◀ Back to PLD1

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