William Jeffries, Bryan M Delfing, Xavier E Laracuente, Xingyu Luo, Audrey Olson, Kenneth W Foreman, Kyung Hyeon Lee, Greg Petruncio, Vito De Benedictis, Mikell Paige, Kylene Kehn-Hall, Christopher Lockhart, Dmitri K Klimov
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Our previous simulations of non-competitive binding of the coreNLS, in which it natively binds to importin-α, are used as a reference. Both inhibitors abrogate native peptide binding and reduce the fraction of its native interactions, but they fail to prevent its non-native binding to importin-α. As a result, these inhibitors turn the coreNLS into diffusive binder, which adopts a manifold of non-native binding poses. Competition from the inhibitors compromises the free energy of coreNLS binding to importin-α showing that they reduce its binding affinity. The inhibition mechanism is based on masking the native binding interactions formed by the coreNLS amino acids. Surprisingly, ligand interference with the binding interactions formed by importin-α amino acids contributes little to inhibition. We show that DP9 is a stronger inhibitor than DP9o. By comparative analysis of DP9 and DP9o interactions we determine the atomistic reason for a relative \"success\" of DP9, which is due to the intercalation of this inhibitor between the side chains of NLS lysine residues. To test our simulations, we performed AlphaScreen experiments measuring IC50 values for the inhibitors. AlphaScreen data confirmed in silico ranking of the inhibitors. By combining our recent studies, we discuss the putative mechanism by which diffusively binding inhibitors impact protein-protein interactions.</p>","PeriodicalId":20241,"journal":{"name":"PLoS Computational Biology","volume":"21 9","pages":"e1013495"},"PeriodicalIF":3.6000,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456801/pdf/","citationCount":"0","resultStr":"{\"title\":\"Ligands binding diffusively to protein target act as inhibitors of protein-protein interactions.\",\"authors\":\"William Jeffries, Bryan M Delfing, Xavier E Laracuente, Xingyu Luo, Audrey Olson, Kenneth W Foreman, Kyung Hyeon Lee, Greg Petruncio, Vito De Benedictis, Mikell Paige, Kylene Kehn-Hall, Christopher Lockhart, Dmitri K Klimov\",\"doi\":\"10.1371/journal.pcbi.1013495\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Nuclear localization signal (NLS) sequence from capsid protein of Venezuelan equine encephalitis virus (VEEV) binds to importin-α transport protein and clogs nuclear import. Prevention of viral NLS binding to importin-α may represent a viable therapeutic route. Here, we investigate the molecular mechanism by which two diffusively binding inhibitors, DP9 and DP9o, interfere with the binding of VEEV's NLS peptide to importin-α. Our study uses all-atom replica exchange molecular dynamics simulations, which probe the competitive binding of the VEEV NLS fragment, the coreNLS peptide, and the inhibitors to importin-α. Our previous simulations of non-competitive binding of the coreNLS, in which it natively binds to importin-α, are used as a reference. Both inhibitors abrogate native peptide binding and reduce the fraction of its native interactions, but they fail to prevent its non-native binding to importin-α. As a result, these inhibitors turn the coreNLS into diffusive binder, which adopts a manifold of non-native binding poses. Competition from the inhibitors compromises the free energy of coreNLS binding to importin-α showing that they reduce its binding affinity. The inhibition mechanism is based on masking the native binding interactions formed by the coreNLS amino acids. Surprisingly, ligand interference with the binding interactions formed by importin-α amino acids contributes little to inhibition. We show that DP9 is a stronger inhibitor than DP9o. By comparative analysis of DP9 and DP9o interactions we determine the atomistic reason for a relative \\\"success\\\" of DP9, which is due to the intercalation of this inhibitor between the side chains of NLS lysine residues. To test our simulations, we performed AlphaScreen experiments measuring IC50 values for the inhibitors. AlphaScreen data confirmed in silico ranking of the inhibitors. 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Ligands binding diffusively to protein target act as inhibitors of protein-protein interactions.
Nuclear localization signal (NLS) sequence from capsid protein of Venezuelan equine encephalitis virus (VEEV) binds to importin-α transport protein and clogs nuclear import. Prevention of viral NLS binding to importin-α may represent a viable therapeutic route. Here, we investigate the molecular mechanism by which two diffusively binding inhibitors, DP9 and DP9o, interfere with the binding of VEEV's NLS peptide to importin-α. Our study uses all-atom replica exchange molecular dynamics simulations, which probe the competitive binding of the VEEV NLS fragment, the coreNLS peptide, and the inhibitors to importin-α. Our previous simulations of non-competitive binding of the coreNLS, in which it natively binds to importin-α, are used as a reference. Both inhibitors abrogate native peptide binding and reduce the fraction of its native interactions, but they fail to prevent its non-native binding to importin-α. As a result, these inhibitors turn the coreNLS into diffusive binder, which adopts a manifold of non-native binding poses. Competition from the inhibitors compromises the free energy of coreNLS binding to importin-α showing that they reduce its binding affinity. The inhibition mechanism is based on masking the native binding interactions formed by the coreNLS amino acids. Surprisingly, ligand interference with the binding interactions formed by importin-α amino acids contributes little to inhibition. We show that DP9 is a stronger inhibitor than DP9o. By comparative analysis of DP9 and DP9o interactions we determine the atomistic reason for a relative "success" of DP9, which is due to the intercalation of this inhibitor between the side chains of NLS lysine residues. To test our simulations, we performed AlphaScreen experiments measuring IC50 values for the inhibitors. AlphaScreen data confirmed in silico ranking of the inhibitors. By combining our recent studies, we discuss the putative mechanism by which diffusively binding inhibitors impact protein-protein interactions.
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