Corrigendum to “The Effects and Mechanisms of Myeloid Differentiation Protein 2 on Intestinal Mucosal Permeability in Mice With Chronic Colitis”

IF 4 2区 生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2025-02-26 DOI:10.1002/jcp.70009
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Abstract

Han C., Q. Guan, L. Guo, Y. Yang, S. Ruan, and X. Zhang. 2019. “The Effects and Mechanisms of Myeloid Differentiation Protein 2 on Intestinal Mucosal Permeability in Mice With Chronic Colitis.” Journal of Cellular Physiology 234, no. 11: 21089–21099. https://doi.org/10.1002/jcp.28711.

In the initial version of the proof stage, We mistakenly inserted incorrect panels in Figure 2d, Figure 3a, Figure 4d, Figure 5a, and Figure 6c. Specifically:

Figure 2c: We have confused the panels of Con and DSS, and the magnification is not consistent. We will present the correct results as follows:

Figure 3a: Strip insertion error for MD2. We will present the correct results as follows:

Figure 4d: TLR4 strip insertion error. We will present the correct results as follows:

Figure 5a: MD2 and GAPDH strip insertion error. We will present the correct results as follows:

Figure 6c: GAPDH strip insertion error. We will present the correct results as follows:

This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.

Abstract Image

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髓系分化蛋白 2 对慢性结肠炎小鼠肠黏膜通透性的影响和机制 "的更正
韩超,关琪,郭亮,杨勇,阮生,张晓明。2019。髓样分化蛋白2对慢性结肠炎小鼠肠黏膜通透性的影响及机制细胞生理学杂志,第234期。11: 21089 - 21099。https://doi.org/10.1002/jcp.28711.In初版校对阶段,我们错误地插入了图2d、图3a、图4d、图5a和图6c中的错误面板。图2c:我们混淆了Con和DSS面板,放大倍率不一致。我们将给出正确的结果如下:图3a: MD2条带插入错误。我们将给出正确的结果如下:图4d: TLR4条带插入错误。我们将给出如下正确结果:图5a: MD2和GAPDH条带插入错误。我们将给出正确的结果如下:图6c: GAPDH条带插入错误我们将以如下方式呈现正确的结果:此更正不会改变结果和结论。作者对这些错误可能造成的任何混淆表示歉意。
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来源期刊
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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