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. 2010 Nov 24;39(7):2503–2518. doi: 10.1093/nar/gkq1178

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© The Author(s) 2010. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 9. — A model of stress-dependent transcriptional activation of IEGs including the proposed p38 MAPK/MK2/3/SRF/SRE pathway. PMA and anisomycin are indicated as stimuli which are specific for ERK and p38MAPK/JNK activation, respectively. A typical IEG promoter contains SREs and CREs. SRF together with ternary complex factors, such as ELk1, bind to SRE. Elk1 may also bind directly to the ETS-Box (58). CRE-binding protein, CREB, and activating transcription factor (ATF) 1 bind to CRE. Phosphorylations of the different factors at the amino acids indicated contribute to transactivation. MSK1 is activated by both ERKs and p38a and increases CREB/ATF1 activity. ERKs and JNKs directly phosphorylate and activate the TCF Elk1. RSK and MK2/3 are activated by ERKs and p38a, respectively, and stimulate SRF activity. Chromatin remodelling via phosphorylation of histone H3 by MSK1 and components of the PRC 1 by MK2/3 or p38 might further contribute to IEG transcription.