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孕酮诱导两栖类卵母细胞第一次减数分裂期间电生性钠钾ATP酶的下调。

Progesterone-induced down-regulation of electrogenic Na+, K+-ATPase during the first meiotic division in amphibian oocytes.

作者信息

Weinstein S P, Kostellow A B, Ziegler D H, Morrill G A

出版信息

J Membr Biol. 1982;69(1):41-8. doi: 10.1007/BF01871240.

Abstract

Progesterone initiates the resumption of the meiotic divisions in the amphibian oocyte. Depolarization of the Rama pipiens oocyte plasma membrane begins 6-10 hr after exposure to progesterone (1-2 hr before nuclear breakdown). The oocyte cytoplasm becomes essentially isopotential with the medium by the end of the first meiotic division (20-22 hr). Voltage-clamp studies indicate that the depolarization coincides with the disappearance of an electrogenic Na+, K+-pump, and other electrophysiological studies indicate a decrease in both K+ and Cl- conductances of the oocyte plasma membrane. Measurement of [3H]-ouabain binding to the plasma-vitelline membrane complex indicates that there are high-affinity (Kd = 4.2 x 10-8M), K+-sensitive ouabain-binding sites on the unstimulated (prophase-arrest) oocyte and that ouabain binding virtually disappears during membrane depolarization. [3H]-Leucine incorporation into the plasma-vitelline membrane complex increased ninefold during depolarization with no significant change in uptake or incorporation into cytoplasmic proteins or acid soluble pool(s). This together with previous findings suggest that progesterone acts at a translational level to produce a cytoplasmic factor(s) that down-regulates the membrane Na+, K+-ATPase and alters the ion permeability and transport properties of both nuclear and plasma membranes.

摘要

孕酮启动两栖类卵母细胞减数分裂的恢复。在暴露于孕酮后6 - 10小时(核破裂前1 - 2小时),牛蛙卵母细胞质膜开始去极化。到第一次减数分裂结束时(20 - 22小时),卵母细胞的细胞质与培养基基本等电位。电压钳研究表明,去极化与生电钠钾泵的消失同时发生,其他电生理研究表明卵母细胞质膜的钾离子和氯离子电导均降低。对结合于质膜 - 卵黄膜复合物的[³H] - 哇巴因的测量表明,在未受刺激(减数分裂前期停滞)的卵母细胞上存在高亲和力(Kd = 4.2×10⁻⁸M)、对钾离子敏感的哇巴因结合位点,且在膜去极化过程中哇巴因结合几乎消失。在去极化过程中,[³H] - 亮氨酸掺入质膜 - 卵黄膜复合物增加了9倍,但对细胞质蛋白或酸溶性池的摄取或掺入没有显著变化。这与先前的研究结果共同表明,孕酮在翻译水平起作用,产生一种细胞质因子,该因子下调膜钠钾ATP酶,并改变核膜和质膜的离子通透性及转运特性。

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