Molecular mechanism of induction of labor via placental protein kinase Nrk

Nrk（NIK-related kinase）是一种功能未知的丝氨酸/苏氨酸蛋白激酶。为了阐明Nrk的生理作用，我们培养了一种靶向破坏X染色体上Nrk基因的小鼠。Nrk基因敲除导致胎盘过度生长，表明Nrk是胎盘细胞增殖的关键调节因子。此外，当Nrk-null胎儿占主导地位时，怀孕的水坝无法在足月分娩后代。因此，Nrk似乎对分娩很重要。为了研究导致Nrk敲除表型的分子机制，我们利用高效双向电泳方法，将Nrk敲除胎盘中的蛋白表达水平与野生型组织中的蛋白表达水平进行了比较，发现Nrk敲除胎盘中有几个显著的蛋白点的表达水平显著增强或降低。我们的检查是胎盘还是胎儿对分娩至关重要，目前正在进行中。

Nrk(NIK-related kinase) is a functionally unknown Ser/Thr protein kinase. To elucidate the physiological roles of Nrk, we generated a strain of mice with targeted disruption of the Nrk gene in the X chromosome. The Nrk gene knockout causes overgrowth of the placenta, indicating that Nrk is a key regulator of placental cellular proliferation. In addition, when the Nrk-null fetuses were dominant, the pregnant dam failed to deliver offspring at term. Thus, Nrk appears to be important for performing parturition.In order to investigate the molecular mechanisms leading to the Nrk knockout phenotype, protein expression levels in the Nrk knockout placenta were compared with those in wild type tissues by using high-performance two-dimensional electrophoresis methodology, and found several significant protein spots whose expression levels were enhanced or diminished significantly in the Nrk knockout placenta. Our examine whether placentas or fetus are essential for labor is now in progress.