返回：LGI1 基因表达的增加会引发神经母细胞瘤细胞的生长抑制和凋亡。

IF 4.5 2区生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2024-09-02 DOI:10.1002/jcp.31411

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引用次数: 0

摘要

撤回：N. Gabellini, V. Masola, S. Quartesan, B. Oselladore, C. Nobile, R. Michelucci, M. Curtarello, C. Parolin, and G. Palù, Journal of Cellular Physiology 207, no.3 (2006):711-721. https://doi.org/10.1002/jcp.20627.上述文章于 2006 年 3 月 3 日在线发表于 Wiley Online Library (wileyonlinelibrary.com)，经期刊主编罗伯特-希思（Robert Heath）和 Wiley Periodicals LLC 协议撤回。第三方报告称，图 1 和图 6 中的 GAPDH 印迹有图像处理痕迹。出版商调查后发现，图 1B 和图 6B 之间有重复、调整大小和拼接的迹象，图 1A 和图 6A 也有拼接的迹象。作者没有回应出版商的询问和提供原始数据的要求。由于文章中提供的结果不再可靠，因此同意撤稿。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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RETRACTION: Increased expression of LGI1 gene triggers growth inhibition and apoptosis of neuroblastoma cells.

Retraction: N. Gabellini, V. Masola, S. Quartesan, B. Oselladore, C. Nobile, R. Michelucci, M. Curtarello, C. Parolin, and G. Palù, Journal of Cellular Physiology 207, no. 3 (2006): 711-721. https://doi.org/10.1002/jcp.20627. The above article, published online on 03 March 2006, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. A third party reported that the GAPDH blots in Figure 1 and Figure 6 showed evidence of image manipulation. An investigation by the publisher found evidence of duplication, resizing, and splicing between Figures 1B and 6B as well as evidence of splicing in Figures 1A and 6A. The authors did not respond to an inquiry by the publisher and a request for original data. The retraction has been agreed to because the results presented in the article can no longer be considered reliable.

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来源期刊

Journal of Cellular Physiology 生物-生理学

CiteScore

14.70

自引率

0.00%

发文量

256

审稿时长

1 months

期刊介绍： The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.

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