Journal of Cellular Physiology最新文献

Transmembrane protein 175 (TMEM175) is an endolysosomal cation channel, which has attracted much attention recently from academics and the pharmaceutical industry alike since human mutations in TMEM175 were found to be associated with the development of Parkinson's disease (PD). Thus, gain-of-function mutations were identified, which reduce and loss-of-function mutations, which increase the risk of developing PD. After having been characterized as an endolysosomal potassium channel initially, soon after TMEM175 was claimed to act as a proton channel. In fact, recent evidence suggests that depending on the conditions, TMEM175 can act as either a potassium or proton channel, without acting as an antiporter or exchanger. A recent work has now identified amino acid H57 to be directly involved in gating, increasing proton conductance of the channel while leaving the potassium conductance unaffected. We review here the current knowledge of TMEM175 function, pharmacology, physiology, and pathophysiology. We discuss the potential of this ion channel as a novel drug target for the treatment of neurodegenerative diseases such as PD, and we discuss the discovery of H57 as proton sensor.

RETRACTION: Y. Shi, M. Liu, Y. Huang, J. Zhang, and L. Yin, “Promotion of Cell Autophagy and Apoptosis in Cervical Cancer by Inhibition of Long Noncoding RNA LINC00511 via Transcription Factor RXRA-regulated PLD1,” Journal of Cellular Physiology 235, no. 10 (2020): 6592-6604. https://doi.org/10.1002/jcp.29529.

The above article, published online on 17 February 2020 in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.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 images shared overlapping sections in Figure 5D in this article, and this duplication was confirmed by the publisher. The third party also reported that the tumor measurement ruler used in Figure 5 A is identical to the ruler used in the figures of previously published articles from different authors, each of which describes a different scientific context (Chen, et al. 2019 [https://doi.org/10.1002/jcp.28911]) and (Feng, et al. 2019 [https://doi.org/10.1186/s13287-022-02841-z]). The use of the identical ruler in the figures of different articles from unrelated research groups at different institutions puts in doubt the veracity of the data reported. The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication within this article, as well as unexplained duplication of image elements and equipment with other experiments by different authors, fundamentally compromises the conclusions reported in this article. The authors did not respond to our notice regarding the retraction.

RETRACTION: A. Uddin and S. Chakraborty, “Role of miRNAs in Lung Cancer,” Journal of Cellular Physiology (Early View), https://doi.org/10.1002/jcp.26607.

The above article, published online on 20 April 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed major textual overlap between this article and two previously published articles by different groups of authors elsewhere (Guz et al. 2014; Hubaux 2012).

The authors noted the major textual overlap and revised their manuscript during the proofing stage, yet the wrong version of the manuscript was published in Early View by mistake. The editors and the publisher apologize for this oversight. During the investigation, the authors were able to provide their revised article, however, also the revised version shows high textual and conceptual similarity to the two previously published review articles (Guz et al. 2014; Hubaux 2012). The authors disagree with the retraction.

References

Guz, M., A. Rivero-Müller, E. Okoń, et al. 2014. “Micrornas-Role in Lung Cancer.” Disease Markers 2014, no. 1: 1–13. https://doi.org/10.1155/2014/218169.

Hubaux, R. 2012. “Micrornas as Biomarkers for Clinical Features of Lung Cancer.” Journal of Postgenomics: Drug & Biomarker Development 2, no. 3: 1000108. https://doi.org/10.4172/2153-0769.1000108.

Carboxyl terminal modulator protein (CTMP) may be involved in various physiological and pathological processes, such as inflammation, tumor growth, and cardiac hypertrophy. Our recent study has shown that CTMP is increased with aging and plays a role in determining brain ischemic tolerance. However, it is not known how CTMP expression with aging is regulated and whether the changed CTMP expression has an effect on cell senescence. Here, cells that stably overexpressed CTMP were generated and cell senescence biomarkers were determined. The brains of Fischer 344 male rats were harvested for Western blot analysis and immunostaining to detect CTMP and the Zinc finger protein Zic2. The regulations of CTMP expression by Zic2 were examined by promoter activity assays. Increasing CTMP enhanced cells expressing senescence-associated β-galactosidase staining but without expression of Ki67, decreased cell proliferation and colony formation, and increased cells with condensed DNA of more than one pair of homologous chromosomes caused by senescence. Zic2 was decreased with aging in rats. Zic2 and CTMP were mainly expressed in the neurons in rats. Similarly, CTMP protein was expressed in the neurons of human brain. An anti-Zic2 antibody immunoprecipitated DNA fragments of ctmp gene. Zic2 inhibited the activity of presumptive ctmp promoter. Overexpressing Zic2 decreased CTMP in cells. These results suggest that CTMP induces cell senescence and that Zic2 is a suppressor of CTMP expression. The decrease of Zic2 contributes to CTMP increase with aging.

This article corrects the following:

Defining Early Hematopoietic-Fated Primitive Streak Specification of Human Pluripotent Stem Cells by the Orchestrated Balance of Wnt, Activin, and BMP Signaling

Jun Shen, Cuicui Lyu, Yaoyao Zhu, Zicen Feng, Shuo Zhang, Dixie L. Hoyle, Guangzhen Ji, Robert A. Brodsky, Tao Cheng, Zack Z. Wang.

Journal of Cell Physiology

https://doi.org/10.1002/jcp.28272

First published: 10 February 2019

Correction text:

The authors made two inadvertent mistakes in the original figures, as follows:

1. The flow cytometry image in the left panel of the original Figure 2e was inadvertently duplicated from the far-right panel of the original Figure 3d.

2. In the original Figure 1d, a duplication of flow figures, for +BMP4 (B) and +BC, occurred. The +BMP4 (B) panel of Figure 1d was incorrectly selected.

The corrected Figure 1 and Figure 2 are as follows:

This correction does not alter the interpretation of the data or the conclusions presented in the paper. The figure legends remain unchanged.

The authors sincerely apologize for any confusion this error may have caused.

This article corrects the following:

Immortalized Hertwig's epithelial root sheath cell line works as a model for epithelial-mesenchymal interaction during tooth root formation

Sicheng Zhang, Xuebing Li, Shikai Wang, Yan Yang, Weihua Guo, Guoqing Chen, Weidong Tian

Journal of Cellular Physiology

https://doi.org/10.1002/jcp.29174

First Published Online: 12 September 2019

Correction text:

During manuscript preparation the authors inadvertently presented a duplicated version of the H&E staining image for the DPC group in Figure 6a as the anti-DMP1 staining group image. The corrected Figure 1 is presented below:

The authors apologize for this oversight and any confusion that may have arisen as a result.