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c-mos蛋白激酶的抑制作用使小鼠受精卵阻滞在原核期。

Inhibition of c-mos protein kinase blocks mouse zygotes at the pronuclei stage.

作者信息

Zhao X, Singh B, Arlinghaus R B

机构信息

Department of Medicine, Stanford University School of Medicine, California 94305.

出版信息

Oncogene. 1991 Aug;6(8):1423-6.

PMID:1832216
Abstract

The c-mos gene product is required for activation of the maturation-promoting factor (MPF) during oocyte maturation. The c-mos protein also acts as a cytostatic factor which is responsible for meiotic metaphase arrest of vertebrate eggs via stabilization of MPF. Here we show that mouse zygotes contain the c-mos protein. Introduction of a kinase-inhibitory anti-mos antibody into mouse zygotes 12 h after fertilization prevented the first cleavage of zygotes at the pronuclei stage. A second anti-mos antibody, known to allow the mos kinase to function, did not interfere with the formation of two-cell embryos. In addition to its known role in MPF activation in oocyte maturation and meiotic metaphase arrest, our findings indicate that the c-mos protein kinase is also required for completion of pronuclei breakdown following fertilization of mouse eggs.

摘要

c-mos基因产物是卵母细胞成熟过程中激活促成熟因子(MPF)所必需的。c-mos蛋白还作为一种细胞静止因子,通过稳定MPF负责脊椎动物卵子的减数分裂中期阻滞。在此我们表明,小鼠受精卵含有c-mos蛋白。在受精后12小时将一种激酶抑制性抗mos抗体引入小鼠受精卵,可阻止受精卵在原核阶段的首次卵裂。另一种已知可使mos激酶发挥功能的抗mos抗体,不会干扰二细胞胚胎的形成。除了其在卵母细胞成熟和减数分裂中期阻滞中MPF激活的已知作用外,我们的研究结果表明,c-mos蛋白激酶对于小鼠卵子受精后原核破裂的完成也是必需的。

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