ERK5 and ERK2 Cooperate to Regulate NF-κB and Cell Transformation*

By G. Pearson, J. English, M. White, M. Cobb. Journal of Biological Chemistry, 2001

124 citations recorded by the source corpus.

We have previously demonstrated an involvement of MEK5 and ERK5 in RafBXB-stimulated focus formation in NIH3T3 cells. We find here that MEK5 and ERK5 cooperate with the RafBXB effectors MEK1/2 and ERK1/2 to induce foci. To further understand MEK5-ERK5-dependent signaling, we examined potential MEK5-ERK5 effectors that might influence focus-forming activity. Consistent with results from our focus-formation assays, constitutively active variants of MEK5 and MEK1 synergize to activate NF-κB, and MEK5 and ERK5 are required for activation of NF-κB by RafBXB. The MEK5-ERK5 pathway is also sufficient to activate both NF-κB and p90 ribosomal S6 kinase. Our results support the hypothesis that NF-κB and p90 ribosomal S6 kinase are involved in MEK5-ERK5-dependent focus formation and may serve as integration points for ERK5 and ERK1/2 signaling.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7da877f80b0c27bde0495a3ff1f65baf58c52622

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In Molecular Biology

Citations in the corpus

Mitogen-activated protein kinases in apoptosis regulation (2004, background): “The ERK5 pathway is also upregulated in cancer cells (Robinson et al., 1996; Pearson et al., 2001; Mehta et al., 2003).”