@article{oai:nagoya.repo.nii.ac.jp:00012294,
 author = {Xu, Feng and Ito, Satoko and Hamaguchi, Michinari and Senga, Takeshi},
 issue = {3-4},
 journal = {Nagoya Journal of Medical Science},
 month = {Aug},
 note = {We previously reported that the disruption of cell spreading by v-Crk was dependent on the activation of the MEK/ERK pathway. Here we demonstrate that the activation of that pathway is sufficient to suppress cell spreading. The MEK/ERK pathway regulates the activity of various proteins including AP-1, which is a transcriptional factor composed of heterodimeric proteins. To examine whether AP-1 activity is required for the suppression of cell spreading by the activation of the MEK/ERK pathway, we expressed BATF, which is a negative regulator of AP-1. The expression of BATF clearly restored cell spreading that was suppressed by the activation of MEK/ERK pathway. In addition, a disrupted formation of stress fibers and focal adhesions by such activation was restored by the suppression of AP-1. Our results define an essential role of the MEK/ERK/AP-1 pathway in the disruption of actin cytoskeleton and cell spreading.},
 pages = {139--144},
 title = {Disruption of Cell Spreading by the Activation of MEK/ERK Pathway is Dependent on AP-1 Activity},
 volume = {72},
 year = {2010}
}