Yamashita H, Okadome T, Franzén P, ten Dijke P, Heldin C H, Miyazono K
Ludwig Institute for Cancer Research, Uppsala, Sweden.
J Biol Chem. 1995 Jan 13;270(2):770-4. doi: 10.1074/jbc.270.2.770.
A rat pituitary tumor cell line (GH3) has been reported to express transforming growth factor-beta (TGF-beta) binding components of 70-74 kDa (ligand included), denoted TGF-beta type IV receptor. We investigated whether the type IV receptor corresponds to any of the recently cloned type I receptors for proteins in the TGF-beta super-family. TGF-beta type I receptor (T beta R-I) complexes of 69-72 kDa formed a heteromeric complex with T beta R-II in GH3 cells, as detected by immunoprecipitation. In addition, TGF-beta formed complexes of 72-74 kDa, which were different from T beta R-I and the other known type I receptors, and were not dependent on T beta R-II for binding. The GH3 cells were resistant to the growth inhibitory activity of TGF-beta, but a transcriptional response was activated by TGF-beta in this cell line, presumably through the T beta R-II and T beta R-I complex. These results indicate that GH3 cells have T beta R-I and T beta R-II and, in addition, other binding protein(s) which form 72-74-kDa complexes with TGF-beta; the function of the latter component(s) remains to be elucidated.
据报道,大鼠垂体肿瘤细胞系(GH3)可表达70 - 74 kDa的转化生长因子β(TGF-β)结合成分(包括配体),称为TGF-β IV型受体。我们研究了IV型受体是否与TGF-β超家族中最近克隆的任何一种I型受体相对应。通过免疫沉淀检测发现,69 - 72 kDa的TGF-β I型受体(TβR-I)复合物在GH3细胞中与TβR-II形成异源复合物。此外,TGF-β形成了72 - 74 kDa的复合物,该复合物不同于TβR-I和其他已知的I型受体,且其结合不依赖于TβR-II。GH3细胞对TGF-β的生长抑制活性具有抗性,但在该细胞系中TGF-β可激活转录反应,推测是通过TβR-II和TβR-I复合物实现的。这些结果表明,GH3细胞具有TβR-I和TβR-II,此外,还有其他与TGF-β形成72 - 74 kDa复合物的结合蛋白;后者的功能仍有待阐明。