Wang Dandan, Zhou Weijie, Chen Jingyu, Wei Wei
Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China.
Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Hefei, China.
J Cell Physiol. 2019 Sep;234(9):14460-14472. doi: 10.1002/jcp.28215. Epub 2019 Feb 2.
Phosphoinositide 3-kinase (PI3K), a crucial signaling molecule, is regulated by various upstream regulators. Traditionally, receptor tyrosine kinases and G protein-coupled receptor are regarded as its principle upstream regulators; however, recent reports have indicated that spleen tyrosine kinase, β-arrestin2, Janus kinase, and RAS can also perform this role. Dysregulation of PI3K is common in the progression of various diseases, including, but not limited to, tumors, Alzheimer's disease, Parkinson's disease, rheumatoid arthritis, and acute myelogenous leukemia. The aim of this review is to provide a perspective on PI3K-related diseases examining both the classical and nonclassical upstream regulators of PI3K in detail.
磷脂酰肌醇3激酶（PI3K）是一种关键的信号分子，受多种上游调节因子调控。传统上，受体酪氨酸激酶和G蛋白偶联受体被视为其主要上游调节因子；然而，最近的报道表明，脾酪氨酸激酶、β-抑制蛋白2、Janus激酶和RAS也能发挥这一作用。PI3K失调在各种疾病的进展中很常见，包括但不限于肿瘤、阿尔茨海默病、帕金森病、类风湿性关节炎和急性髓性白血病。本综述的目的是详细研究PI3K的经典和非经典上游调节因子，从而对PI3K相关疾病提供一种观点。
