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. 2023 Feb 10;23:138. doi: 10.1186/s12885-023-10559-1

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© This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Mechanism of GDNF-EGR1 positive feedback loop. A UCSC genome browser data showing p-ELK-1 binding motif located at EGR1 promoter. B ChIP-qPCR data showing increased p-ELK-1 binding after rGDNF treatment. C UCSC genome browser data showing EGR1 binding motif located at the GDNF promoter. D ChIP-qPCR data showing increased EGR1 binding to the GDNF promoter. *p < 0.05, **p < 0.005. Student’s paired t-test was used for statistical analyses