Journal
JOURNAL OF CELL BIOLOGY
Volume 177, Issue 2, Pages 253-264Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200609166
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Funding
- NCI NIH HHS [CA100849, R01 CA100849] Funding Source: Medline
- NIA NIH HHS [R01 AG019193, AG19193] Funding Source: Medline
- NIDCR NIH HHS [DE015973, R01 DE015973] Funding Source: Medline
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Elucidation of mechanisms regulating cell cycle progression is of fundamental importance for cell and cancer biology. Although several genes and signaling pathways are implicated in G1-S regulation, less is known regarding the mechanisms controlling cell cycle progression through G2 and M phases. We report that extracellular signal-regulated kinase 5 (ERK5), a member of the mitogen-activated protein kinases, is activated at G2-M and required for timely mitotic entry. Stimulation of ERK5 activated nuclear factor kappa B (NF kappa B) through ribosomal S6 kinase 2 (RSK2)-mediated phosphorylation and degradation of I kappa B. Furthermore, selective inhibition of NF kappa B at G2-M phases substantially delayed mitotic entry and inhibited transcription of G2-M-specific genes, including cyclin B1, cyclin B2, Plk-1, and cdc25B. Moreover, inhibition of NF kappa B at G2-M diminished mitosis induced by constitutive activation of ERK5, providing a direct link between ERK5, NF kappa B, and regulation of G2-M progression. We conclude that a novel ERK5-NF kappa B signaling pathway plays a key role in regulation of the G2-M progression.
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