回归:Bach2的过度表达通过抑制系统性红斑狼疮中IRF4的表达来抑制Th9细胞的分化。

IF 2.8 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY FEBS Open Bio Pub Date : 2024-11-01 DOI:10.1002/2211-5463.13922
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引用次数: 0

摘要

撤回:Y. Sheng, J. Zhang, K. Li, H. Wang, W. Wang, L. Wen, J. Gao, X. Tang, H. Tang, H. Huang, M. Cai, T. Yuan, L. Liu, X. Zheng, Z. Zhu and Y. Cui, "Bach2 Overexpression Represses Th9 Cell Differentiation by Suppressing IRF4 Expression in Systemic Lupus Erythematosus," FEBS Open Bio 11, no:395-403, https://doi.org/10.1002/2211-5463.13050.上述文章于 2020 年 11 月 28 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编 Miguel A. De la Rosa、FEBS Press 和 John Wiley and Sons Ltd.同意,已被撤回。作者在该研究中使用的患者样本中发现了诊断错误,因此同意撤稿。基于所发现的问题,编辑和作者认为研究结论已大打折扣。
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RETRACTION: Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus

RETRACTION: Y. Sheng, J. Zhang, K. Li, H. Wang, W. Wang, L. Wen, J. Gao, X. Tang, H. Tang, H. Huang, M. Cai, T. Yuan, L. Liu, X. Zheng, Z. Zhu and Y. Cui, “Bach2 Overexpression Represses Th9 Cell Differentiation by Suppressing IRF4 Expression in Systemic Lupus Erythematosus,” FEBS Open Bio 11, no. 2 (2021): 395–403, https://doi.org/10.1002/2211-5463.13050.

The above article, published online on 28 November 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed following diagnostic errors identified by the authors in the patient samples used in this study. Based on the issues identified, the editors and authors consider the conclusions substantially compromised.

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来源期刊
FEBS Open Bio
FEBS Open Bio BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
5.10
自引率
0.00%
发文量
173
审稿时长
10 weeks
期刊介绍: FEBS Open Bio is an online-only open access journal for the rapid publication of research articles in molecular and cellular life sciences in both health and disease. The journal''s peer review process focuses on the technical soundness of papers, leaving the assessment of their impact and importance to the scientific community. FEBS Open Bio is owned by the Federation of European Biochemical Societies (FEBS), a not-for-profit organization, and is published on behalf of FEBS by FEBS Press and Wiley. Any income from the journal will be used to support scientists through fellowships, courses, travel grants, prizes and other FEBS initiatives.
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Beyond digital twins: the role of foundation models in enhancing the interpretability of multiomics modalities in precision medicine. Mapping Hsp104 interactions using cross-linking mass spectrometry. Characterisation of the role played by ELMO1, GPR141 and the intergenic polymorphism rs918980 in Fuchs' dystrophy in the Indian population. Piezo1 channels enhance anabolic signaling activation induced by electrical stimulation of cultured myotubes. Identification of inhibitors of the Salmonella FraB deglycase, a drug target.
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