Correction to: Concomitant blockade of A2AR and CTLA-4 by siRNA-loaded polyethylene glycol-chitosan-alginate nanoparticles synergistically enhances antitumor T-cell responses
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引用次数: 0
Abstract
M. Ghasemi-Chaleshtari, S. H. Kiaie, M. Irandoust, H. Karami, M. N. Afjadi, S. Ghani, N. A. Vanda, M. J. Ghaderi Sede, A. Ahmadi, A. Masjedi, H. Hassannia, F. Atyabi, M. Hojjat-Farsangi, A. Namdar, G. Ghalamfarsa, F. Jadidi-Niaragh, “Concomitant blockade of A2AR and CTLA-4 by siRNA-loaded polyethylene glycol-chitosan-alginate nanoparticles synergistically enhances antitumor T-cell responses,” Journal of Cellular Physiology 235, no. 12 (2020): 10068-10080, https://doi.org/10.1002/jcp.29822.
In the original version of this article, the authors mistakenly duplicated the panels showing the β-actin bands across Figure 2b, 2f and Figure 4e. While Figure 2b and 2f share the same cellular origin and treatment, the β-actin bands in Figure 4e have been mistakenly used. The corrected Figure 4e is shown below.
This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.
M.M. Ghasemi-Chaleshtari、S. H. Kiaie、M. Irandoust、H. Karami、M. N. Afjadi、S. Ghani、N. A. Vanda、M. J. Ghaderi Sede、A. Ahmadi、A. Masjedi、H. Hassannia、F. Atyabi、M. Hojjat-Farsangi、A. Namdar、G. Ghalamfarsa、F. Jadidi-Niaragh, "Concomitant blockade A2AR and CTLA-4 by siRNA-loaded polyethylene glycol-chitosan-alginate nanopartart.Jadidi-Niaragh，"siRNA负载的聚乙二醇-壳聚糖-海藻酸盐纳米颗粒对A2AR和CTLA-4的协同阻断可协同增强抗肿瘤T细胞反应，"《细胞生理学杂志》第235期，第12号（2020年）：10068-10080，https://doi.org/10.1002/jcp.29822。在本文的原始版本中，作者错误地重复了图 2b、2f 和图 4e 中显示 β-肌动蛋白条带的面板。虽然图 2b 和图 2f 的细胞来源和处理方法相同，但图 4e 中的β-肌动蛋白条带却被误用了。更正后的图 4e 如下。这项更正不会改变结果和结论。作者对这些错误可能造成的混淆表示歉意。
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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