{"title":"Correction to: Clusterin enhances AKT2-mediated motility of normal and cancer prostate cells through a PTEN and PHLPP1 circuit","authors":"","doi":"10.1002/jcp.31377","DOIUrl":null,"url":null,"abstract":"<p>Bertacchini J, Mediani L, Beretti F, et al. Clusterin enhances AKT2-mediated motility of normal and cancer prostate cells through a PTEN and PHLPP1 circuit. <i>J Cell Physiol</i>. 2019;234:11188–11199. https://doi.org/10.1002/jcp.27768</p><p>In the original version of this article, the authors mistakenly duplicated the panels showing AKT1 levels in Figure 1c and the panels showing clusterin (CLU) levels in Figure 3c.</p><p>In the correct Figure 1c below, the authors replaced the lower right panels (CLU cells transfected with scramble shRNA or shAkt2) with a replicate experiment showing the proper anti-Akt1 blot. Equal loading of CLU cell lysates was probed by anti-CLU.</p><p>In the correct Figure 3c below, the author replaced the panels showing CLU and ACTIN levels in the PC3 cell line with a replicate experiment.</p><p>This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5000,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31377","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cellular Physiology","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jcp.31377","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Bertacchini J, Mediani L, Beretti F, et al. Clusterin enhances AKT2-mediated motility of normal and cancer prostate cells through a PTEN and PHLPP1 circuit. J Cell Physiol. 2019;234:11188–11199. https://doi.org/10.1002/jcp.27768
In the original version of this article, the authors mistakenly duplicated the panels showing AKT1 levels in Figure 1c and the panels showing clusterin (CLU) levels in Figure 3c.
In the correct Figure 1c below, the authors replaced the lower right panels (CLU cells transfected with scramble shRNA or shAkt2) with a replicate experiment showing the proper anti-Akt1 blot. Equal loading of CLU cell lysates was probed by anti-CLU.
In the correct Figure 3c below, the author replaced the panels showing CLU and ACTIN levels in the PC3 cell line with a replicate experiment.
This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.
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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