Induction of the mammalian GRP78/BiP gene by Ca2+ depletion and formation of aberrant proteins: activation of the conserved stress-inducible grp core promoter element by the human nuclear factor YY1.

W W Li; Y Hsiung; Y Zhou; B Roy; A S Lee

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Induction of the mammalian GRP78/BiP gene by Ca2+ depletion and formation of aberrant proteins: activation of the conserved stress-inducible grp core promoter element by the human nuclear factor YY1.

机译：Ca2 +耗尽诱导哺乳动物GRP78 / BiP基因并形成异常蛋白：人核因子YY1激活保守的应激诱导性grp核心启动子元件。

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Previously, we have identified a constitutive nuclear factor, p70CORE, from HeLa cell nuclear extract which interacts specifically with the stress-inducible change region (SICR) of the grp78 promoter. Here we report that p70CORE is identical to YY1, a member of the GLI zinc finger family, by criteria of biochemical properties including apparent molecular weight, binding site homology, immunoreactivity, and affinity purification. Recombinant YY1 binds the double-stranded SICR with high specificity but has no affinity for its single-stranded form. In cotransfection studies, YY1 specifically enhanced the transcriptional activation of the grp78 promoter under a variety of stress conditions: depletion of the endoplasmic reticulum calcium stores, protein glycosylation block, and formation of aberrant proteins by azetidine treatment. In contrast, YY1 has minimal effect on the stress induction of the hsp70 promoter. YY1 enhancement of the grp78 stress response is dependent on its DNA-binding domain, with little effect on the basal expression of the promoter. The effect of YY1 transactivation may be mediated by the highly conserved grp78 core element. This is the first example of the ubiquitous factor YY1 involved in regulating inducible gene expression and its involvement in mediating stress signals generated from the endoplasmic reticulum to the nucleus.

机译：以前，我们从HeLa细胞核提取物中鉴定出一个组成性核因子p70CORE，它与grp78启动子的应激诱导变化区（SICR）特异性相互作用。在这里，我们报道了通过生化特性（包括表观分子量，结合位点同源性，免疫反应性和亲和力纯化）的标准，p70CORE与YY1（GLI锌指家族的成员）相同。重组YY1以高特异性结合双链SICR，但对其单链形式没有亲和力。在共转染研究中，YY1在多种胁迫条件下特异性增强了grp78启动子的转录激活：内质网钙存储的耗尽，蛋白质糖基化阻滞和通过氮杂环丁烷处理形成异常蛋白质。相反，YY1对hsp70启动子的应激诱导影响最小。 YY1对grp78应激反应的增强取决于其DNA结合结构域，对启动子的基础表达影响很小。 YY1反式激活的作用可能是由高度保守的grp78核心元件介导的。这是泛在因子YY1参与调节可诱导基因表达及其参与介导从内质网到细胞核的应激信号的第一个例子。

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《Molecular and Cellular Biology》 |1997年第1期|共7页
作者
W W Li; Y Hsiung; Y Zhou; B Roy; A S Lee;
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中图分类细胞生物学;
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1. Stress induction of the mammalian GRP78/BiP protein gene: in vivo genomic footprinting and identification of p70CORE from human nuclear extract as a DNA-binding component specific to the stress regulatory element. [J] . W W Li, L Sistonen, R I Morimoto, Molecular and Cellular Biology . 1994,第8期

机译：应力诱导哺乳动物GRP78 / BiP蛋白基因：体内基因组足迹和人核提取物中p70CORE的鉴定，作为应力调节元件特有的DNA结合成分。
2. Common sets of nuclear factors binding to the conserved promoter sequence motif of two coordinately regulated ER protein genes,GRP78 and GRP94 [J] . Amy S. Lee, Eva S. Liu Nucleic acids research . 1991,第19期

机译：与两个协调调节的ER蛋白基因GRP78和GRP94的保守启动子序列基序结合的常见核因子集
3. Cloning of a functional Burkitt's lymphoma polypeptide-binding protein/78 kDa glucose-regulated protein (BiP/GRP78) gene promoter by the polymerase chain reaction, and its interaction with inducible cellular factors [J] . C C K Chao, L K Chen, S Lin-Chao, The biochemical journal . 1992,第2期

机译：通过聚合酶链反应克隆功能性伯基特氏淋巴瘤多肽结合蛋白/ 78 kDa葡萄糖调节蛋白（BiP / GRP78）基因启动子及其与诱导性细胞因子的相互作用
4. Disulfide bond formation in the nuclear factor-kappaB essential modulator and gene expression profiling of a human B-lymphoma cell line expressing an activated REL transcription factor. [D] . Herscovitch, Melanie I. 2010

机译：核因子-κB必需调节剂中的二硫键形成和表达激活的REL转录因子的人B淋巴瘤细胞系的基因表达谱。
5. Induction of the mammalian GRP78/BiP gene by Ca2+ depletion and formation of aberrant proteins: activation of the conserved stress-inducible grp core promoter element by the human nuclear factor YY1. [O] . W W Li, Y Hsiung, Y Zhou, 1997

机译：Ca2 +耗尽诱导哺乳动物GRP78 / BiP基因并形成异常蛋白：人核因子YY1激活保守的应激诱导性grp核心启动子元件。
6. Induction of the mammalian GRP78/BiP gene by Ca2+ depletion and formation of aberrant proteins: activation of the conserved stress-inducible grp core promoter element by the human nuclear factor YY1. [O] . Li, W W, Hsiung, Y, Zhou, Y, 1997

机译：Ca2 +耗尽诱导哺乳动物GRP78 / BiP基因并形成异常蛋白：人核因子YY1激活保守的应激诱导性grp核心启动子元件。

Induction of the mammalian GRP78/BiP gene by Ca2+ depletion and formation of aberrant proteins: activation of the conserved stress-inducible grp core promoter element by the human nuclear factor YY1.

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