中文摘要：

转变生长因素 -- 尾(发信号的 TGF- 尾) 紧被调整在不同细胞和纸巾保证它的合适的生理的功能。象另外的房间表面受体一样， TGF- 尾受体被使内在化进房间，并且这个过程在 TGF- 尾发信号起一个重要规章的作用。当 TGF- 尾 endocytosis 能被钾弄空和 GTPase 缺乏的 dynamin K44A 异种堵住， TGF- 尾受体是经由 clathrin 涂的泡的 endocytosed，这很好被记录当 TGF- 尾 endocytosis 能被钾弄空和 GTPase 缺乏的 dynamin K44A 异种堵住。TGF- 尾受体可以也经由充满胆固醇的膜 microdomain 类脂化合物 rafts/caveolae 进入房间并且在 caveolin-1-positive 泡被发现。尽管受体 endocytosis 不为 TGF- 尾是必要的发信号，调停 clathrin 的 endocytosis 被显示了支持 TGF- 尾 - 导致的 Smad 激活和 transcriptional 回答。类脂化合物 rafts/caveolae 广泛地被认为是为 G 联合蛋白质的受体和酷氨酸 kinase 受体表明中心，但是他们被显示便于 TGF- 尾受体并且因此的降级 TGF- 尾发信号的转弯。这评论在 TGF- 尾发信号的调整总结 TGF- 尾受体 endocytosis，位于这个过程下面的可能的机制，和 endocytosis 的角色的当前的理解。

英文摘要：

Transforming growth factor-β （TGF-β） signaling is tightly regulated to ensure its proper physiological functions in different cells and tissues. Like other cell surface receptors, TGF-β receptors are internalized into the cell, and this process plays an important regulatory role in TGF-β signaling. It is well documented that TGF-β receptors are endocytosed via clathrin-coated vesicles as TGF-β endocytosis can be blocked by potassium depletion and the GTPasedeficient dynamin K44A mutant. TGF-β receptors may also enter cells via cholesterol-rich membrane microdomain lipid rafts/caveolae and are found in caveolin-l-positive vesicles. Although receptor endocytosis is not essential for TGF-β signaling, clathrin-mediated endocytosis has been shown to promote TGF-β-induced Smad activation and transcriptional responses. Lipid rafts/caveolae are widely regarded as signaling centers for G protein-coupled recep- tors and tyrosine kinase receptors, but they are indicated to facilitate the degradation of TGF-β receptors and there- fore turnoff of TGF-β signaling. This review summarizes current understanding of TGF-β receptor endocytosis, the possible mechanisms underlying this process, and the role of endocytosis in modulation of TGF-β signaling.