Here, we discuss the transition model of receptor tyrosine kinase (RTK) activation, which is derived from biophysical investigations of RTK interactions and signaling. The model postulates that (1) RTKs can interact laterally to form dimers even in the absence of ligand, (2) different unliganded RTK dimers have different stabilities, (3) ligand binding stabilizes the RTK dimers, and (4) ligand binding causes structural changes in the RTK dimer. The model is grounded in the principles of physical chemistry and provides a framework to understand RTK activity and to make predictions in quantitative terms. It can guide basic research aimed at uncovering the mechanism of RTK activation and, in the long run, can empower the search for modulators of RTK function.

在这里，我们讨论受体酪氨酸激酶 (RTK) 激活的转变模型，该模型源自 RTK 相互作用和信号传导的生物物理学研究。该模型假设 (1) 即使在没有配体的情况下，RTK 也可以横向相互作用形成二聚体，(2) 不同的未配体 RTK 二聚体具有不同的稳定性，(3) 配体结合稳定 RTK 二聚体，(4) 配体结合导致结构RTK 二聚体的变化。该模型以物理化学原理为基础，提供了一个了解 RTK 活动并进行定量预测的框架。它可以指导旨在揭示 RTK 激活机制的基础研究，从长远来看，可以促进 RTK 功能调节剂的寻找。