Correction to “Discovery of Novel Histone Deacetylase 6 (HDAC6) Inhibitors with Enhanced Antitumor Immunity of Anti-PD-L1 Immunotherapy in Melanoma”

IF 6.8 1区 医学 Q1 CHEMISTRY, MEDICINAL Journal of Medicinal Chemistry Pub Date : 2024-10-19 DOI:10.1021/acs.jmedchem.4c02486
Xiaopeng Peng, Ling Li, Jingxuan Chen, Yichang Ren, Jin Liu, Ziwen Yu, Hao Cao, Jianjun Chen
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引用次数: 0

Abstract

In our study to investigate the impact of two newly synthesized compounds (XP5 and XP19) alongside a positive control drug (CAY10603) on the expression levels of various target proteins─specifically, AC-α-Tubulin, α-Tubulin, SMC3, Ac-H3, H3, Ac-SMC3, and apoptosis-related antibodies (Ac-Ku70, Ku70, Bcl-2, Bax)─we conducted a series of experiments on different tumor cell lines, including Jurkat-T cells and B16-F10 cells. This comprehensive analysis yielded a substantial amount of experimental data and protein bands. Regrettably, during the assembly of Figure 7 and Figure 8 in the original manuscript, we inadvertently used a wrong image of Ac-Ku70 and Ku70 in Figure 7A and of Ac-SMC3, SMC3, and Ac-H3 in Figure 8E,F. Upon recent and careful review of the original manuscript, we identified this error and have replaced the wrong image with the correct one in the corrected Figure 7 and Figure 8. This corrected result still demonstrates that XP5 and XP19 can upregulate the expression levels of acetylated Ku70 significantly and dose-dependently but showed no effect on the Ku70 levels and had little effect on the levels of acetyl-SMC3 and acetyl-H3, and these corrections do not change the scientific conclusions of the article in any way. Figure 7. Analysis of acetylated Ku70, Ku70, Bcl-2, and Bax by Western blot. Jurkat T cells were treated with dimethyl sulfoxide (DMSO) or XP5, and XP19 for 6 h. The levels of acetylated Ku70, Ku70, Bcl-2, and Bax were examined by Western blot (A). Quantitative analysis of the levels of acetylated Ku70 (B), Bcl-2 (C), and Bax (D). All data are representative of three independent experiments and shown as mean ± SD. ***p < 0.001, **p < 0.01, *p < 0.05 compared with the control group, ###p < 0.001. One-way ANOVA for the above analysis, Dunnett test. Figure 8. Analysis of acetylated α-tubulin/acetylated-SMC3 and acetylated-H3 by Western blot. The levels of acetyl-α-tubulin (Ac-α-Tub) and α-tubulin in B16-F10 cells (A) and Jurkat T cells (B) treated with DMSO or XP5, XP19, and CAY10603 for 6 h. Quantitative analysis of the level of acetyl-α-tubulin (Ac-α-Tub) by Western blotting assay obtained in B16-F10 cells (C) and Jurkat T cells (D). The levels of acetylated-SMC3, total SMC3, acetylated-H3, and total H3 in B16-F10 cells (E) and Jurkat T cells (F) treated with DMSO or XP5, XP19, and CAY10603 for 6 h. All data are representative of three independent experiments and shown as mean ± SD. ***p < 0.001, **p < 0.01 compared with the control group, ###p < 0.001, &p < 0.05, &&p < 0.01. One-way ANOVA for the above analysis, Dunnett test. We have now corrected the original Figure 7 and Figure 8, and all authors have agreed to the changes. We apologize for any confusion this may have caused and appreciate your understanding as we make these necessary corrections to ensure the integrity of our research findings. This article has not yet been cited by other publications.

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对 "发现新型组蛋白去乙酰化酶 6 (HDAC6) 抑制剂,增强黑色素瘤中抗 PD-L1 免疫疗法的抗肿瘤免疫力 "的更正
我们的研究旨在探讨两种新合成的化合物(XP5和XP19)与阳性对照药物(CAY10603)一起对多种靶蛋白表达水平的影响,具体包括AC-α-Tubulin、α-Tubulin、SMC3、Ac-H3、H3、Ac-SMC3和凋亡相关抗体(Ac-Ku70、Ku70、Bcl-2、Baxwe)、α-微管蛋白、SMC3、Ac-H3、H3、Ac-SMC3 和凋亡相关抗体(Ac-Ku70、Ku70、Bcl-2、Bax)的表达水平--我们在不同的肿瘤细胞系(包括 Jurkat-T 细胞和 B16-F10 细胞)上进行了一系列实验。这项综合分析获得了大量的实验数据和蛋白质条带。遗憾的是,在绘制原稿中的图 7 和图 8 时,我们不小心用错了图 7A 中 Ac-Ku70 和 Ku70 的图像,以及图 8E,F 中 Ac-SMC3、SMC3 和 Ac-H3 的图像。在最近仔细审阅原稿后,我们发现了这个错误,并在更正后的图 7 和图 8 中用正确的图像替换了错误的图像。改正后的结果仍然表明,XP5和XP19能显著上调乙酰化Ku70的表达水平,且呈剂量依赖性,但对Ku70的水平没有影响,对乙酰化-SMC3和乙酰化-H3的水平影响也不大,这些改正丝毫没有改变文章的科学结论。图 7.通过 Western 印迹分析乙酰化 Ku70、Ku70、Bcl-2 和 Bax。用二甲基亚砜(DMSO)或 XP5 和 XP19 处理 Jurkat T 细胞 6 小时,用 Western 印迹法检测乙酰化 Ku70、Ku70、Bcl-2 和 Bax 的水平(A)。乙酰化 Ku70(B)、Bcl-2(C)和 Bax(D)水平的定量分析。所有数据均代表三个独立实验的结果,以平均值 ± SD 表示。与对照组相比,***p < 0.001,**p < 0.01,*p < 0.05,###p < 0.001。上述分析采用单因素方差分析,Dunnett 检验。图 8.通过 Western 印迹分析乙酰化 α-微管蛋白/乙酰化-SMC3 和乙酰化-H3。用 DMSO 或 XP5、XP19 和 CAY10603 处理 6 小时的 B16-F10 细胞(A)和 Jurkat T 细胞(B)中乙酰化-α-微管蛋白(Ac-α-Tub)和α-微管蛋白的水平。用 Western 印迹法定量分析 B16-F10 细胞(C)和 Jurkat T 细胞(D)中乙酰化-α-微管蛋白(Ac-α-Tub)的水平。用 DMSO 或 XP5、XP19 和 CAY10603 处理 6 h 的 B16-F10 细胞(E)和 Jurkat T 细胞(F)中乙酰化-SMC3、总 SMC3、乙酰化-H3 和总 H3 的水平。 所有数据均代表三个独立实验,以均数 ± SD 表示。与对照组相比,***p < 0.001,**p < 0.01,###p < 0.001,&p < 0.05,&&p < 0.01。上述分析采用单因素方差分析,Dunnett 检验。我们现已对最初的图 7 和图 8 进行了修改,所有作者均已同意。我们对由此可能造成的任何混淆表示歉意,并感谢您的理解,我们将进行这些必要的更正,以确保我们研究成果的完整性。本文尚未被其他出版物引用。
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来源期刊
Journal of Medicinal Chemistry
Journal of Medicinal Chemistry 医学-医药化学
CiteScore
4.00
自引率
11.00%
发文量
804
审稿时长
1.9 months
期刊介绍: The Journal of Medicinal Chemistry is a prestigious biweekly peer-reviewed publication that focuses on the multifaceted field of medicinal chemistry. Since its inception in 1959 as the Journal of Medicinal and Pharmaceutical Chemistry, it has evolved to become a cornerstone in the dissemination of research findings related to the design, synthesis, and development of therapeutic agents. The Journal of Medicinal Chemistry is recognized for its significant impact in the scientific community, as evidenced by its 2022 impact factor of 7.3. This metric reflects the journal's influence and the importance of its content in shaping the future of drug discovery and development. The journal serves as a vital resource for chemists, pharmacologists, and other researchers interested in the molecular mechanisms of drug action and the optimization of therapeutic compounds.
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