Skip to main content
. Author manuscript; available in PMC: 2015 Jan 10.
Published in final edited form as: Biochem Biophys Res Commun. 2013 Dec 12;443(2):743–748. doi: 10.1016/j.bbrc.2013.12.037

Figure 3.

Figure 3

GSK3 inactivation in sensory neurons of GSK3α-S21A/GSK3β-S9A double knockin mice is necessary for regenerative axon growth. (A) Representative immunoblots of GSK3α, GSK3β and phosphorylated CRMP2 in adult sensory neurons from wild type (WT) or GSK3α-S21A/GSK3β-S9A double knockin (DKI) mice. Note the complete lack of phospho-GSK3α/β in the double knockin mice and similar levels of total GSK3α/β. (B) Representative immunoblots of GSK3α, GSK3β and phosphorylated CRMP2 in naïve (Nai.) adult sensory neurons or neurons with peripheral axotomy (Axt.) from wild type (WT) or double knockin (DKI) mice. Note that the levels of phosphorylated CRMP2 were reduced in adult sensory neurons from both wild type (WT) and double knockin (DKI) mice in response to peripheral axotomy. (C) Quantification of the levels of phosphorylated CRMP2 from 3 independent experiments. Error bars represent s.e.m. * indicates significant difference between indicated conditions. P<0.0001. (D) Quantification of axon growth from at least 3 independent experiments. Error bars represent s.e.m. * indicates significant difference from control (EGFP), P<0.0001. (E) Representative images of adult sensory neurons from GSK3α-S21A/GSK3β-S9A double knockin mice transfected with plasmids encoding EGFP or GSK3β-S9A. Scale bar, 100 μm.