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首页> 外文期刊>Journal of Molecular Biology >Retraction notice to 'Peroxisome proliferator-activated receptor alpha controls hepatic heme biosynthesis through ALAS1' J. Mol. Biol. 388/2 (2010) 225-238.
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Retraction notice to 'Peroxisome proliferator-activated receptor alpha controls hepatic heme biosynthesis through ALAS1' J. Mol. Biol. 388/2 (2010) 225-238.

机译：撤回有关“过氧化物酶体增殖物激活的受体α通过ALAS1控制肝血红素生物合成”的通知。生物学388/2（2010）225-238。

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In this paper the authors described six of eight genes encoding for human heme biosynthesis pathway as primary targets of the nuclear receptor PPAR alpha. The most responsive and rate-limiting gene was ALAS1, which has several putative PPAR alpha binding sites in its regulatory region. It came to the attention of the corresponding author that the first author has performed incorrect data handling for the ChIP analysis described in Figs. 4 and 5B and has also used wrong gel pictures as representatives in gel shift assays shown in Fig. 5A. In the following the ChIP data were re-analyzed and the gelshifts were repeated. The claims of Fig. 4 on the binding of PPAR alpha, RXR alpha, PGC1 alpha and pPol II to the transcription start site (TSS) region of the six PPAR alpha responsive heme biosynthesis pathway still hold true but the numerical values changed. Also the claim of Fig. 5A on in vitro binding of PPAR alpha -RXR alpha heterodimers to putative response elements (REs) of the ALAS1 gene could be reproduced. New versions of Figs. 4 and 5 can be found at www.uku.fi/biokem/research/carlberg/Errata/errata.shtml. However, together with the reanalyzed ChIP data of Fig. 5B and the reporter gene data of Fig. 5C, the authors have to change their conclusion about the functional PPAR a binding sites of the ALAS1 gene: not RE1 and RE2, but RE1 and RE3 being located 9 and 0.7 kB upstream of the ALAS1 TSS seem to be the correct sites mediating the effects of PPAR a on the regulation of the gene.
机译：在本文中，作者将八个编码人类血红素生物合成途径的基因中的六个描述为核受体PPARα的主要靶标。最具响应性和速率限制的基因是ALAS1，该基因在其调控区具有几个推定的PPARα结合位点。引起相应作者注意的是，第一作者对图1和2中描述的ChIP分析执行了不正确的数据处理。在图4和图5B中，并且还使用了错误的凝胶图片作为图5A中所示的凝胶位移测定中的代表。接下来，重新分析ChIP数据，并重复凝胶位移。关于PPARα，RXRα，PGC1α和pPol II与六个PPARα反应性血红素生物合成途径的转录起始位点（TSS）区域结合的图4的主张仍然成立，但数值有所变化。还可以再现图5A关于PPARα-RXRα异二聚体与ALAS1基因的假定反应元件（RE）的体外结合的主张。无花果的新版本。可以在www.uku.fi/biokem/research/carlberg/Errata/errata.shtml中找到第4和第5段。但是，连同重新分析的图5B的ChIP数据和图5C的报告基因数据，作者必须更改有关ALAS1基因的功能性PPAR a结合位点的结论：不是RE1和RE2，而是RE1和RE3。位于ALAS1 TSS上游9和0.7 kB的位置似乎是介导PPAR a对基因调控作用的正确位点。

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