The molecular mechanism and physiological significance of thyroid hormone non-genomic action

我们以前已经报道，甲状腺激素(T3)通过甲状腺激素受体(TR)刺激PI3K/Akt通路，这是一种非基因组作用，因为新的蛋白质合成不参与。在本研究中，我们证明了T3促进了tr/src/p85复合体的形成，进而诱导src和p85的磷酸化，导致PI3K→Akt的激活。这种新的T3作用在神经细胞的存活中起着重要作用。

We have reported previously that thyroid hormone (T3) stimulates the PI3K/Akt pathway through thyroid hormone receptor (TR).It is a non-genomic action since the novel protein synthesis is not involved in. In the present study we demonstrated that T3 promotes the complex formation of TR/Src/p85, which induces the phosphorylation of Src and p85 sequentially and results in the activation of PI3K→Akt. This novel T3 action plays important role in neuronal cell survival.