Kelkar Nyaya, Delmotte Marie-Helene, Weston Claire R, Barrett Tamera, Sheppard Barbara J, Flavell Richard A, Davis Roger J
Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.
Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9843-8. doi: 10.1073/pnas.1733944100. Epub 2003 Aug 1.
The murine JNK-interacting protein 3 (JIP3) protein (also known as JSAP1) is expressed exclusively in neurons and has been identified as a scaffold protein for the c-Jun NH2-terminal kinase (JNK) signaling pathway and as an adapter protein for cargo transport by the microtubule motor protein kinesin. To investigate the physiological function of JIP3, we examined the effect of Jip3 gene disruption in mice. The Jip3-/- mice were unable to breathe and died shortly after birth. Microscopic analysis demonstrated that Jip3 gene disruption causes severe defects in the morphogenesis of the telencephalon. Jip3-/- mice lack the telencephalic commissure, a major connection between the left and right hemispheres of the brain. The central nervous system abnormalities of Jip3-/- mice may be accounted for in part by a reduction in signal transduction by RhoA and its effector ROCK.
小鼠JNK相互作用蛋白3（JIP3）（也称为JSAP1）仅在神经元中表达，并且已被鉴定为c-Jun NH2末端激酶（JNK）信号通路的支架蛋白以及微管运动蛋白驱动蛋白进行货物运输的衔接蛋白。为了研究JIP3的生理功能，我们检测了Jip3基因敲除对小鼠的影响。Jip3基因敲除小鼠无法呼吸，出生后不久即死亡。显微镜分析表明，Jip3基因敲除会导致端脑形态发生严重缺陷。Jip3基因敲除小鼠缺乏脑连合，而脑连合是大脑左右半球之间的主要连接。Jip3基因敲除小鼠的中枢神经系统异常可能部分归因于RhoA及其效应器ROCK的信号转导减少。
