Wiley H S, Burke P M
Environmental and Health Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA.
Traffic. 2001 Jan;2(1):12-8. doi: 10.1034/j.1600-0854.2001.020103.x.
Activated receptor tyrosine kinase (RTK) receptors are rapidly internalized and eventually delivered to the lysosomes. Although ligand-induced endocytosis was originally thought to be a mechanism of receptor inactivation, many studies suggest that receptors remain active within endosomes. This review discusses the role that internalized signaling complexes may play in different RTK systems including recent data on how ubiquitination may regulate this process. In general, it appears that some receptor systems have evolved to enhance endosomal signaling, as is the case for TrkA and NGF. In contrast, the insulin receptor system appears to limit the extent of endosomal signaling. The EGFR system is the intermediate example. In this case, some signals are specifically generated from the cell surface while others appear to be generated from within endosomes. This may act as a mechanism to produce ligand-specific signals. Thus, trafficking could play diverse roles in receptor signaling, depending on the specific cell and tissue type.
活化的受体酪氨酸激酶(RTK)受体迅速内化,最终被转运至溶酶体。尽管配体诱导的内吞作用最初被认为是一种受体失活机制,但许多研究表明,受体在内体中仍保持活性。本综述讨论了内化信号复合物在不同RTK系统中可能发挥的作用,包括关于泛素化如何调节这一过程的最新数据。一般来说,某些受体系统似乎已经进化以增强内体信号传导,如TrkA和神经生长因子(NGF)的情况。相反,胰岛素受体系统似乎限制了内体信号传导的程度。表皮生长因子受体(EGFR)系统则是中间例子。在这种情况下,一些信号是在细胞表面特异性产生的,而其他信号似乎是在内体中产生的。这可能作为产生配体特异性信号的一种机制。因此,根据特定的细胞和组织类型,转运在受体信号传导中可能发挥多种作用。