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首页> 外文期刊>Cellular Physiology and Biochemistry >The transcription factors NFAT and CREB have different susceptibilities to the reduced ca responses caused by the knock down of inositol trisphosphate receptor in HEK 293A cells
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The transcription factors NFAT and CREB have different susceptibilities to the reduced ca responses caused by the knock down of inositol trisphosphate receptor in HEK 293A cells

机译：转录因子NFAT和CREB对HEK 293A细胞中的肌醇三磷酸受体敲低引起的ca反应减少的敏感性不同

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Background/Aims: The inositol 1,4,5-trisphosphate receptor (IP _3R), a ligand-gated Ca~(2+) channel, plays an important role in the control of intracellular Ca~(2+). Three isoforms of IP _3R have been identified and most cell types express different proportions of these isoforms. The purpose of this study was to investigate how IP_3R signalling is involved in the activation of the Ca ~(2+)-sensitive transcription factors NFAT and CREB. Methods: Each IP_3R isoform expressed in HEK 293A cells was knocked down using selective siRNA. Free intracellular Ca~(2+) was monitored spectrofluometrically. NFAT and CREB activities were measured with luciferase reporter constructs. Results: IP_3R-2-knocked down HEK 293A cells showed a deficient CCh-induced Ca~(2+) response that could be rescued by co-stimulation with VIP, a cAMP increasing agonist. NFAT transcriptional activity, but not CREB transcriptional activity, was significantly reduced in IP_3R-2-knocked down HEK 293A cells. Overexpression of IP _3R-1 could fully compensate for IP_3R-2 knock down to mobilize Ca~(2+) and to activate NFAT. Conclusion: Our results show that the knock down of IP_3R-2 significantly reduced the intracellular Ca~(2+) response of HEK 293 cells. This reduced Ca~(2+) response did not affect the activation of CREB but significantly decreased the activation of NFAT, suggesting that the Ca~(2+) signals required for the activation of NFAT are stronger than those required for the activation of CREB.
机译：背景/目的：肌醇1,4,5-三磷酸受体（IP _3R）是配体门控的Ca〜（2+）通道，在细胞内Ca〜（2+）的控制中起着重要的作用。已鉴定出IP _3R的三种同工型，大多数细胞类型表达这些同工型的不同比例。这项研究的目的是调查IP_3R信号如何参与Ca〜（2+）敏感转录因子NFAT和CREB的激活。方法：使用选择性siRNA敲除HEK 293A细胞中表达的每个IP_3R同工型。分光光度法监测游离的细胞内Ca〜（2+）。用荧光素酶报道基因构建物测量NFAT和CREB活性。结果：击倒的IP_3R-2-HEK 293A细胞显示出不足的CCh诱导的Ca〜（2+）反应，可以通过与cAMP增加的激动剂VIP共同刺激来挽救。在IP_3R-2-敲低的HEK 293A细胞中，NFAT转录活性而不是CREB转录活性显着降低。 IP _3R-1的过表达可以完全补偿IP_3R-2的敲低，从而动员Ca〜（2+）和激活NFAT。结论：我们的结果表明，敲低IP_3R-2可以显着降低HEK 293细胞的细胞内Ca〜（2+）反应。这种降低的Ca〜（2+）反应不会影响CREB的激活，但会显着降低NFAT的激活，这表明NFAT激活所需的Ca〜（2+）信号比CREB激活所需的信号更强。 。

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