◀ Back to AKT2
AKT2 — PLD1
Text-mined interactions from Literome
Wang et al., Biochem Pharmacol 2003
:
Collectively, these results indicate that the inhibition by CCY1a of fMLP induced O2 ( .- ) generation in rat neutrophils can probably be attributed to the increase in cAMP levels, and to the blockade of Ca2+ entry, suppression of
Akt , and
PLD activation via cAMP independent mechanisms
Kam et al., FASEB J 2004
:
PDGF induced marked phosphorylation of
Akt ( a PI3K target ) but this was not
affected by
PLD deficiency ... LPA caused much less phosphorylation of
Akt and this was
dependent on
PLD activity
Li et al., J Pharmacol Exp Ther 2005
:
Diacylglycerol kinase inhibitor II diminished Ang II-induced and diC8-phosphatidic acid ( PA ) -increased Akt phosphorylation, suggesting that
PLD dependent
Akt activation is mediated by PA
Kim et al., Cancer Res 2006
:
Etoposide induced activation of
Akt was
potentiated by overexpression of
PLD and PLD stimulated suppression of Egr-1 was blocked by inhibition of phosphatidylinositol 3-kinase/Akt survival pathway at the both transcriptional and posttranscriptional levels
Toschi et al., Mol Cell Biol 2009
:
Suppression of
PLD also
blocked insulin stimulated
Akt phosphorylation at Ser473 and the mTORC2 dependent phosphorylation of PRAS40
Chen et al., Science signaling 2012
(Breast Neoplasms...) :
PLD1 deficiency
suppressed the activation of
Akt and mitogen activated protein kinase signaling pathways by vascular endothelial growth factor in vascular endothelial cells, resulting in decreased integrin dependent cell adhesion to, and migration on, extracellular matrices, as well as reduced tumor angiogenesis in a xenograft model