共查询到20条相似文献,搜索用时 31 毫秒
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Cooperative interactions between CBP and TORC2 confer selectivity to CREB target gene expression 总被引:2,自引:0,他引:2
Ravnskjaer K Kester H Liu Y Zhang X Lee D Yates JR Montminy M 《The EMBO journal》2007,26(12):2880-2889
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为了研究 C B P在胰岛 H I T 细胞中调节基因转录的机制,将不同的 C B P片段瞬时转染到细胞中,观察其转录活性.实验表明,在胰岛 H I T 细胞中,膜去极化及 c A M P 均可诱导 C B P30( C R E B结合功能区)转录活性增强,并有协同效应. P K C对 C B P30 的转录活性无影响;与 C R E B有更强结合力的 C B P K I X S/ B(氨基酸序列短于 C B P30 的 C R E B结合功能区)其基本转录活性及膜去极化、c A M P诱导下的转录活性均比 C B P30 更强.反义 C R E B 的过度表达可降低 c A M P诱导的 C B P的转录活性.提示在胰岛 H I T 细胞中,膜去极化及 c A M P对共转录因子 C B P转录活性的调节作用通过 C R E B介导. 相似文献
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Ng SW di Capite J Singaravelu K Parekh AB 《The Journal of biological chemistry》2008,283(46):31348-31355
Mast cell activation involves cross-linking of IgE receptors followed by phosphorylation of the non-receptor tyrosine kinase Syk. This results in activation of the plasma membrane-bound enzyme phospholipase Cgamma1, which hydrolyzes the minor membrane phospholipid phosphatidylinositol 4,5-bisphosphate to generate diacylglycerol and inositol trisphosphate. Inositol trisphosphate raises cytoplasmic Ca2+ concentration by releasing Ca2+ from intracellular stores. This Ca2+ release phase is accompanied by sustained Ca2+ influx through store-operated Ca2+ release-activated Ca2+ (CRAC) channels. Here, we find that engagement of IgE receptors activates Syk, and this leads to Ca2+ release from stores followed by Ca2+ influx. The Ca2+ influx phase then sustains Syk activity. The Ca2+ influx pathway activated by these receptors was identified as the CRAC channel, because pharmacological block of the channels with either a low concentration of Gd3+ or exposure to the novel CRAC channel blocker 3-fluoropyridine-4-carboxylic acid (2',5'-dimethoxybiphenyl-4-yl)amide or RNA interference knockdown of Orai1, which encodes the CRAC channel pore, all prevented the increase in Syk activity triggered by Ca2+ entry. CRAC channels and Syk are spatially close together, because increasing cytoplasmic Ca2+ buffering with the fast Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis failed to prevent activation of Syk by Ca2+ entry. Our results reveal a positive feedback step in mast cell activation where receptor-triggered Syk activation and subsequent Ca2+ release opens CRAC channels, and the ensuing local Ca2+ entry then maintains Syk activity. Ca2+ entry through CRAC channels therefore provides a means whereby the Ca2+ and tyrosine kinase signaling pathways can interact with one another. 相似文献
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在胰岛细胞株 H I T 细胞中,用瞬时转染法观察高 K+ 导致的膜去极化与c A M P对 C B P C端片段转录活性的影响.发现二者均可诱导 C B P C端片段的转录活性增强,并有协同效应; C B P C端片段的突变体( Ser 1 772 突变为 Ala)表现相同的诱导特性,但其基本转录活性降低.说明膜去极化和 c A M P对 C B P C 端片段转录活性的诱导作用与 P K A 磷酸化位点 Ser 1 772 无关,而该位点的磷酸化对调节 C B P C 端片段的基本转录活性起重要作用.蛋白激酶 C 通路对 C B P Ti的转录活性无影响. 相似文献
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