RETRACTION: Epac1-Induced Cellular Proliferation in Prostate Cancer Cells Is Mediated by B-Raf/ERK and mTOR Signaling Cascades

IF 2.8 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of cellular biochemistry Pub Date : 2025-07-15 DOI:10.1002/jcb.70046

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引用次数: 0

Abstract

RETRACTION: U. K. Misra and S. V. Pizzo, “Epac1-Induced Cellular Proliferation in Prostate Cancer Cells Is Mediated by B-Raf/ERK and mTOR Signaling Cascades,” Journal of Cellular Biochemistry 108, no. 4 (2009): 998–1011, https://doi.org/10.1002/jcb.22333.

The above article, published online on 1 September 2009 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.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. Specifically, duplication of image elements has been detected between Figures 2A and 4B, between Figure 3B and 3D, and between Figures 3B and 4C. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.

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撤回：epac1诱导的前列腺癌细胞增殖是由B-Raf/ERK和mTOR信号级联介导的

引用本文：U. K. Misra和S. V. Pizzo，“epac1诱导前列腺癌细胞增殖的B-Raf/ERK和mTOR信号级联介导”，《细胞生物化学杂志》第108期。4 (2009): 998-1011, https://doi.org/10.1002/jcb.22333.The上述文章于2009年9月1日在线发表在Wiley在线图书馆（wileyonlinelibrary.com）上，经期刊主编Christian Behl；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。具体来说，在图2A和4B之间、图3B和3D之间以及图3B和4C之间发现了图像元素的重复。在所有情况下，这些图像元素被用来表示不同的实验条件。一项机构审查证实了这些担忧的有效性。因此，由于编辑对整个数据的准确性和完整性失去信任，并认为文章的结论无效，文章被撤回。作者已被告知撤稿的决定。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

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.