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ANGPT2 — PLD2

Text-mined interactions from Literome

Andresen et al., Hypertension 2001 (Hypertension) : Therefore, we conclude that in PGSMCs, the effect of Ang II on PLD activity is ( 1 ) greater in SHR ; ( 2 ) mediated by AT(1) receptors signaling to PLD2 ; ( 3 ) transduced primarily by Rho proteins ; and ( 4 ) inhibited in SHR by brefeldin A ... Inhibitors of phosphoinositol-3-kinase and protein kinase C did not block Ang II-induced PLD activity in SHR and WKY PGSMCs. Catalytically-inactive constructs of PLD2 and RhoA, but not PLD1, ADP ribosylation factor 1 (ARF1), ARF6, or ADP ribosylation factor nucleotide exchange factor ( ARNO ) blocked Ang II-induced PLD activity in SHR and WKY PGSMCs. Brefeldin A completely blocked Ang II-induced PLD activity in SHR but only slightly reduced Ang II-induced PLD activity in WKY PGSMCs
Li et al., J Pharmacol Exp Ther 2005 : These data indicate that Ang II-stimulated Akt activity is mediated by cPLA(2) dependent, p38 MAPK regulated PLD(2) activation and EGFR transactivation
Andresen et al., American journal of physiology. Renal physiology 2005 (Hypertension, Renal) : ANG II activation of phospholipase D ( PLD ) is required for ERK and NAD ( P ) H oxidase activation, both of which are involved in hypertension
Parmentier et al., Am J Physiol Heart Circ Physiol 2006 (Hypertrophy) : ANG II stimulates phospholipase D ( PLD ) activity and growth of vascular smooth muscle cells ( VSMC ) ... ANG II stimulated PKCzeta activity with maximal activation at 30 s followed by a decline in its activity to 45 % above basal at 5 min. Inhibition of PKCzeta activity with a myristoylated pseudosubstrate peptide or overexpression of a kinase-inactive form of PKCzeta decreased ANG II-induced PLD activity
Touyz et al., Methods Mol Med 2001 : The Gß? subunits as well as their associated Ga ( 12 ) subunits, mediate Ang II-induced PLD activation via Src dependent mechanisms in vascular smooth muscle cells
Freeman et al., Arch Biochem Biophys 1995 : To determine whether PLD stimulation by Ang II is the result of PLC activation and the subsequent elevation of cytosolic free Ca2+ and PKC activation, we investigated the role of Ca2+ and PKC in the activation of PLD
Freeman et al., Biochem J 1994 : Alternatively, PLD may be sequentially activated in response to Ang II activation of PLC and a subsequent increase in calcium concentration
Freeman et al., Am J Hypertens 1995 (Hypertension) : Furthermore, Ang II-induced activation of PLD in VSMC from hypertensive rats was significant within 1 min, whereas significant increases in PLD activity in cells from normotensive rats were not seen until 10 min after exposure to Ang II
Suzuki et al., Atherosclerosis 1996 : These results suggest that Ang II stimulates phosphatidylcholine hydrolyzing phospholipase D due to Ca2+ influx from the extracellular space in rat aortic SMC, and that protein tyrosine kinase is involved in the Ang II-induced Ca2+ influx, resulting in the promotion of phosphatidylcholine hydrolysis
Jung et al., Biochem J 1998 : These results suggest that the Ang II-elicited activation of PLD is associated with a sustained increase in aldosterone secretion from glomerulosa cells and further provide the first evidence, to our knowledge, of differences in the kinetics of PLD activation in response to two physiologically relevant agonists
Ushio-Fukai et al., Mol Pharmacol 1999 : In intact cells, Ang II activation of PLD was pertussis toxin-insensitive and was not additive with sodium fluoride, a cell-permeant activator of heterotrimeric G proteins, indicating that AT1 receptor-PLD coupling requires pertussis toxin-insensitive heterotrimeric G proteins