Miyazono K
Department of Biochemistry, Cancer Institute, Tokyo, Japan.
Int J Hematol. 1997 Feb;65(2):97-104. doi: 10.1016/s0925-5710(96)00542-7.
TGF-beta inhibits the growth of many cell types, including hematopoietic cells and lymphocytes. TGF-beta transduces signals through two different types of serine/threonine kinase receptors, type I (T beta R-I) and type II (T beta R-II). T beta R-II is a primary binding protein for the ligands, and T beta R-I is an effector protein, which determines the specificity of signals. Type III receptor (betaglycan) and endoglin play more indirect roles; i.e. delivery of ligands to the signaling receptors. Various molecules, including farnesyl transferase-alpha, Mothers against dpp (Mad)-related proteins, and a novel MAPKKK (TAK1), have been suggested to participate in the signal transduction of TGF-beta receptors. TGF-beta receptors and Mad-related proteins have been found to act as tumor suppressor genes in various tumors, including colorectal cancers and T-cell lymphoma.
转化生长因子-β（TGF-β）抑制多种细胞类型的生长，包括造血细胞和淋巴细胞。TGF-β通过两种不同类型的丝氨酸/苏氨酸激酶受体，即I型（TβR-I）和II型（TβR-II）转导信号。TβR-II是配体的主要结合蛋白，而TβR-I是效应蛋白，它决定信号的特异性。III型受体（β聚糖）和内皮糖蛋白发挥更间接的作用；即，将配体递送至信号受体。包括法尼基转移酶-α、抗dpp母亲相关蛋白（Mad）和一种新型丝裂原活化蛋白激酶激酶激酶（TAK1）在内的各种分子已被认为参与TGF-β受体的信号转导。TGF-β受体和Mad相关蛋白已被发现在包括结直肠癌和T细胞淋巴瘤在内的各种肿瘤中作为肿瘤抑制基因发挥作用。
