Kuida Keisuke, Boucher Diane M
Vertex Pharmaceuticals, 130 Waverly Street, Cambridge, MA 02139, USA.
J Biochem. 2004 Jun;135(6):653-6. doi: 10.1093/jb/mvh078.
Mitogen-activated protein kinases (MAPKs) comprise a family of well-conserved serine/threonine kinases that control a vast array of physiological functions in a number of organisms ranging from yeast to mammals. Recently gene-targeting experiments have shed light on in vivo functions of MAPKs. In particular, embryos deficient in extracellular signal-regulated kinase (ERK) 2 lack mesoderm differentiation and placental angiogenesis. Knockout mice for c-Jun amino-terminal kinases have revealed roles for these kinases in neural apoptosis and activation/differentiation of T cells. Deletion of p38alpha MAPK results in angiogenic defects in the placenta and peripheral vessels. ERK5-deficient embryos are embryonic lethal due to defects in angiogenesis and cardiovascular development. Although these results have provided new insights for MAPK research, development and analysis of conditional knockout mice are required in order to investigate roles of MAPKs, especially, in other biological processes such as disease pathogenesis.
丝裂原活化蛋白激酶（MAPK）是一类高度保守的丝氨酸/苏氨酸激酶家族，在从酵母到哺乳动物的多种生物中控制着大量的生理功能。最近，基因靶向实验揭示了MAPK的体内功能。特别是，缺乏细胞外信号调节激酶（ERK）2的胚胎缺乏中胚层分化和胎盘血管生成。c-Jun氨基末端激酶基因敲除小鼠揭示了这些激酶在神经细胞凋亡以及T细胞活化/分化中的作用。p38α MAPK的缺失导致胎盘和外周血管的血管生成缺陷。ERK5缺陷型胚胎由于血管生成和心血管发育缺陷而胚胎致死。尽管这些结果为MAPK研究提供了新的见解，但仍需要开发和分析条件性基因敲除小鼠，以便研究MAPK在其他生物学过程（尤其是疾病发病机制）中的作用。
