Xia Ying, Karin Michael
Center for Environmental Genetics and Department of Environmental Health, University of Cincinnati Medical Center, 123 East Shields Street, Cincinnati, OH 45267-0056, USA.
Trends Cell Biol. 2004 Feb;14(2):94-101. doi: 10.1016/j.tcb.2003.12.005.
Originally identified as stress-activated protein kinases that control cell survival and proliferation through transcription factor c-Jun, the Jun N-terminal kinase (JNK) subgroup of MAP kinases (MAPKs) have recently emerged as crucial regulators of cell migration and the morphogenetic movement of epithelial sheets. In Drosophila, a well-orchestrated JNK signaling pathway controls formation of actin stress fibers and cell shape changes, which are required for the sealing of embryonic epidermis in a process known as dorsal closure. The JNK pathway is also involved in morphogenetic processes in mice including closure of the eyelid, neural tube and optic fissure. This article focuses on recent advances in understanding the role of JNK pathway in the regulation of cell migration, cytoskeleton rearrangement and the morphogenesis of epithelial sheets.
最初被鉴定为通过转录因子c-Jun控制细胞存活和增殖的应激激活蛋白激酶，丝裂原活化蛋白激酶（MAPKs）的Jun氨基末端激酶（JNK）亚组最近已成为细胞迁移和上皮细胞层形态发生运动的关键调节因子。在果蝇中，一条精心编排的JNK信号通路控制着肌动蛋白应激纤维的形成和细胞形状的变化，这是胚胎表皮在一个称为背侧闭合的过程中密封所必需的。JNK通路也参与小鼠的形态发生过程，包括眼睑、神经管和视裂的闭合。本文重点介绍了在理解JNK通路在调节细胞迁移、细胞骨架重排和上皮细胞层形态发生中的作用方面的最新进展。
