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CCND1 — FOXM1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Leung et al., FEBS Lett 2001
:
Quantitation of cyclin B1 and D1 levels using flow cytometric, Western and Northern analyses reveals that elevated
FoxM1 levels
lead to stimulation of cyclin B1 but not
cyclin D1 expression
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
Dai et al., Cancer Res 2010
(Brain Neoplasms...) :
Furthermore, overexpression of
FoxM1B in immortalized NHAs
increased the expression of survivin,
cyclin D1 , and cyclin E, which are important molecules for tumor growth
Wierstra et al., Biochem Biophys Res Commun 2013
:
Cyclin D1/Cdk4 increases the transcriptional activity of
FOXM1c without phosphorylating FOXM1c ... Anders et al. ( 2011 ) [ 11 ] reported that
cyclinD1/Cdk4 and cyclinD3/Cdk6
enhance the transcriptional activity of
FOXM1c by phosphorylating its TAD ... They defined 12 Cdk consensus sites as essential for the
activation of
FOXM1c by
cyclinD1/Cdk4 and cyclinD3/Cdk6 and stated that the 12 Cdk-sites are positioned within the TAD of FOXM1c ... This study shows that the
activation of
FOXM1c by
cyclinD1/Cdk4 is lost without removal of any cyclin/Cdk site and gained without addition of any cyclin/Cdk site because it depends on a FOXM1c domain with no potential cyclin/Cdk site, namely on the interaction domain for the tumor suppressor RB, which binds to and represses FOXM1c ...
CyclinD1/Cdk4 activates
FOXM1c because cyclinD1/Cdk4 releases FOXM1c from its repression by RB through removal of RB from FOXM1c ... For this purpose,
cyclinD1/Cdk4 phosphorylates only RB, but not FOXM1c, so that cyclinD1/Cdk4 increases the transcriptional activity of FOXM1c without phosphorylating FOXM1c and
activates FOXM1c independently of cyclin/Cdk phosphorylation sites in FOXM1c ... For this purpose,
cyclinD1/Cdk4 phosphorylates only RB, but not FOXM1c, so that cyclinD1/Cdk4 increases the transcriptional activity of FOXM1c without phosphorylating FOXM1c and
activates FOXM1c independently of cyclin/Cdk phosphorylation sites in FOXM1c ... In summary, this study changes the model of Anders et al. ( 2011 ) [ 11 ] completely because it disproves their central conclusion that
cyclinD1/Cdk4 and cyclinD3/Cdk6
enhance the transcriptional activity of
FOXM1c by phosphorylating its TAD at the 12 Cdk-sites