Correction to “The Oncolytic Virus H101 Combined with Gnaq Sirna-Mediated Knockdown Reduces Uveal Melanoma Cell Viability”

IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

Abstract

Li Y, He J, Qiu C, et al. The oncolytic virus H101 combined with GNAQ siRNA-mediated knockdown reduces uveal melanoma cell viability. J Cell Biochem. 2019;120:5766-5776. https://doi.org/10.1002/jcb.27863.

In the original version of this article, the authors mistakenly duplicated panels in Figure 2A showing the morphological changes of OMM2.3 cells treated with “H101” and “H101+siNC,” as well as in Figure 3A, showing the flow cytometric analysis of OMM2.3 cells in the “NC” and “siGNAQ” groups. In the corrected Figures 2A and 3A below, the authors have replaced the duplicated “H101+siNC” and “siGNAQ” panels with the correct ones, respectively. Additionally, in the correct Figure 3 below, the axis labels have been corrected from “PMT4 Log” to “PI” (Propidium Iodide) and from “PMT2 Log” to “Annexin V-FITC”.

The legend for Figure 3 is corrected as per below (changes in bold):

Figure 3. Apoptosis was modulated by cotreatment with H101 and siGNAQ. A, Apoptosis of the OMM2.3, 92.1, and OCM1 cell lines was detected with an annexin-V kit and a flow-cytometric analysis. B, At 48 h after transfection, the proportion of early apoptotic cells (Annexin V+ PI-) was calculated. When H101 was combined with siGNAQ, the apoptosis of UM cells was enhanced relative to that induced by H101 alone. The results are presented as the means and standard error of the mean; *P < 0.05. UM, uveal melanoma.

Additionally, there is a typographical error in the sequence of the reverse primer for GADPH amplification. The correct sequence is “CAAAGTTGTCATGGATGACC”.

Finally, the author omitted to mention that the bands for GNAQ and β-actin in Figure 5A are referenced from Figure 1C.

The authors apologize for these mistakes and for any inconvenience these may have caused.

Abstract Image

对 "溶瘤病毒 H101 与 Gnaq Sirna 基因敲除相结合可降低葡萄膜黑色素瘤细胞活力 "的更正。
Li Y, He J, Qiu C, et al.溶瘤病毒H101结合GNAQ siRNA介导的基因敲除降低了葡萄膜黑色素瘤细胞的存活率。J Cell Biochem.2019;120:5766-5776。 https://doi.org/10.1002/jcb.27863.In 在本文的原始版本中,作者错误地重复了图2A中显示经 "H101 "和 "H101+siNC "处理的OMM2.3细胞形态变化的面板,以及图3A中显示 "NC "和 "siGNAQ "组OMM2.3细胞流式细胞分析的面板。在更正后的图 2A 和图 3A 中,作者分别用正确的面板替换了重复的 "H101+siNC "和 "siGNAQ "面板。此外,在下面正确的图 3 中,坐标轴标签已从 "PMT4 Log "更正为 "PI"(碘化丙啶),从 "PMT2 Log "更正为 "Annexin V-FITC"。H101 和 siGNAQ 共处理调节细胞凋亡。A、用附件素-V试剂盒和流式细胞仪检测 OMM2.3、92.1 和 OCM1 细胞系的细胞凋亡。B、转染 48 小时后,计算早期凋亡细胞(Annexin V+ PI-)的比例。当 H101 与 siGNAQ 联用时,UM 细胞的凋亡相对于 H101 单独诱导的凋亡更强。结果以平均值和平均值的标准误表示;*P < 0.05。UM,葡萄膜黑色素瘤。此外,用于 GADPH 扩增的反向引物序列存在印刷错误。最后,作者没有提到图 5A 中 GNAQ 和 β-actin 的条带是从图 1C 中引用的。作者对这些错误和可能造成的不便表示歉意。
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
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.
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