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Correction

Correction: Zhang et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage. Antioxidants 2022, 11, 1787

1
Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education & Key Lab of Swine Genetics and Breeding of Ministry of Agriculture and Rural Affairs, Huazhong Agricultural University, Wuhan 430070, China
2
Guangdong Laboratory of Lingnan Modern Agriculture, Guangzhou 510642, China
3
National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan 430070, China
4
Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan 430070, China
5
The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan 430070, China
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Antioxidants 2023, 12(2), 446; https://doi.org/10.3390/antiox12020446
Submission received: 6 February 2023 / Accepted: 7 February 2023 / Published: 10 February 2023
In the original publication [1], a mistake was identified in Figure 4 as published. The explanation in Figure 4E is wrong. The corrected Figure 4 appears below. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.

Reference

  1. Zhang, J.; Hu, S.; Zhao, C.; Zhou, Y.; Zhang, L.; Liu, H.; Zhou, P.; Li, S.; Fu, L.; Zheng, Z.; et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage. Antioxidants 2022, 11, 1787. [Google Scholar] [CrossRef] [PubMed]
Figure 4. Treatment with inhibitor M2 leads to the highest resistance to aflatoxin B1 in vitro. (A) Workflow of the structure-based virtual screening to identify inhibitors targeting BACH1. (B) Validation of the top three inhibitors (M1, M2, and M3) in Huh7 cells by CCK-8 assays. (C) Comparation of Huh7 tolerance to different AFB1 concentrations with and without M2 treatment. (D) The relative fluorescence intensity of AFB1-DNA adducts in Huh7 cells with and without M2 treatment. (E) Representative light microscopy images of AFB1-treated PK-15 cells with or without M2 treatment. Scale bar, 100 μm. (F) The IC50 assays for AFB1 in PK-15 cells with and without M2 treatment determined with CCK-8 assays. (G) The relative fluorescence intensity of AFB1-DNA adducts in PK-15 cells with and without M2 treatment. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant. p values were determined with two-tailed Student’s t-tests. AFB1, aflatoxin B1; M1, 1-Piperazineethanol, 4-phenyl-α-[[(3,4,5-trimethoxyphenyl)methoxy]methyl]; M2, 1-Piperazineethanol,α-[(1,3-benzodioxol-5-yloxy)methyl]-4-(2-methoxyphenyl); M3, 1,2-Ethanediamine, N1, N1, N2, N2-tetrakis (1H-benzimidazol-2-ylmethyl).
Figure 4. Treatment with inhibitor M2 leads to the highest resistance to aflatoxin B1 in vitro. (A) Workflow of the structure-based virtual screening to identify inhibitors targeting BACH1. (B) Validation of the top three inhibitors (M1, M2, and M3) in Huh7 cells by CCK-8 assays. (C) Comparation of Huh7 tolerance to different AFB1 concentrations with and without M2 treatment. (D) The relative fluorescence intensity of AFB1-DNA adducts in Huh7 cells with and without M2 treatment. (E) Representative light microscopy images of AFB1-treated PK-15 cells with or without M2 treatment. Scale bar, 100 μm. (F) The IC50 assays for AFB1 in PK-15 cells with and without M2 treatment determined with CCK-8 assays. (G) The relative fluorescence intensity of AFB1-DNA adducts in PK-15 cells with and without M2 treatment. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant. p values were determined with two-tailed Student’s t-tests. AFB1, aflatoxin B1; M1, 1-Piperazineethanol, 4-phenyl-α-[[(3,4,5-trimethoxyphenyl)methoxy]methyl]; M2, 1-Piperazineethanol,α-[(1,3-benzodioxol-5-yloxy)methyl]-4-(2-methoxyphenyl); M3, 1,2-Ethanediamine, N1, N1, N2, N2-tetrakis (1H-benzimidazol-2-ylmethyl).
Antioxidants 12 00446 g001
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MDPI and ACS Style

Zhang, J.; Hu, S.; Zhao, C.; Zhou, Y.; Zhang, L.; Liu, H.; Zhou, P.; Li, S.; Fu, L.; Zheng, Z.; et al. Correction: Zhang et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage. Antioxidants 2022, 11, 1787. Antioxidants 2023, 12, 446. https://doi.org/10.3390/antiox12020446

AMA Style

Zhang J, Hu S, Zhao C, Zhou Y, Zhang L, Liu H, Zhou P, Li S, Fu L, Zheng Z, et al. Correction: Zhang et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage. Antioxidants 2022, 11, 1787. Antioxidants. 2023; 12(2):446. https://doi.org/10.3390/antiox12020446

Chicago/Turabian Style

Zhang, Jinfu, Siyi Hu, Changzhi Zhao, Yuan Zhou, Lu Zhang, Hailong Liu, Peng Zhou, Sheng Li, Liangliang Fu, Zhuqing Zheng, and et al. 2023. "Correction: Zhang et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage. Antioxidants 2022, 11, 1787" Antioxidants 12, no. 2: 446. https://doi.org/10.3390/antiox12020446

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