p14-MP1-MEK1 signaling regulates endosomal traffic and cellular proliferation during tissue homeostasis.
p14-MP1-MEK1 signaling regulates endosomal traffic and cellular proliferation during tissue homeostasis.
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P14-MP1-MEK1信号传导调节组织稳态期间的内体流量和细胞增殖。
DOI：
10.1083/jcb.200607025
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发表时间：
2006-12-18
影响因子：
7.8
通讯作者：
Huber, Lukas A.
中科院分区：
文献类型：
--
作者：
Teis, David;Taub, Nicole;Kurzbauer, Robert;Hilber, Diana;de Araujo, Mariana E.;Erlacher, Miriam;Offterdinger, Martin;Villunger, Andreas;Geley, Stephan;Bohn, Georg;Klein, Christoph;Hess, Michael W.;Huber, Lukas A.
细胞外信号调节激酶(ERK)级联调控多细胞生物体的增殖、分化和生存。支架蛋白通过提供关键的空间和时间特异性来调节细胞内的信号传递。支架蛋白MEK1(丝裂原活化蛋白激酶和ERK激酶1)伴侣(MP1)通过适配蛋白p14定位于晚期内吞体内。通过在小鼠中有条件地破坏p14基因，我们现在证明了p14-MP1-MEK1信号复合体调节晚期内体运输和细胞增殖。这一功能对早期胚胎发育和组织动态平衡是必不可少的，如表皮特异性缺失p14所揭示的那样。这些发现表明，内体p14-MP1-MEK1信号在体内具有特定和基本的功能，因此，表明细胞外信号对晚期内体运输的调节是维持组织内稳态所必需的。
The extracellular signal-regulated kinase (ERK) cascade regulates proliferation, differentiation, and survival in multicellular organisms. Scaffold proteins regulate intracellular signaling by providing critical spatial and temporal specificity. The scaffold protein MEK1 (mitogen-activated protein kinase and ERK kinase 1) partner (MP1) is localized to late endosomes by the adaptor protein p14. Using conditional gene disruption of p14 in mice, we now demonstrate that the p14–MP1-MEK1 signaling complex regulates late endosomal traffic and cellular proliferation. This function its essential for early embryogenesis and during tissue homeostasis, as revealed by epidermis-specific deletion of p14. These findings show that endosomal p14–MP1-MEK1 signaling has a specific and essential function in vivo and, therefore, indicate that regulation of late endosomal traffic by extracellular signals is required to maintain tissue homeostasis.
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影响因子：
9.2
作者：
Giroux, S;Tremblay, M;Charron, J
通讯作者：
Charron, J
DOI：
10.1073/pnas.90.14.6786
发表时间：
1993-07-15
影响因子：
11.1
作者：
JIANG, CK;MAGNALDO, T;BLUMENBERG, M
通讯作者：
BLUMENBERG, M
影响因子：
64.8
作者：
Pelkmans, L;Fava, E;Zerial, M
通讯作者：
Zerial, M
影响因子：
64.5
作者：
THERRIEN, M;CHANG, HC;RUBIN, GM
通讯作者：
RUBIN, GM
影响因子：
64.5
作者：
Acharya, U;Mallabiabarrena, A;Malhotra, V
通讯作者：
Malhotra, V