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CDK2 — FOXM1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database FOXM1 transcription factor network:
RB1/FOXM1C complex (FOXM1-RB1)
→
Cyclin A-E1/CDK1-2 complex (CCNA2_CCNE1-CDK2)
(modification, collaborate)
Lüscher-Firzlaff et al., FEBS Lett 2006, Wierstra et al., Biochem Biophys Res Commun 2006, Wierstra et al., Biol Chem 2006
Evidence: mutant phenotype, assay, reporter gene, physical interaction
-
Reactome Reaction:
FOXM1
→
CDK2
(reaction)
Major et al., Mol Cell Biol 2004, Laoukili et al., Mol Cell Biol 2008*, Fu et al., Nat Cell Biol 2008*
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Major et al., Mol Cell Biol 2004
(MAP Kinase Signaling System) :
We demonstrated that
FoxM1B transcriptional activity
requires binding of either S-phase or M-phase
Cdk-cyclin complexes to mediate efficient Cdk phosphorylation of the FoxM1B Thr 596 residue, which is essential for recruitment of p300/CBP coactivator proteins
Lüscher-Firzlaff et al., FEBS Lett 2006
:
Regulation of the transcription factor
FOXM1c by
Cyclin E/CDK2
Wierstra et al., Biochem Biophys Res Commun 2006
:
FOXM1c is
activated by cyclin
E/Cdk2 , cyclin A/Cdk2, and cyclin A/Cdk1, but repressed by GSK-3alpha ... Here, we demonstrate that cyclin
E/Cdk2 , cyclin A/Cdk2, and cyclin A/Cdk1
activate FOXM1c ...
Cyclin E/Cdk2 activates
FOXM1c by releasing its transactivation domain from the repression by these two inhibitory domains
Wierstra et al., Biochem Biophys Res Commun 2008
:
In contrast, we now demonstrate that this LXL-motif is not required for the activation of FOXM1c by cyclin D1/Cdk4, cyclin
E/Cdk and cyclin A/Cdk2 or for the
repression of
FOXM1c by p27
Alvarez-Fernández et al., EMBO Rep 2010
:
Recovery from a DNA-damage induced G2 arrest requires
Cdk dependent activation of
FoxM1 ... We have shown recently that
Cdk activity is
required for activation of the Forkhead transcription factor
FoxM1 , an important regulator of gene expression in the G2 phase of the cell cycle