摘要
目的:探讨小鼠卵母细胞G2期阻滞中,AKAP7γ是否是介导蛋白激酶A(protein kinaseA,PKA)锚定在Cdc25B底物蛋白处的A型激酶锚定蛋白(A-kinase anchoring proteins,AKAPs)。方法:以PKA锚定阻断剂Ht31处理G2期阻滞的小鼠卵母细胞,观察Cdc25B-S321的磷酸化状态,以免疫共沉淀方法检测PKA RII-AKAP7γ-Cdc25B的相互作用。结果:在G2期阻滞的小鼠卵母细胞中,Ht31处理后Cdc25B-S321不能被PKA磷酸化,同时PKA RII-AKAP7γ及AKAP7γ-Cdc25B存在相互作用。结论:在小鼠卵母细胞中,PKA通过AKAP7γ锚定在胞质中的Cdc25B底物蛋白处,磷酸化其321位丝氨酸,使卵母细胞减数分裂阻滞在G2期,PKA RII-AKAP7γ/Cdc25B通路在小鼠卵母细胞减数分裂阻滞中发挥重要作用。
Objective： To seek whether the A-kinase anchoring proteins 7y（AKAPs） regulates the association of PKA and Cdc25B in G2-arrested mouse oocytes, Methods： Ht31 was used to disrupt the association of PKA and its substrates and phosphorylation status of Cdc25B-S321 was examined. The co-immunoprecipita- tion was used to examine the interaction of PKA RII-AKAP7y and AKAP7y-Cdc25B. Results： Phosphorylation reaction mediated by Cdc25B-S321 associated PKA II was inhibited by Ht31 peptide but not by the control peptide Ht31-P. AKAP7y bound PKA RII in overlay assays and also was immunoprecipitated with Cdc25B from G2-arrested mouse oocytes. Conclusion： PKA II is linked physically and functionally to Cdc25B by AKAP interaction, and AKAP7y serves as an AKAP for PKA-mediated phosphorylation of Cdc25B-S321.
出处
《生殖与避孕》
CAS
CSCD
2012年第5期289-292,共4页
Reproduction and Contraception
基金
国家自然科学基金青年基金项目(30800392)
辽宁省教育厅一般项目(2008807)资助
