Journal: Bioinformatics and Biology Insights

Article Title: Computational and Experimental Characterization of Mycobacterium marinum β-Carbonic Anhydrase Inhibitors

doi: 10.1177/11779322261427120

Figure Lengend Snippet: Docking pose of protein and ligand complex file while images (A-C) show for compound F2686-0257, and images (D-F) show for compound F1011-1367.

Article Snippet: Molecular dynamics simulations more than 100 ns confirmed stable backbones and conserved binding pockets, with F2686-0257 stabilized by aromatic anchoring and F1011-1367 by polar interactions.

Techniques:

Journal: Bioinformatics and Biology Insights

Article Title: Computational and Experimental Characterization of Mycobacterium marinum β-Carbonic Anhydrase Inhibitors

doi: 10.1177/11779322261427120

Figure Lengend Snippet: RMSD and RMSF plots of molecular dynamics (MD) of complexes of 2 compounds docked with the CA model protein, while images (A-B) show for compound F2686-0257, and images (C-D) show for compound F1011-1367.

Article Snippet: Molecular dynamics simulations more than 100 ns confirmed stable backbones and conserved binding pockets, with F2686-0257 stabilized by aromatic anchoring and F1011-1367 by polar interactions.

Techniques:

Journal: Bioinformatics and Biology Insights

Article Title: Computational and Experimental Characterization of Mycobacterium marinum β-Carbonic Anhydrase Inhibitors

doi: 10.1177/11779322261427120

Figure Lengend Snippet: Ligand property plots (RMSD, Radius of Gyration, Intra HB, MoLSA, SASA, and PSA) of molecular dynamics (MD) of protein-ligand complexes of hit compounds F2686-0257 and F1011-1367, respectively.

Article Snippet: Molecular dynamics simulations more than 100 ns confirmed stable backbones and conserved binding pockets, with F2686-0257 stabilized by aromatic anchoring and F1011-1367 by polar interactions.

Techniques:

Journal: Medicine

Article Title: Prediction of the therapeutic mechanism of Sugemule-4 in insomnia treatment using network pharmacology and molecular docking

doi: 10.1097/MD.0000000000046489

Figure Lengend Snippet: Results of molecular docking of EGFR with 5 active ingredients. (A) Apigenin, (B) luteolin, (C) piplartine, (D) dauricine, and (E) pinocembrin. EGFR = epidermal growth factor receptor.

Article Snippet: Molecular dynamics confirmed stable interactions of EGFR with apigenin, luteolin, and piplartine.

Techniques:

Journal: Medicine

Article Title: Prediction of the therapeutic mechanism of Sugemule-4 in insomnia treatment using network pharmacology and molecular docking

doi: 10.1097/MD.0000000000046489

Figure Lengend Snippet: Protein root mean square deviation. (A) EGFR–apigenin, (B) EGFR–luteolin, and (C) EGFR–piplartine. EGFR = epidermal growth factor receptor.

Article Snippet: Molecular dynamics confirmed stable interactions of EGFR with apigenin, luteolin, and piplartine.

Techniques:

Journal: Medicine

Article Title: Prediction of the therapeutic mechanism of Sugemule-4 in insomnia treatment using network pharmacology and molecular docking

doi: 10.1097/MD.0000000000046489

Figure Lengend Snippet: Radius of gyration. (A) EGFR–apigenin, (B) EGFR–luteolin, and (C) EGFR–piplartine. EGFR = epidermal growth factor receptor.

Article Snippet: Molecular dynamics confirmed stable interactions of EGFR with apigenin, luteolin, and piplartine.

Techniques:

Journal: Clinical immunology (Orlando, Fla.)

Article Title: Characterization of Vibrio cholerae neuraminidase as an immunomodulator for novel formulation of oral allergy immunotherapy

doi: 10.1016/j.clim.2018.03.017

Figure Lengend Snippet: NA, AAL and WGA remained stable up to 180 min in SGF experiments (A) and bound to Caco-2 cells in a dose-dependent manner (B; FITC-NA: 16 μg: blue line, 32 μg: orange line, 64 μg: light green line, 128 μg: dark green line versus MFI control (red line) left panel, WGA: light blue line, AAL: orange line versus MFI control (red line). AAL was inhibited by α-L fucose and WGA by TCT. GM1 and α-L fucose inhibited NA binding to Caco-2 cells in a dose-dependent manner (C, n = 3). Data are presented as mean ± standard error of mean (SEM). #P, statistical significant differences to the uninhibited control (0 μM); *P, significant differences between α-L fucose and TCT inhibitions at same concentrations. *P/#P < 0.05, **P/##P < 0.01, ###P < 0.001, ####P < 0.0001. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The targeting molecule NA from Vibrio cholerae (Type III, sterile filtered, 1–5 units/mg protein, N7885, Sigma-Aldrich, St. Louis, MO) was tested for its gastric stability in simulated gastric fluid (SGF) as described previously and compared to the lectins AAL (L-1390) and WGA (L-1020, both from Vector Laboratories, Burlingame, CA, USA) [ 19 ].

Techniques: Binding Assay

Journal: Clinical immunology (Orlando, Fla.)

Article Title: Characterization of Vibrio cholerae neuraminidase as an immunomodulator for novel formulation of oral allergy immunotherapy

doi: 10.1016/j.clim.2018.03.017

Figure Lengend Snippet: Encapsulation of OVA in uncoated MPs (Plain-MPs) or functionalized MPs (NA-MPs, AAL-MPs, WGA-MPs) ensured protein integrity up to 120 min in SGF experiments in contrast to unprotected OVA.

Article Snippet: The targeting molecule NA from Vibrio cholerae (Type III, sterile filtered, 1–5 units/mg protein, N7885, Sigma-Aldrich, St. Louis, MO) was tested for its gastric stability in simulated gastric fluid (SGF) as described previously and compared to the lectins AAL (L-1390) and WGA (L-1020, both from Vector Laboratories, Burlingame, CA, USA) [ 19 ].

Techniques:

Journal: Scientific Reports

Article Title: Comparative assessment of favipiravir and remdesivir against human coronavirus NL63 in molecular docking and cell culture models

doi: 10.1038/s41598-021-02972-y

Figure Lengend Snippet: Binding mode of favipiravir to the SARS-CoV-2 and HCoV-NL63 RdRp. ( A ) Favipiravir, bound to the SARS-CoV-2 RdRp (atom color ribbons) binding site, was depicted as surface representation with H-bond donor (purple) and acceptor (green). ( B ) Molecular interactions of favipiravir (atom color sticks) with the SARS-CoV-2 RdRp residues (yellow sticks). ( C ) 2D diagram of interactions between SARS-CoV-2 RdRp and favipiravir. ( D ) Favipiravir, bound to the HCoV-NL63 RdRp (atom color ribbons) binding site, was depicted as surface representation with H-bond donor (purple) and acceptor (green). ( E ) Molecular interactions of favipiravir (atom color sticks) with the HCoV-NL63 RdRp residues (yellow sticks). ( F ) 2D diagram of interactions between HCoV-NL63 RdRp and favipiravir.

Article Snippet: Molecular dynamics simulation further confirmed the stability of favipiravir and remdesivir binding to the SARS-CoV-2 and HCoV-NL63 RdRp.

Techniques: Binding Assay

Journal: Scientific Reports

Article Title: Comparative assessment of favipiravir and remdesivir against human coronavirus NL63 in molecular docking and cell culture models

doi: 10.1038/s41598-021-02972-y

Figure Lengend Snippet: The root-mean-square deviations (RMSDs) of the backbone atoms and its ligands complex relative to their coordinates as a function of simulation time. ( A ) The average RMSDs of SARS-CoV-2 RdRp backbone atoms (Blue line) and its complexes with favipiravir (Green Line) or remdesivir (Red line) were plotted against the total simulation time. ( B ) The average RMSDs of HCoV-NL63 RdRp backbone atoms (Blue line) and its complexes with favipiravir (Green Line) or remdesivir (Red line) were plotted against the total simulation time.

Article Snippet: Molecular dynamics simulation further confirmed the stability of favipiravir and remdesivir binding to the SARS-CoV-2 and HCoV-NL63 RdRp.

Techniques:

Journal: Scientific Reports

Article Title: Comparative assessment of favipiravir and remdesivir against human coronavirus NL63 in molecular docking and cell culture models

doi: 10.1038/s41598-021-02972-y

Figure Lengend Snippet: Antiviral effects of favipiravir against HCoV-NL63 in cell culture models. ( A ) Dose-dependent inhibition of HCoV-NL63 replication in LLC-MK2 cell line by favipiravir treatment. Intracellular viral RNA quantified by qRT-PCR was normalized to housekeeping gene GAPDH and presented relative to the control (CTR) (set as 1) (n = 6). ( B ) Immunofluorescence microscopy analysis of dsRNA, the intermediate of replicating HCoV-NL63 genomic RNA, upon treatment of different concentrations of favipiravir in LLC-MK2 and Caco-2 cell lines. Nuclei were visualized by DAPI (blue). ( C ) Dose-dependent inhibition of HCoV-NL63 replication by favipiravir in Caco-2 cell line (n = 6). ( D ) Caco-2 cells were infected with 0.1 MOI HCoV-NL63 and treated with different concentrations of favipiravir for 48 h. 50% effective concentration (EC50) curve was quantified by qRT-PCR, and 50% cytotoxic concentration (CC50) curve was determined by MTT assay. The left and right Y-axis of the graphs represent mean % inhibition of virus yield and cytotoxicity of the drug, respectively (n = 6–8). ( E ) Caco-2 cells were infected with 0.1 MOI HCoV-NL63, and then untreated or treated with 10 μM favipiravir for 5 days. Supernatant was collected every day to quantify secreted viruses by qRT-PCR, calculated as genomic copy numbers (n = 6). Standard curve for calculation of genomic copy numbers is included in Supplementary Fig. . ( F ) Caco-2 cells were infected with 0.1 MOI HCoV-NL63, and then untreated or treated with 1 or 100 μM favipiravir for 48 h. Virus titers from different groups was determined by TCID50 assay (n = 6). Data represent as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Molecular dynamics simulation further confirmed the stability of favipiravir and remdesivir binding to the SARS-CoV-2 and HCoV-NL63 RdRp.

Techniques: Cell Culture, Inhibition, Quantitative RT-PCR, Immunofluorescence, Microscopy, Infection, Concentration Assay, MTT Assay, TCID50 Assay

Journal: Scientific Reports

Article Title: Comparative assessment of favipiravir and remdesivir against human coronavirus NL63 in molecular docking and cell culture models

doi: 10.1038/s41598-021-02972-y

Figure Lengend Snippet: Antiviral effects of remdesivir against HCoV-NL63 in vitro. ( A ) Dose-dependent inhibition of HCoV-NL63 replication by remdesivir in LLC-MK2 cell line. Intracellular viral RNA quantified by qRT-PCR was normalized to housekeeping gene GAPDH and presented relative to the control (CTR) (set as 1) (n = 6–8). ( B ) Immunofluorescence microscopy analysis of dsRNA, the replicating HCoV-NL63 genomic RNA, upon treatment of different concentrations of remdesivir in LLC-MK2 and Caco-2 cell lines. Nuclei were visualized by DAPI (blue). ( C ) Dose-dependent inhibition of HCoV-NL63 replication by remdesivir on in Caco-2 cell line (n = 6). ( D ) Caco-2 cells were infected with 0.1 MOI HCoV-NL63 and treated with different concentrations of remdesivir for 48 h. 50% effective concentration (EC50) curve was quantified by qRT-PCR, and 50% cytotoxic concentration (CC50) curve was determined by MTT assay. The left and right Y-axis of the graphs represent mean % inhibition of virus yield and cytotoxicity of the drug, respectively (n = 6–8). ( E ) Caco-2 cells were infected with 0.1 MOI HCoV-NL63, and then untreated or treated with 1 μM remdesivir for 5 days. Supernatant was collected every day to quantify secreted viruses by qRT-PCR and calculated as genomic copy numbers (n = 6). Standard curve for calculation of genomic copy numbers is included in Supplementary Fig. . ( F ) Caco-2 cells were infected with HCoV-NL63 at an MOI of 0.1, then untreated or treated with 0.3 or 3 μM remdesivir for 48 h. Virus titers from different groups was determined by TCID50 assay (n = 6). Data represent as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001. ( G ) Comparing the inhibitory potency of favipiravir and remdesivir in Caco-2 cells infected with HCoV-NL63. ( H ) HCoV-NL63 was serially passaged in Caco-2 cells exposed to no remdesivir (as control) or increasing concentrations of remdesivir for 20 passages. 1 μM remdesivir was used in passage 1–10, which was increased to 2 μM at the subsequent passages. The effect of remdesivir (1 μM) on HCoV-NL63 harvested at passage 5, 10, 15 and 20 was quantified using qRT-PCR. Data represent as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Molecular dynamics simulation further confirmed the stability of favipiravir and remdesivir binding to the SARS-CoV-2 and HCoV-NL63 RdRp.

Techniques: In Vitro, Inhibition, Quantitative RT-PCR, Immunofluorescence, Microscopy, Infection, Concentration Assay, MTT Assay, TCID50 Assay

Journal: Scientific Reports

Article Title: Comparative assessment of favipiravir and remdesivir against human coronavirus NL63 in molecular docking and cell culture models

doi: 10.1038/s41598-021-02972-y

Figure Lengend Snippet: The effects of combining antivirals in Caco-2 cells infected with HCoV-NL63. The antiviral effects of favipiravir in combination with remdesivir ( A ), or IFN-α in combination with favipiravir ( B ) or remdesivir ( C ) respectively. The results were analyzed by the MacSynergyII model. The three-dimensional surface plot represents the differences (within 95% confidence interval) between actual experimental effects and theoretical additive effects of the combination at various concentrations (n = 4).

Article Snippet: Molecular dynamics simulation further confirmed the stability of favipiravir and remdesivir binding to the SARS-CoV-2 and HCoV-NL63 RdRp.

Techniques: Infection