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. 2010 Apr 1;5(4):e9982. doi: 10.1371/journal.pone.0009982

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Southgate et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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WT MEF exhibited an increase in ERK phosphorylation in response to CXCL12 stimulation that was prevented by the MEK1 inhibitor PD98059 (M, 50 µM) and the CXCR4 inhibitor AMD3100 (C, 10 µM) but not by the PI3K inhibitor LY294002 (P, 50 µM). 5T4KO MEF did not respond to CXCL12 stimulation, and this lack of response was specifically related to CXCR4 function and not due to a generalized disruption of MAPK/ERK signaling as both WT and KO MEF exhibited an increase in ERK1/2 phosphorylation in response to PMA stimulation, which was blocked by MEK1 inhibition but independent of both CXCR4 and PI3K activity. Total ERK was used as a loading control.