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28 June 2024

Correction: Shokeer et al. Mutational Analysis of the Binding of Alternative Substrates and Inhibitors to the Active Site of Human Glutathione Transferase P1–1. Processes 2020, 8, 1232

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1
Department of Molecular Biology, Genetic Engineering and Biotechnology Research Division, National Research Centre, Dokki, Giza 126 22, Egypt
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Department of Biochemistry and Biophysics, Stockholm University, 106 91 Stockholm, Sweden
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Author to whom correspondence should be addressed.
This article belongs to the Special Issue Synthesis, Biological Evaluation and Molecular Modeling of Enzyme Inhibitors
The changes below represent the corrections the authors wish to make to the original paper [1].

Errors in Tables

The authors wish to make changes to Tables 2–4. In the original publication, one of the values in Table 2 was not consistent with the text. For Tables 3 and 4, several values were missing a decimal point. The new Table 2, Table 3 and Table 4 are attached below.
Table 2. Steady-state kinetic parameters of wild-type human GST P1–1 and mutants.
Table 3. Saturation kinetics in three dimensions.
Table 4. Catalytic efficiency (kcat/Km) of GST P1–1 variants with alternative thiol substrates.

Changes to Figure and Figure Legend

The authors wish to make changes to Figure 3 and the Figure legend. In the original publication, some values were miscalculated, and a minor typographical error was detected in the Figure legend. The new Figure 3 with the Figure legend has been updated below.
Figure 3. Schemes of incremental binding energies (kJ mol−1) compared to the binding of five different glutathione derivatives to wild-type GST P1–1 and mutants K45A, Q52A, and Q52K. The complexes with S-hexylglutathione, γE-C(Hx)-G (upper left corners), serve as references. Positive values indicate increased binding affinities.

Correction to Equation

The equation present in the original publication had a typographical error in it. The adjusted equation is attached below.
ΔΔG = −RT ln (Ki/Ki*)

Correction to Text

The authors wish to make changes to errors found in the main text.
3.3. Steady-State Kinetics
Paragraph 1: Original text: Mutant Q52K is most strongly affected with a nine-fold increase of KMCDNB, an eight-fold decrease of kcat, and a resulting 70-fold decrease of kcat/KMGSH (Table 2).
New text: Mutant Q52K is most strongly affected with a nine-fold increase in KMGSH, an eight-fold decrease in kcat, and a resulting seventy-fold decrease in kcat/KMGSH (Table 2).
Paragraph 3: Original text: However, the catalytic efficiency could be determined and showed that mutant Q52K was 50% more efficient than the wild-type enzyme with GSH as the varied thiol substrate.
New text: However, the catalytic efficiency could be determined and showed that the mutant Q52K only displayed a fraction (1.5%) of the efficiency of the wild-type enzyme with GSH as the varied thiol substrate.
3.4. Inhibition Studies
Paragraph 8: Original text: a potent ligand.
New text: a potent inhibitor.
The authors apologize for any inconvenience caused and state that the scientific conclusion of the paper is unaffected. The original publication has also been updated.

Reference

  1. Shokeer, A.; Ismail, A.; Hegazy, U.M.; Kolm, R.H.; Mannervik, B. Mutational Analysis of the Binding of Alternative Substrates and Inhibitors to the Active Site of Human Glutathione Transferase P1–1. Processes 2020, 8, 1232. [Google Scholar] [CrossRef]
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