外在因素包括生长因子对少突胶质祖细胞（OPCs）的影响决定了该细胞的细胞周期进程以及末期产生髓鞘的少突胶质细胞分化。
多项研究已经阐明了G1/S在OPCs中是人合伙被调控的，然而很少有人知道如何S期和G2/M过渡期在这些细胞中是如何被调控的。
近日，一项研究报告阐明了胰岛素样生长因子（IGF）与FGF-2共同促进S期进展，但胰岛素样生长因子能单独影响G2/M期的进展。
在S期中，I GF-I/FGF-2提高蛋白cyclin A和CDK2的表达，并进一步增加有效复合物的形成，增强CDK2的活性。
然而，令人惊讶的是，OPCs只暴露在FGF-2环境下，在不存在IGF-I时，少突胶质祖细胞不会进入G2/M期。而OPCs暴露于IGF-I环境下，但FGF-2不存在的情况下，细胞数目持续增加超过48小时。研究数据表明IGF-I对少突胶质祖细胞G2/M的调控作用。（生物谷：Bioon.com）
编译自：Insulin-like growth factor I regulates G2/M progression through mammalian target of rapamycin signaling in oligodendrocyte progenitors
doi:10.1002/glia.22387
PMC:
PMID:
Insulin-like growth factor I regulates G2/M progression through mammalian target of rapamycin signaling in oligodendrocyte progenitors
Jungsoo Min1, Sukhwinder Singh2, Patricia Fitzgerald-Bocarsly2, Teresa L. Wood1,*
Extrinsic factors including growth factors influence decisions of oligodendrocyte progenitor cells (OPCs) to continue cell cycle progression or exit the cell cycle and terminally differentiate into oligodendrocytes capable of producing myelin. Multiple studies have elucidated how the G1/S transition is regulated in OPCs; however, little is known about how S phase progression and the G2/M transition are regulated in these cells. Herein, we report that insulin-like growth factor (IGF)-I coordinates with FGF-2 to promote S phase progression but regulates G2/M progression independently. During S phase, IGF-I/FGF-2 enhances protein expression of cyclin A and cdk2, and further increases effective complex formation resulting in enhanced cdk2 activity. Surprisingly, however, OPCs exposed to FGF-2 in the absence of IGF-I fail to traverse through G2/M. Consistent with this observation, OPCs exposed to IGF-I, but not FGF-2, increase cell number over 48 h. IGF-I enhances cdk1 kinase activity during G2/M by promoting nuclear localization of cyclin B/cdk1 as well as of Cdc25C, an activator of cdkIGF-I also induces phosphorylation of histone 3 indicating traverse of cells through mitosis. Finally, we demonstrate that IGF-I-mediated G2/M regulation requires mammalian target of rapamycin activity. These data support an important function for IGF-I in G2/M progression in OPCs.
