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CREB5 — MAP2K1
Text-mined interactions from Literome
Gubina et al., J Immunol 2001
:
Inhibition of
mitogen activated protein kinase kinase activity also
inhibited IL3 induced
CREB phosphorylation
Kolonics et al., Cell Signal 2001
(MAP Kinase Signaling System) :
The GM-CSF promoted cell survival and proliferation correlated with
MEK-1 dependent ERK1/2, Elk-1 and
CREB phosphorylation and Egr-1, c-Fos expression as well as with increased STAT-5, AP-1, c-Myb and NF-kappaB DNA binding
Mehrhof et al., Circulation 2001
:
IGF-I also induced phosphorylation of cAMP response element binding protein (
CREB ) in a PI3K- and
MEK1 dependent manner
Qiao et al., Mol Cell Biol 2003
:
Inhibition of C/EBPbeta,
CREB , and c-Jun function promoted apoptosis following DCA treatment, and the level of apoptosis was further
increased in the case of CREB and c-Jun, but not C/EBPbeta, by inhibition of
MEK1/2
Zhang et al., Brain Res Bull 2003
(Hypothalamic Neoplasms) :
However,
MEK1/2 inhibitor, CaMKII inhibitor, and PKC inhibitor significantly
suppressed lead induced
CREB phosphorylation
Maldonado et al., Biochem Biophys Res Commun 2005
(Calcium Signaling) :
IGF-1 induced
CREB phosphorylation was
mediated by
MEK1/ERK , PI3-K, p38-MAPK, as well as Ca ( 2+ ) /calmodulin kinase and calcineurin
Keeley et al., Biotechniques 2005
(MAP Kinase Signaling System) :
The novel hybrid transcription factor TetR-Elk-1 was regulated by
MAPK ERK kinase 1 (MEK-1) overexpression, and
TetR-CREB was
regulated by protein kinase A (PKA) overexpression or elevation of cyclic AMP levels
Suzuki et al., J Comp Neurol 2007
:
MKK1 is
required to reduce spine head size when spine density is high, whereas
CREB is required to enlarge spines when spine density is low
Rosethorne et al., Biochem Pharmacol 2008
(Neuroblastoma...) :
In contrast, inhibition of
MEK1/2 by U0126
resulted in significantly reduced
CREB phosphorylation levels after B2 bradykinin, but not M3 mACh receptor activation
Ozgen et al., Mol Pharmacol 2009
:
Rather, the H2O2 dependent decrease in
CREB protein is
prevented by the proteasome inhibitor lactacystin, by inhibitors of
mitogen activated protein kinase kinase or protein kinase C activity, or by adenoviral mediated delivery of a small interfering RNA that decreases PKD1 expression