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CREB1 — INS
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Ban et al., Diabetes 2000
:
Furthermore, when transfected into rat primary cultured islets, ATF-2
enhanced glucose induced
insulin promoter activity, whereas cAMP response element binding protein (
CREB ) repressed it
Grimes et al., J Neurochem 2001
:
Conversely, overexpression of active GSK3 beta to 3.5-fold the normal levels completely blocked increases in
CREB DNA binding activity
induced by epidermal growth factor,
insulin-like growth factor-1, forskolin, and cyclic AMP
Huang et al., Mol Cell Neurosci 2005
:
Insulin also
induced rapid and long-term ( 30 h ) PI 3-K dependent phosphorylation of Akt and cAMP response element binding protein (
CREB )
Canettieri et al., Cell Metab 2005
:
Here, we show that, in parallel with their effects on glucose output,
CREB and TORC2 also
enhance insulin signaling in liver by stimulating expression of the insulin receptor substrate 2 (IRS2) gene
Schnoke et al., J Orthop Res 2007
:
Some signaling molecules like the extracellular response kinases 1/2 ( Erk1/2 ) and the cAMP response element binding protein (
CREB ) were
activated by
insulin and PTH, respectively, but not by PEMF treatment
Wang et al., Cell Metab 2008
(Starvation) :
The
insulin regulated
CREB coactivator TORC promotes stress resistance in Drosophila
Liu et al., Am J Physiol Endocrinol Metab 2012
(Diabetes Mellitus, Type 2...) :
Furthermore,
d-INS increased ß-catenin phosphorylation, its nuclear translocation, and
enhanced cAMP response element binding protein (
CREB ) phosphorylation in a phosphatidylinositol 3-kinase and/or mitogen activated protein kinase kinase/extracellular signal regulated kinase-sensitive manner
Reusch et al., Endocrinology 1994
:
Insulin increased in vivo phosphorylation of
CREB by 40 %
Klemm et al., J Biol Chem 1998
:
Earlier studies from our laboratory demonstrated an
insulin mediated
increase in cAMP-response element binding protein (
CREB ) phosphorylation ...
Insulin stimulated the phosphorylation of
CREB at serine 133, the protein kinase A site, and mutation of serine 133 to alanine blocked the insulin effect ... The ability of
insulin to
induce CREB phosphorylation and activity was efficiently blocked by PD98059, a potent inhibitor of mitogen activated protein kinase kinase ( MEK1 ), but not significantly by rapamycin or wortmannin ... Likewise, expression of dominant negative forms of Ras or Raf-1 completely blocked
insulin stimulated
CREB transcriptional activity ... Finally, we demonstrate an essential
role for
CREB in
insulin activation of fatty-acid synthase and fatty acid binding protein (FABP) indicating the potential physiologic relevance of insulin regulation of CREB ... In summary,
insulin regulates
CREB transcriptional activity in insulin-sensitive tissues via the Raf -- > MEK pathway and has an impact on physiologically relevant genes in these cells
Pugazhenthi et al., J Biol Chem 1999
:
CREB phosphorylation at serine 133 and its transcriptional activation as measured by a CREB-specific Gal4-CREB reporter and the neuroendocrine-specific gene chromogranin A was
induced 2-3.3-fold by
insulin-like growth factor (IGF)-I