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. 2016 Aug 31;6(8):160091. doi: 10.1098/rsob.160091

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© 2016 The Authors.

Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

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Figure 12. — Summary of ATF3's function in facial nerve regeneration. (a) In injured wild-type mice, ATF3 is involved in transcriptional activation of the RAGs Gal, Vip, Wnt2, Grp and Ngf, whereas Ccl2 is repressed. Neuropeptides would stimulate axonal growth and thereby increase axonal regeneration. By contrast, CCL2 levels in FMNs are suppressed by ATF3 and therefore CCL2's potential to decrease axon growth is reduced. (b) In lesioned Atf3 mutant mice, induction of Gal, Vip, Wnt2, Grp and Ngf is reduced, resulting in weaker stimulation of axonal growth and also reduced regeneration potential of FMNs. In addition, Ccl2 is not repressed by ATF3 anymore and enhanced CCL2 levels in injured FMNs decrease axonal growth and regeneration.