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pubmed-article:20942268pubmed:abstractTextWe 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.lld:pubmed
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pubmed-article:20942268pubmed:articleTitleDisruption of cell spreading by the activation of MEK/ERK pathway is dependent on AP-1 activity.lld:pubmed
pubmed-article:20942268pubmed:affiliationDepartment of Cancer Biology, Nagoya University Graduate School of Medicine.lld:pubmed
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