Cdo interacts with APPL1 and activates Akt in myoblast differentiation.
Cdo interacts with APPL1 and activates Akt in myoblast differentiation.
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DOI：
10.1091/mbc.e09-12-1011
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发表时间：
2010-07-15
影响因子：
3.3
通讯作者：
Kang JS
中科院分区：
文献类型：
--
作者：
Bae GU;Lee JR;Kim BG;Han JW;Leem YE;Lee HJ;Ho SM;Hahn MJ;Kang JS
在成肌细胞分化过程中，Cdo通过与APPL1的间接相互作用激活Akt，这一复合物可能介导了细胞间相互作用的部分早生肌效应。Cdo的促生功能涉及通过与支架蛋白、JLP和Bnip-2 （p38MAPK）和APPL1 （Akt）相互作用协调激活p38MAPK和Akt。肌肉前体细胞之间的相互作用是肌源性分化所必需的；然而，潜在的机制在很大程度上是未知的。早生肌细胞表面蛋白Cdo作为含有其他细胞粘附分子Boc、Neogenin和N-cadherin的多蛋白复合物的组分，介导肌肉前体细胞间相互作用触发的一些信号。Cdo通过与两种支架蛋白JLP和Bnip-2相互作用激活p38MAPK，促进肌肉形成。p38MAPK和Akt信号通路是肌源性分化所必需的，这两个信号通路的激活对于有效的肌源性分化至关重要。我们在这里报道了Akt的相互作用伙伴APPL1在分化成肌细胞时与Cdo和Boc形成复合物。在成肌细胞分化过程中，Akt的有效激活需要Cdo和APPL1。过表达一种构成活性形式的Akt可完全挽救cdo缺失细胞的分化缺陷，而过表达APPL1则不能。综上所述，在成肌细胞分化过程中，Cdo通过与APPL1的关联激活Akt，该复合物可能介导了细胞间相互作用的一些早生肌效应。Cdo的促生功能涉及通过与支架蛋白、JLP和Bnip-2 （p38MAPK）和APPL1 （Akt）的关联，协调激活p38MAPK和Akt。
Cdo activates Akt via indirect interaction with APPL1 during myoblast differentiation, and this complex likely mediates some of the promyogenic effect of cell–cell interaction. The promyogenic function of Cdo involves a coordinated activation of p38MAPK and Akt via interaction with scaffold proteins, JLP and Bnip-2 for p38MAPK and APPL1 for Akt. Cell–cell interactions between muscle precursors are required for myogenic differentiation; however, underlying mechanisms are largely unknown. Promyogenic cell surface protein Cdo functions as a component of multiprotein complexes containing other cell adhesion molecules, Boc, Neogenin and N-cadherin, and mediates some of signals triggered by cell–cell interactions between muscle precursors. Cdo activates p38MAPK via interaction with two scaffold proteins JLP and Bnip-2 to promote myogenesis. p38MAPK and Akt signaling are required for myogenic differentiation and activation of both signaling pathways is crucial for efficient myogenic differentiation. We report here that APPL1, an interacting partner of Akt, forms complexes with Cdo and Boc in differentiating myoblasts. Both Cdo and APPL1 are required for efficient Akt activation during myoblast differentiation. The defective differentiation of Cdo-depleted cells is fully rescued by overexpression of a constitutively active form of Akt, whereas overexpression of APPL1 fails to do so. Taken together, Cdo activates Akt through association with APPL1 during myoblast differentiation, and this complex likely mediates some of the promyogenic effect of cell–cell interaction. The promyogenic function of Cdo involves a coordinated activation of p38MAPK and Akt via association with scaffold proteins, JLP and Bnip-2 for p38MAPK and APPL1 for Akt.
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影响因子：
11.8
作者：
Griffin CA;Kafadar KA;Pavlath GK
通讯作者：
Pavlath GK
影响因子：
3.3
作者：
Bae, Gyu-Un;Yang, Youn-Joo;Krauss, Robert S.
通讯作者：
Krauss, Robert S.
影响因子：
2.7
作者：
Lee, JR;Chang, YY;Hahn, MJ
通讯作者：
Hahn, MJ
影响因子：
16
作者：
Bergstrom, DA;Penn, BH;Tapscott, SJ
通讯作者：
Tapscott, SJ
影响因子：
11.4
作者：
Lluís, F;Ballestar, E;Muñoz-Cánoves, P
通讯作者：
Muñoz-Cánoves, P