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首页> 外文期刊>The European Journal of Neuroscience >Inactivation and activation of Ras by the neurotrophin receptor p75.
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Inactivation and activation of Ras by the neurotrophin receptor p75.

机译：神经营养蛋白受体p75使Ras失活和激活。

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摘要

The neurotrophin receptor p75 induces neurotrophic and/or apoptotic signalling pathways and can also cooperate with the neurotrophic Trk receptor tyrosine kinases. Its intracellular part encloses a so-called 'death domain' with a segment similar to the wasp venom mastoparan which binds small GTPases such as Rho. To study possible interactions of p75 and Ras (and Rho) we used wild-type and mutant genes of p75 stably expressed by MDCK cells which normally have neither Trk nor p75. We found that p75 can directly bind the GTPases Ras and Rho and that the unstimulated p75 inactivates total cellular Ras through a differential influence on the dissociation of GDP and GTP from Ras and an exchange of bound Ras.GDP for free Ras.GTP. These properties of p75 could also be demonstrated in vitro and should therefore be cell type-independent. Stimulation of p75 with nerve growth factor causes Ras activation via adapter proteins known from Trk signalling and induces rapid outgrowth of cellular processes. Both inactivation and activation of Ras by p75 are controlled by the phosphorylation state of the receptor's two intracellular tyrosines. p75 also influences Rho activation and inactivation, and the combined interactions of the receptor with the two GTPases Ras and Rho can regulate neurite formation in an efficient, synergistic way.
机译：神经营养蛋白受体p75诱导神经营养和/或凋亡信号通路，并且还可以与神经营养性Trk受体酪氨酸激酶协同作用。它的细胞内部分围绕着一个所谓的“死亡结构域”，该区域的片段类似于黄蜂毒液马索帕兰，它结合了诸如Rho的小GTPase。为了研究p75与Ras（和Rho）的可能相互作用，我们使用了由MDCK细胞稳定表达的p75野生型和突变基因，这些细胞通常既没有Trk也没有p75。我们发现p75可以直接结合GTPases Ras和Rho，而未受刺激的p75通过对Ras分离GDP和GTP以及将结合的Ras.GDP交换为自由Ras.GTP的不同影响而使总细胞Ras失活。 p75的这些特性也可以在体外得到证实，因此应该与细胞类型无关。用神经生长因子刺激p75会通过Trk信号已知的衔接蛋白引起Ras活化，并诱导细胞过程快速生长。 p75的失活和激活Ras均受受体两个细胞内酪氨酸的磷酸化状态控制。 p75还影响Rho的激活和失活，并且受体与两个GTPases Ras和Rho的结合相互作用可以有效，协同地调节神经突的形成。

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