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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 8. — ATF3 mediates neuropeptide and Wnt2b expression in primary PNS neurons. (a–d) Adult wt or ATF3-deficient mouse DRG neurons were infected with adenoviral (AV) particles resulting in GFP (control) or ATF3 expression. mRNA levels of Atf3 (a), Wnt2b (b), Galanin (c) and Grp (d) were analysed by qPCR. Viral infection strongly enhanced Atf3 mRNA abundance in wt and Atf3 mutant neurons (a). Wnt2b (b), Galanin (c) and Grp (d) mRNA levels were augmented upon viral ATF3 overexpression in wt and Atf3 mutant DRG neurons. (e,f) Primary wt neurons overexpressing GFP or ATF3 were subjected to ChIP analysis with anti-ATF3 or IgG (control) antibodies. ATF3 occupancy at potential ATF3 binding sites of the Galanin (e) and Grp (f) promoter was tested with qPCR. ATF3 promoter occupancy was observed in ATF3-overexpressing samples only in the presence of anti-ATF3 but not IgG antibodies suggesting ATF3 binding at the Galanin (e) and Grp (f) promoter. Numbers in bars reflect independent numbers of experiments. Data are presented as mean ± s.d. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001.