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小鼠减数分裂成熟对c-mos蛋白激酶的需求。

Requirement of the c-mos protein kinase for murine meiotic maturation.

作者信息

Zhao X, Batten B, Singh B, Arlinghaus R B

机构信息

Department of Anatomy, Ohio State University, Columbus 43210.

出版信息

Oncogene. 1990 Nov;5(11):1727-30.

PMID:2176285
Abstract

Anti-sense mos oligonucleotides have been shown to block steps required for meiotic maturation of oocytes. In Xenopus oocytes, the block prevents germinal vesicle breakdown (GVBD), an early step in oocyte maturation. In mice the block induced by anti-sense mos occurs at a later step in oocyte maturation concerned with the first polar body emission. Here, we show that mouse oocyte maturation is blocked by introduction of anti-mos antibodies into immature functional oocytes. Antibodies that inhibit the mos kinase blocked GVBD. In contrast, anti-mos antibodies that permit the mos kinase to function do not block GVBD, but interfere with polar body formation. Antibodies pre-reacted with excess cognate peptide had no observable effects on maturation. These results indicate that the c-mos kinase function is required for activation of maturation-promoting factor (MPF) during meiosis. These findings are also consistent with our previous studies which show that the mos kinase directly phosphorylates cyclin B2, a component of MPF (Roy et al., 1990).

摘要

反义mos寡核苷酸已被证明可阻断卵母细胞减数分裂成熟所需的步骤。在非洲爪蟾卵母细胞中,这种阻断可防止生发泡破裂(GVBD),这是卵母细胞成熟的早期步骤。在小鼠中,反义mos诱导的阻断发生在卵母细胞成熟的后期,与第一极体排放有关。在此,我们表明,将抗mos抗体引入未成熟的功能性卵母细胞可阻断小鼠卵母细胞的成熟。抑制mos激酶的抗体可阻断GVBD。相反,允许mos激酶发挥作用的抗mos抗体不会阻断GVBD,但会干扰极体形成。与过量同源肽预反应的抗体对成熟没有可观察到的影响。这些结果表明,c-mos激酶功能是减数分裂期间激活成熟促进因子(MPF)所必需的。这些发现也与我们之前的研究一致,我们之前的研究表明mos激酶直接磷酸化MPF的一个组分细胞周期蛋白B2(罗伊等人,1990年)。

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