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首页> 外文期刊>Journal of cellular biochemistry. >Regulation of inducible bradykinin B1 receptor gene expression through absence of internalization and resensitization.
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Regulation of inducible bradykinin B1 receptor gene expression through absence of internalization and resensitization.

机译：通过缺乏内在化和重新敏化来调节诱导型缓激肽B1受体基因的表达。

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Rapid induction and down-regulation of bradykinin B1 receptor (BKB1R) gene expression is tightly regulated at the transcriptional and mRNA levels (Zhou et al. [1998] Biochem. J. 330:361-366; Zhou et al. [1999] Mol. Cell Biol. Res. Commun. 1:29-35). Here we explore regulation of BKB1R expression at the protein level. To make this inducible gene express constitutively, we utilized a bicistronic mammalian expression vector (pCMin) for stable transfection of the BKB1R gene into human lung fibroblasts, IMR90SV40. The BKB1R displayed a high affinity and specificity (K(d) = 0.5 nM) for desArg(10)-kallidin. The receptor mediated such signaling events as arachidonic acid (ARA) release, phosphoinositide (PI) turnover and Ca(2+)-flux. The receptor function proved differentially desensitized. For example, after initial exposure to desArg(10)-kallidin, a second stimulation with desArg(10)-kallidin did not induce further Ca(2+)-flux or ARA-release while PI-turnover continued unabated. Unlike most of the G-protein coupled receptors, the BKB1R did not internalize within 60 min of exposure to 10 nM desArg(10)-kallidin. It also did not resensitize. Thus, the duration and signal capacity of the BKB1R at the protein level is regulated through lack of internalization, an absence of resensitization and a lack of desensitization for certain events such as PI turnover. In fact, the absence of BKB1R resensitization is likely a very important contributor to the rapid disappearance of this inducible receptor. Copyright 2000 Wiley-Liss, Inc.
机译：缓激肽B1受体（BKB1R）基因表达的快速诱导和下调在转录和mRNA水平上受到严格调节（Zhou等[1998] Biochem。J. 330：361-366; Zhou等[1999] Mol （Cell Biol.Res.Commun.1：29-35）。在这里，我们探讨蛋白质水平上的BKB1R表达的调节。为了使该可诱导基因组成型表达，我们利用双顺反子哺乳动物表达载体（pCMin）将BKB1R基因稳定转染到人肺成纤维细胞IMR90SV40中。 BKB1R对desArg（10）-kallidin表现出高亲和力和特异性（K（d）= 0.5 nM）。该受体介导诸如花生四烯酸（ARA）释放，磷酸肌醇（PI）营业额和Ca（2 +）-通量这样的信号事件。受体功能被证明是差异性脱敏的。例如，在最初暴露于desArg（10）-kallidin之后，使用desArg（10）-kallidin进行的第二次刺激不会诱导进一步的Ca（2+）助焊剂或ARA释放，而PI转换持续不断。与大多数G蛋白偶联受体不同，BKB1R在暴露于10 nM desArg（10）-kallidin的60分钟内没有内在化。它也没有重新敏感。因此，BKB1R在蛋白质水平上的持续时间和信号容量是通过缺乏内在化，缺乏重新敏感性和缺乏对某些事件（如PI转换）的脱敏性来调节的。实际上，缺乏BKB1R再敏化可能是该诱导型受体迅速消失的重要原因。版权所有2000 Wiley-Liss，Inc.

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