摘要
转变生长因素的成员 -- 尾(TGF- 尾) 家庭经由 autocrine， paracrine，和内分泌的模式在后生动物的有机体控制大量细胞的回答。因此，发信号的异常 TGF- 尾能在几疾病的致病起一个关键作用，包括癌症。TGF- 尾发信号小径被短 phospho 串联激活，从受体 phosphorylation 到随后的 phosphorylation，下游的信号变换器的激活叫了 R-Smads。R-Smad phosphorylation 状态决定 Smad 复杂集会 / 拆卸，原子进口 / 出口， transcriptional 活动和稳定性，并且因此是在 TGF- 尾发信号的最批评的事件。由特定的磷酸酶的 R-Smads 的 Dephosphorylation 阻止或终止 TGF- 尾发信号，加亮需要认为 Smad (de ) 是 phosphorylation 作为一紧控制了并且动态事件。这篇文章在控制 TGF- 尾发信号和随后的生理的回答的力量和持续时间说明可逆 phosphorylation 的必要角色。
Members of the transforming growth factor-β （TGF-β） family control a broad range of cellular responses in metazoan organisms via autocrine, paracrine, and endocrine modes. Thus, aberrant TGF-β signaling can play a key role in the pathogenesis of several diseases, including cancer. TGF-β signaling pathways are activated by a short phospho-cascade, from receptor phosphorylation to the subsequent phosphorylation and activation of downstream signal transducers called R-Smads. R-Smad phosphorylation state determines Smad complex assembly/disassembly, nuclear import/export, transcriptional activity and stability, and is thus the most critical event in TGF-β signaling. Dephosphorylation of R-Smads by specific phosphatases prevents or terminates TGF-β signaling, highlighting the need to consider Smad （de）phosphorylation as a tightly controlled and dynamic event. This article illustrates the es- sential roles of reversible phosphorylation in controlling the strength and duration of TGF-β signaling and the ensu- ing physiological responses.
