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非洲爪蟾卵母细胞成熟过程中成熟促进因子的诱导使钙库耗竭与钙库操纵性钙内流解偶联。

Induction of maturation-promoting factor during Xenopus oocyte maturation uncouples Ca(2+) store depletion from store-operated Ca(2+) entry.

作者信息

Machaca Khaled, Haun Shirley

机构信息

Department of Physiology and Biophysics, University of Arkansas Medical Science, Little Rock, 72205, USA.

出版信息

J Cell Biol. 2002 Jan 7;156(1):75-85. doi: 10.1083/jcb.200110059.

Abstract

During oocyte maturation, eggs acquire the ability to generate specialized Ca(2+) signals in response to sperm entry. Such Ca(2+) signals are crucial for egg activation and the initiation of embryonic development. We examined the regulation during Xenopus oocyte maturation of store-operated Ca(2+) entry (SOCE), an important Ca(2+) influx pathway in oocytes and other nonexcitable cells. We have previously shown that SOCE inactivates during Xenopus oocyte meiosis. SOCE inactivation may be important in preventing premature egg activation. In this study, we investigated the correlation between SOCE inactivation and the Mos-mitogen-activated protein kinase (MAPK)-maturation-promoting factor (MPF) kinase cascade, which drives Xenopus oocyte maturation. SOCE inactivation at germinal vesicle breakdown coincides with an increase in the levels of MAPK and MPF. By differentially inducing Mos, MAPK, and MPF, we demonstrate that the activation of MPF is necessary for SOCE inactivation during oocyte maturation. In contrast, sustained high levels of Mos kinase and the MAPK cascade have no effect on SOCE activation. We further show that preactivated SOCE is not inactivated by MPF, suggesting that MPF does not block Ca(2+) influx through SOCE channels, but rather inhibits coupling between store depletion and SOCE activation.

摘要

在卵母细胞成熟过程中,卵子获得了响应精子进入而产生特殊Ca(2+)信号的能力。这种Ca(2+)信号对于卵子激活和胚胎发育的启动至关重要。我们研究了非洲爪蟾卵母细胞成熟过程中储存操纵性Ca(2+)内流(SOCE)的调控,SOCE是卵母细胞和其他非兴奋性细胞中一种重要的Ca(2+)内流途径。我们之前已经表明,非洲爪蟾卵母细胞减数分裂过程中SOCE会失活。SOCE失活可能在防止卵子过早激活方面很重要。在本研究中,我们调查了SOCE失活与Mos-丝裂原活化蛋白激酶(MAPK)-成熟促进因子(MPF)激酶级联反应之间的相关性,该激酶级联反应驱动非洲爪蟾卵母细胞成熟。生发泡破裂时SOCE失活与MAPK和MPF水平的增加同时发生。通过差异诱导Mos、MAPK和MPF,我们证明MPF的激活是卵母细胞成熟过程中SOCE失活所必需的。相反,持续高水平的Mos激酶和MAPK级联反应对SOCE激活没有影响。我们进一步表明,预激活的SOCE不会被MPF失活,这表明MPF不会通过SOCE通道阻断Ca(2+)内流,而是抑制储存耗竭与SOCE激活之间的偶联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b6b/2173586/d56c04542030/0110059f1.jpg

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