摘要:番茄红素通过mTORC2/AKT信号通路负调控FOXO3a,保护角质形成细胞免受UVB辐射诱导的癌变

IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

引用本文:陈鹏,徐世生,曲俊,“番茄红素通过mTORC2/AKT信号通路负调控FOXO3a对UVB辐射诱导的角质形成细胞的保护作用”,《细胞生物化学》,第11期。1 (2018): 366-377, https://doi.org/10.1002/jcb.26189.The上述文章于2017年6月6日在Wiley online Library (wileyonlinelibrary.com)上发表,经主编Christian Behl同意撤回;和Wiley期刊有限责任公司。由于第三方提出的担忧,已同意撤回。图2a和图4a中的多个图像元素被发现在之前和/或之后由不同的作者在不同的科学背景下发表。此外,在图3c中发现了不适当的图像编辑/操作的证据。作者被邀请对这些担忧发表评论,但没有回应。因此,由于编辑对文章中提供的全部数据的完整性和可靠性失去信心,并认为其结论无效,因此文章被撤回。作者被告知撤稿。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RETRACTION: Lycopene Protects Keratinocytes Against UVB Radiation-Induced Carcinogenesis via Negative Regulation of FOXO3a Through the mTORC2/AKT Signaling Pathway

RETRACTION: P. Chen, S. Xu, and J. Qu, “Lycopene Protects Keratinocytes Against UVB Radiation-Induced Carcinogenesis via Negative Regulation of FOXO3a Through the mTORC2/AKT Signaling Pathway,” Journal of Cellular Biochemistry 119, no. 1 (2018): 366-377, https://doi.org/10.1002/jcb.26189.

The above article, published online on 6 June 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Multiple image elements within Figures 2 A and 4 A were found to have been published previously and/or subsequently by different authors in different scientific contexts. Furthermore, evidence of inappropriate image editing/manipulation were found within Figure 3 C. The authors were invited to comment on these concerns but did not respond. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.

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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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