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. 2012 Mar 9;10:6. doi: 10.1186/1478-811X-10-6

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Copyright ©2012 Faust et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Proposed hypothetical model describing different p38 signalling pathways in response to mitogens and cellular stress. Anisomycin leads to a sustained phosphorylation of p38 which is independent of upstream-acting small GTPases and accompanied by an accumulation of p38 in the nucleus. One downstream substrate of p38 is CREB. In contrast, p38 is transiently phosphorylated after serum-stimulation in a GTPase-dependent manner and cyclin D1 is upregulated. The cellular response is proliferation.