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Figure 5 Myostatin-specific inhibition by myostatin-b. HeLa cells cotransfected with Luc and Gal plasmids were treated with recombinant myostatin at concentrations of 0, 20, 40 and 60 ng/mL (A); recombinant growth differentiation factor 11 <t>(GDF11)</t> at concentrations of 0, 10, 20 and 30 ng/mL (B); recombinant transforming growth factor β1 (TGF-β1) at concentrations of 0, 0.5, 1 and 2 ng/mL (C); and activin A at concentrations of 0, 10, 20 and 30 ng/mL (D). In addition, the myostatin-b plasmid was cotransfected into each treated cell. The results of luciferase activity are shown. Myostatin-b inhibited myostatin signalling induced only by recombinant myostatin but not by recombinant GDF11, recombinant TGF-β1 or recombinant activin A (red bars). The data are expressed as the mean ± SEM of three independent experiments. **P < 0.01, ***P < 0.001. RLU, relative luminescence unit.
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Information of antibodies

Journal: Journal of Neuroinflammation

Article Title: Stabilizing histamine release in gut mast cells mitigates peripheral and central inflammation after stroke

doi: 10.1186/s12974-023-02887-7

Figure Lengend Snippet: Information of antibodies

Article Snippet: Recombinant Human GDF11 protein (ab50159) , abcam ab50159 , 1:1000.

Techniques: Recombinant

Figure 5 Myostatin-specific inhibition by myostatin-b. HeLa cells cotransfected with Luc and Gal plasmids were treated with recombinant myostatin at concentrations of 0, 20, 40 and 60 ng/mL (A); recombinant growth differentiation factor 11 (GDF11) at concentrations of 0, 10, 20 and 30 ng/mL (B); recombinant transforming growth factor β1 (TGF-β1) at concentrations of 0, 0.5, 1 and 2 ng/mL (C); and activin A at concentrations of 0, 10, 20 and 30 ng/mL (D). In addition, the myostatin-b plasmid was cotransfected into each treated cell. The results of luciferase activity are shown. Myostatin-b inhibited myostatin signalling induced only by recombinant myostatin but not by recombinant GDF11, recombinant TGF-β1 or recombinant activin A (red bars). The data are expressed as the mean ± SEM of three independent experiments. **P < 0.01, ***P < 0.001. RLU, relative luminescence unit.

Journal: Journal of cachexia, sarcopenia and muscle

Article Title: A novel splice variant of the human MSTN gene encodes a myostatin-specific myostatin inhibitor.

doi: 10.1002/jcsm.13314

Figure Lengend Snippet: Figure 5 Myostatin-specific inhibition by myostatin-b. HeLa cells cotransfected with Luc and Gal plasmids were treated with recombinant myostatin at concentrations of 0, 20, 40 and 60 ng/mL (A); recombinant growth differentiation factor 11 (GDF11) at concentrations of 0, 10, 20 and 30 ng/mL (B); recombinant transforming growth factor β1 (TGF-β1) at concentrations of 0, 0.5, 1 and 2 ng/mL (C); and activin A at concentrations of 0, 10, 20 and 30 ng/mL (D). In addition, the myostatin-b plasmid was cotransfected into each treated cell. The results of luciferase activity are shown. Myostatin-b inhibited myostatin signalling induced only by recombinant myostatin but not by recombinant GDF11, recombinant TGF-β1 or recombinant activin A (red bars). The data are expressed as the mean ± SEM of three independent experiments. **P < 0.01, ***P < 0.001. RLU, relative luminescence unit.

Article Snippet: After 24 h, the medium was replaced with serum-free RPMI 1640 or DMEM containing recombinant myostatin (788-G8, R&D Systems), recombinant growth differentiation factor 11 (GDF11) (1958-GD, R&D Systems), recombinant TGF-β1 (240-B/CF, R&D Systems) or recombinant activin A (338-AC/CF, R&D Systems).

Techniques: Inhibition, Recombinant, Plasmid Preparation, Luciferase, Activity Assay