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. 2020 Feb 7;21(3):e49129. doi: 10.15252/embr.201949129

Figure 1. Identification of E4 as a modulator of retrograde axonal transport.

Figure 1

  1. Small‐molecule kinase inhibitor screen. Data are shown as an XY plot of normalized mean staining intensity of Alexa Fluor 555‐HcT versus α‐p75NTR. The α‐p75NTR was detected using an Alexa Fluor 647‐conjugated donkey anti‐rabbit secondary antibody 12. Compounds that increased the accumulation of HcT or α‐p75NTR by at least three standard deviations (yellow box) were classified as active compounds (A1—light blue; C3—purple; E4—dark blue). The negative control (EHNA) is shown in red (≥ 25 cell bodies were imaged per condition, N = 3 independent experiments).
  2. Speed distribution profile of PMN treated with 0.5 μM E4 or DMSO for 30 min. Graph shows an increase in the rate of axonal transport upon E4 treatment (DMSO, 153 endosomes, 13 axons; E4, 165 endosomes, 13 axons; N = 4 independent experiments; data shown are mean ± SEM).
  3. PMN treated with 0.5 μM E4 for 30 min showed a significant decrease in phospho‐IGF1R levels compared to controls. Protein levels were normalized to β‐actin (***P < 0.001, Student's t‐test, N = 3 independent experiments; data shown are mean ± SEM).