Withdrawn: LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis

IF 3 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of cellular biochemistry Pub Date : 2024-04-03 DOI:10.1002/jcb.30561

引用次数: 0

Abstract

Withdrawn: ‘LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis’ by Su Ni, Chao Xu, Chao Zhuang, Gongyin Zhao, Chenkai Li, Yuji Wang, Xihu Qin, J Cell Biochem (https://doi.org/10.1002/jcb.29637). The above article, published online on 7 February 2020 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcb.29637) has been withdrawn by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The withdrawal has been agreed following no response from the author to requests to sign the Journal's publishing license.

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撤回：LncRNA LUADT1调控miR-34a/SIRT1参与软骨细胞凋亡

撤稿：《LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis》，作者：Su Ni, Chao Xu, Chao Zhuang, Gongyin Zhao, Chenkai Li, Yuji Wang, Xihu Qin，J Cell Biochem (https://doi.org/10.1002/jcb.29637).上述文章于 2020 年 2 月 7 日在线发表于 Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcb.29637)，经期刊主编 Christian Behl 和 Wiley Periodicals LLC 同意，该文章已被撤回。在作者对签署期刊出版许可证的请求没有回应后，双方同意撤回该文章。

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.