回归:通过上调 MDM4,下调 microRNA-23b 可通过 p53 信号通路保护大鼠免受缺血再灌注损伤。

IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of cellular biochemistry Pub Date : 2024-07-17 DOI:10.1002/jcb.30622
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引用次数: 0

摘要

撤回:Z. Zhao, J.-Z. Guan, M. Wu, G.-H.Guan, M. Wu, G.-H. Lai, and Z.-L.Lai, and Z.-L. Zhu.通过上调MDM4,下调microRNA-23b通过p53信号通路保护大鼠免受缺血再灌注损伤。Journal of Cellular Biochemistry 120, no.3 (2019):4599-4612, https://doi.org/10.1002/jcb.27748.上述文章于2018年12月9日在线发表于Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编Christian Behl和Wiley Periodicals LLC三方协商,已被撤回。之所以同意撤稿,是因为第三方对文章中的数据提出了质疑。我们发现,文章中介绍的结果与实验方法之间存在若干缺陷和不一致之处。此外,图 5B 中用于描绘免疫荧光染色的同一样本被发现在不同作者组之前发表的一篇文章中被用于不同的科学背景。因此,编者认为这篇文章的结论无效。
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RETRACTION: Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats

RETRACTION: Z. Zhao, J.-Z. Guan, M. Wu, G.-H. Lai, and Z.-L. Zhu. Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats. Journal of Cellular Biochemistry 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748.

The above article, published online on 9 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, the same sample used to depict the immunofluorescence staining in Figure 5B was found to have been used in a different scientific context in a previous publication from a different author group. Thus, the editors consider the conclusions of this article to be invalid.

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来源期刊
Journal of cellular biochemistry
Journal of cellular biochemistry 生物-生化与分子生物学
CiteScore
9.90
自引率
0.00%
发文量
164
审稿时长
1 months
期刊介绍: The Journal of Cellular Biochemistry publishes descriptions of original research in which complex cellular, pathogenic, clinical, or animal model systems are studied by biochemical, molecular, genetic, epigenetic or quantitative ultrastructural approaches. Submission of papers reporting genomic, proteomic, bioinformatics and systems biology approaches to identify and characterize parameters of biological control in a cellular context are encouraged. The areas covered include, but are not restricted to, conditions, agents, regulatory networks, or differentiation states that influence structure, cell cycle & growth control, structure-function relationships.
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