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促黄体生成素释放激素增强大鼠颗粒细胞中的多磷酸肌醇分解。

Luteinizing hormone-releasing hormone enhances polyphosphoinositide breakdown in rat granulosa cells.

作者信息

Ma F, Leung P C

出版信息

Biochem Biophys Res Commun. 1985 Aug 15;130(3):1201-8. doi: 10.1016/0006-291x(85)91742-5.

Abstract

A 2-min addition of LHRH to [3H]inositol-prelabeled rat granulosa cells in primary culture evoked significant increases in the accumulation of [3H]inositol phosphates, i.e. radiolabeled inositol monophosphate (IP), inositol diphosphate (IP2), and inositol triphosphate (IP3) levels increased to 210, 590 and 520%, respectively, when compared to control cultures. By contrast, addition of FSH failed to elicit such a response. The effect of LHRH was completely blocked by the concomitant presence of a specific LHRH antagonist. LHRH evoked increase in [3H]IP3 and [3H]IP2 accumulation as early as 30 sec, while the increase in [3H]IP became significant at 2 min. These data support the hypothesis that polyphosphoinositide breakdown may be an early step in the intracellular signal mechanism which mediates the action of LHRH.

摘要

在原代培养的[³H]肌醇预标记大鼠颗粒细胞中加入促黄体生成素释放激素(LHRH)2分钟,可引起[³H]肌醇磷酸积累显著增加,即放射性标记的肌醇一磷酸(IP)、肌醇二磷酸(IP₂)和肌醇三磷酸(IP₃)水平分别比对照培养物增加至210%、590%和520%。相比之下,添加促卵泡激素(FSH)未能引发这种反应。LHRH拮抗剂的同时存在完全阻断了LHRH的作用。LHRH早在30秒时就引起[³H]IP₃和[³H]IP₂积累增加,而[³H]IP的增加在2分钟时变得显著。这些数据支持了多磷酸肌醇分解可能是介导LHRH作用的细胞内信号机制的早期步骤这一假说。

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