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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 Ca2+ 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 Ca2+ 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Ca2 +还原反应的敏感性不同。

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Background/Aims The inositol 1,4,5-trisphosphate receptor (IPsub3/subR), a ligand-gated Casup2+/sup channel, plays an important role in the control of intracellular Casup2+/sup. Three isoforms of IPsub3/subR have been identified and most cell types express different proportions of these isoforms. The purpose of this study was to investigate how IPsub3/subR signalling is involved in the activation of the Casup2+/sup-sensitive transcription factors NFAT and CREB. Methods Each IPsub3/subR isoform expressed in HEK 293A cells was knocked down using selective siRNA. Free intracellular Casup2+/sup was monitored spectrofluometrically. NFAT and CREB activities were measured with luciferase reporter constructs. Results IPsub3/subR-2-knocked down HEK 293A cells showed a deficient CCh-induced Casup2+/sup 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 IPsub3/subR-2-knocked down HEK 293A cells. Overexpression of IPsub3/subR-1 could fully compensate for IPsub3/subR-2 knock down to mobilize Casup2+/sup and to activate NFAT. Conclusion Our results show that the knock down of IPsub3/subR-2 significantly reduced the intracellular Casup2+/sup response of HEK 293 cells. This reduced Casup2+/sup response did not affect the activation of CREB but significantly decreased the activation of NFAT, suggesting that the Casup2+/sup 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 3 R）是配体门控的Ca 2 + 通道，在控制肌醇中起重要作用。细胞内Ca 2 + 。已鉴定出IP 3 R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。本研究的目的是研究IP 3 R信号如何参与Ca 2 + 敏感转录因子NFAT和CREB的激活。方法用选择性siRNA敲除HEK 293A细胞中表达的每个IP 3 R同工型。分光光度法监测游离细胞内Ca 2 + 。用荧光素酶报道基因构建物测量NFAT和CREB活性。结果IP 3 R-2-敲除的HEK 293A细胞显示出不足的CCh诱导的Ca 2 + 反应，可以通过与VIP共同刺激来挽救，cAMP增加激动剂。 IP 3 R-2-敲除的HEK 293A细胞的NFAT转录活性显着降低，而CREB转录活性未显着降低。 IP 3 R-1的过表达可以完全补偿IP 3 R-2的敲低，从而动员Ca 2 + 并激活NFAT。结论我们的结果表明，IP 3 R-2的敲低显着降低了HEK 293细胞的细胞内Ca 2 + 反应。减少的Ca 2 + 响应并不影响CREB的激活，但显着降低了NFAT的激活，表明激活NFAT所需的Ca 2 + 信号更强。而不是激活CREB所需的那些。

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