Fig. 2: The designs display potent and specific activity in cell-based assays.
From: A topological refactoring design strategy yields highly stable granulopoietic proteins
A Dose–response curves of NFS-60 proliferation upon 48 h treatment with Filgrastim (rhG-GCSF), Boskar3, or Boskar4. Datapoints and error bars represent mean ± standard deviations of three biologically independent replicates. B Time-dependent proliferation trajectory of surface-immobilised NFS-60 cells over a 10-day treatment. Data points and shades represent mean and standard deviation values of three biologically independent replicates. Experiments were performed three times in triplicates. Data of one representative experiment is shown. C, D Dose- and time-dependent proliferation trajectories over a 5-day treatment of free-floating NFS-60 cells, under the influence of Boskar3 and Boskar4 treatments, respectively. Data points and shades represent mean and standard deviation values of three biologically independent replicates. E G-CSFR-deficient primary stem cells (G-CSFR KO), show abolished proliferative responses to either rhG-CSF or the designs. Experiment was performed twice in triplicates. Data points and shades represent mean and standard deviation values of three biologically independent replicates. F Intracellular levels of phospho-AKT (Thr308), phospho-ERK1/2 (p44/42 MAPK), phospho-STAT3 (Tyr705), and phospho-STAT5 (Tyr694) in CD34+ HSPCs treated with rhG-CSF or the designs (see the “Methods” section). Geometric mean of the expression intensity of each phospho-protein (GeoMean intensity) is shown on the y-axis. The experiment was performed twice.
