴定了几个自身磷酸化位点,包括 Thr348、Thr353、Ser366 和 Ser445,所有这些位点在脊椎动物 eEF2K 中都高度保守。我们还鉴定了许多其他位点,包括 Ser78,这是一个已知的磷酸化位点,以及其他一些位点,其中一些位点的保守性较差。没有一个位点位于催化结构域中,但有三个位点影响 eEF2K 的活性。将 Ser78、Thr348 和 Ser366 突变为非磷酸化的丙氨酸残基会降低 eEF2K 的活性。在用野生型 eEF2K 转染人胚肾 293(HEK293)细胞后,通过免疫印迹检测到 Thr348 的磷酸化,但在用激酶失活构建体转染后未检测到,这证实了这确实是一个自身磷酸化的位点。Thr348 在体外似乎是持续自身磷酸化的。有趣的是,其他最近的数据表明,其他α-激酶中的相应残基也会自身磷酸化,并有助于这些酶的激活[Crawley、Gharaei、Ye、Yang、Raveh、London、Schueler-Furman、Jia 和 Cote(2011)J. Biol. Chem. 286,2607-2616]。Ser366 磷酸化也在完整细胞中被检测到,但在激酶失活构建体中仍被观察到,这表明该位点不仅通过自身催化而且还通过其他激酶的转磷酸化而被磷酸化。