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CREB1 — PI3

Text-mined interactions from Literome

Trümper et al., J Endocrinol 2002 (MAP Kinase Signaling System) : These interactions included : ( i ) a central role of tyrosine phosphorylation for stimulation of PKA/CREB, MAPK and PI3-kinase/PKB, ( ii ) inhibition of PKA/CREB by the MAPK pathway at the level of MAPK kinase-1 or downstream, ( iii ) activation of MAPK signaling by PI3-kinase and PKA at the level of extracellular-signal regulated kinase 1/2 or upstream, and ( iv ) activation of PKB by MAPK and PKA signaling at the level of PKB or upstream
Milani et al., J Neurochem 2003 (Neuroblastoma) : Moreover, TRAIL increased CREB phosphorylation and phospho-CREB DNA binding activity in a phosphatidylinositol 3-kinase (PI 3K)/Akt dependent manner
Lin et al., J Neurosci 2003 : Likewise, PI-3 kinase inhibitor blocked fear training induced cAMP response element binding protein ( CREB ) phosphorylation as well as extinction training induced decrease in CREB phosphorylation, the latter of which was associated with calcineurin expression and could be reversed by a specific calcineurin inhibitor
Misra et al., J Cell Biochem 2004 : Silencing of the CREB gene with dsRNA homologous in sequence to the target gene, markedly reduced the levels of CREB mRNA activation of CREB, PI 3-kinase , Akt, and p70s6k in alpha2M* stimulated macrophages
Wang et al., Mol Biol Cell 2005 (Inflammation) : Moreover, the phosphatidylinositol 3 (PI3)-kinase inhibitor ( wortmannin ) and p38 ( MAPK ) inhibitor ( SB203580 ) inhibited the EGF induced CREB phosphorylation and the expression of NF-IL6beta gene in cells
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
Garat et al., Mol Cell Biol 2006 : Subsequent studies showed that PDGF activated extracellular signal regulated kinase, Jun N-terminal protein kinase, and phosphatidylinositol 3 (PI3)-kinase pathways in SMCs. Inhibition of these pathways blocked SMC proliferation in response to PDGF, but only inhibition of PI3-kinase or its effector, Akt, blocked PDGF induced CREB loss
Husse et al., Heart international 2010 : The inhibition of PKA, PKC, MEK, p38-MAPK or PI3-kinase partially reduced the strain induced CREB phosphorylation