RETRACTION: Upregulation of mTORC2 Activation by the Selective Agonist of EPAC, 8-CPT-2Me-cAMP, in Prostate Cancer Cells: Assembly of a Multiprotein Signaling Complex

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.70048

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引用次数: 0

Abstract

RETRACTION: U. K. Misra and S. V. Pizzo, “Upregulation of mTORC2 Activation by the Selective Agonist of EPAC, 8-CPT-2Me-cAMP, in Prostate Cancer Cells: Assembly of a Multiprotein Signaling Complex,” Journal of Cellular Biochemistry 113, no. 5 (2011): 1488–1500, https://doi.org/10.1002/jcb.24018.

The above article, published online on 15 December 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.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 4C and 7B, between Figure 7A and 7B, and within Figure 6C. 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.

查看原文本刊更多论文

在前列腺癌细胞中，EPAC选择性激动剂8-CPT-2Me-cAMP对mTORC2激活的上调：多蛋白信号复合物的组装

撤回：U. K. Misra和S. V. Pizzo，“选择性激动剂EPAC， 8-CPT-2Me-cAMP在前列腺癌细胞中mTORC2激活的上调：多蛋白信号复合物的组装”，细胞生物化学杂志，第113期。5 (2011): 1488-1500, https://doi.org/10.1002/jcb.24018.The上述文章于2011年12月15日在线发表在Wiley online Library （wileyonlinelibrary.com）上，经主编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4C和图7B之间、图7A和图7B之间以及图6C内部都发现了重复的图像元素。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.