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. 2010 Jan 26;107(7):3216–3221. doi: 10.1073/pnas.0912367107

Fig. 5.

Fig. 5.

Grb7 mediates EGF-induced, KOR-dependent axon extension in primary DRG neurons. (A) Luciferase reporter activity in P19 cells transfected with different KOR UTR reporters shown on the top. Control or EGF treatment are shown with white or gray bars (*, P < 0.05). (B) Luciferase reporter activity in P19 cells transfected with KOR 5′ and 3′-UTR reporter along with either control siRNA (Left) or Grb7-specific siRNA (Right) (*, P < 0.05). Efficient silencing was confirmed by Western blots shown on the top right. (C) Immunohistochemistry (anti-Tau) of rat DRG neurons transfected with control siRNA (first column), Grb7 siRNA (second column), Grb7 siRNA plus KOR-IRES-GFP (third column), or Grb7 siRNA plus 5′-UTR-KOR-IRES-GFP (fourth column) upon EGF treatment. Quantitative analysis of axon length by scoring 50 neurons in each experiment is shown on the right (*, P < 0.05). (Scale bars: 25 μm.) (D) Immunohistochemistry (anti-Tau) of rat DRG neurons transfected with WT or DM Flag-Grb7 or KOR-IRES-GFP constructs as indicated. Quantitative analysis of axon length by scoring 50 neurons of each experiment is shown on the right (*, P < 0.05). (Scale bars: 25 μm.)