• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Biochemical Journal >Extracellular nucleotides stimulate receptor-mediated calcium mobilization and inositol phosphate production in human fibroblasts.
【2h】

Extracellular nucleotides stimulate receptor-mediated calcium mobilization and inositol phosphate production in human fibroblasts.

机译：细胞外核苷酸刺激人类成纤维细胞中受体介导的钙动员和磷酸肌醇生成。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In human skin fibroblasts, low concentrations of extracellular ATP stimulated 45Ca2+ efflux from a slow-turnover intracellular pool, accompanied by inositol phosphate generation. These effects of ATP were not due to a generalized increase in plasma-membrane permeability. The EC50 (concn. giving 50% stimulation) for ATP was dependent on Ca2+ and Mg2+ concentrations in a manner which indicates that a form of ATP uncomplexed with bivalent cations is the active species. The rank order of potency of nucleotides was: ATP = UTP greater than adenosine 5'-[gamma-thio]triphosphate greater than ITP greater than ADP greater than UDP greater than other nucleoside triphosphates. Adenosine 5'-[alpha beta-methylene]triphosphate, adenosine 5'-[beta gamma-methylene]triphosphate and 2-methylthio-ATP were inactive. Thus the nucleotide specificity of this receptor is different from that of previously characterized P2 purinoceptors. Nucleotide-stimulated 45Ca2+ mobilization and inositol phosphate production were markedly inhibited by phorbol ester, and partially inhibited by pertussis-toxin pretreatment. These findings suggest that the coupling of nucleotide receptor to phospholipase C is mediated both by a pertussis-toxin-sensitive G-protein and by a pertussis-toxin-insensitive mechanism.
机译：在人类皮肤成纤维细胞中，低浓度的细胞外ATP刺激了来自缓慢转变的细胞内池的45Ca2 +外排，并伴随着肌醇磷酸的产生。 ATP的这些作用并非归因于血浆膜通透性的普遍提高。 ATP的EC50（持续给予50％的刺激）取决于Ca2 +和Mg2 +的浓度，这表明未与二价阳离子复合的ATP形式是活性物质。核苷酸效力的等级顺序为：ATP = UTP大于腺苷5'-γ-硫代三磷酸大于ITP大于ADP大于UDP大于其他核苷三磷酸。腺苷5'-α-β-亚甲基三磷酸腺苷，腺苷5'-β-γ-亚甲基三磷酸腺苷和2-甲硫基-ATP无效。因此，该受体的核苷酸特异性不同于先前表征的P2嘌呤受体。佛波酯显着抑制核苷酸刺激的45Ca2 +动员和磷酸肌醇生成，而百日咳毒素预处理则部分抑制核苷酸刺激。这些发现表明核苷酸受体与磷脂酶C的偶联是由百日咳毒素敏感的G蛋白和百日咳毒素不敏感的机制介导的。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号