◀ Back to SRC

PLD4 — SRC

Text-mined interactions from Literome

Khare et al., Am J Physiol 1999 : Moreover, 1,25 ( OH ) 2D3, but not TPA, activated pp60(c-src) and treatment with PP1, a specific inhibitor of the pp60(c-src) family, blocked the ability of 1,25 ( OH ) 2D3 to activate PLD ... These findings, taken together with those of the accompanying paper, indicate that although 1,25 ( OH ) 2D3 and TPA each activate PLD in Caco-2 cells in part via PKC-alpha, their stimulation of PLD differs in a number of important aspects, including the requirement for pp60(c-src) and RhoA in the activation of PLD by 1,25 ( OH ) 2D3, but not TPA
Ahn et al., Mol Cell Biol 2003 (Carcinoma, Squamous Cell) : While PLD activity as a lipid hydrolyzing enzyme is not affected by c-Src , wild-type PLDs but not catalytically inactive PLD mutants significantly increase c-Src kinase activity, up-regulating c-Src mediated paxillin phosphorylation and extracellular signal regulated kinase activity ... These results demonstrate the critical role of PLD catalytic activity in the stimulation of Src signaling
Yoon et al., FEBS Lett 2005 : To investigate the involvement of protein kinase A (PKA), Src , and Ras in 8-Br-cAMP induced PLD activation, we used PKA inhibitor, H89 and Rp-cAMPs, and transfections of DN-Src and DN-Ras ... In addition, transfection of ES cells with DN-Src, or DN-Ras partially inhibited 8-Br-cAMP induced ERK1/2 and consequently PLD activation, whereas cotransfection of DN-Src and DN-Ras completely inhibited ERK1/2 and PLD activation, suggesting that Src and Ras independently regulate ERK/PLD activation ... Taken together, these results demonstrate a novel pathway in ES cells that 8-Br-cAMP activate PLD through PKA and ERK1/2 and this ERK/PLD activation by 8-Br-cAMP is mediated by Src and Ras, separately
Oh et al., J Cell Biochem 2007 (Cell Transformation, Viral) : Furthermore, inhibition of Src and Ras partially blocked bFGF induced PLD activation and neurite outgrowth, respectively
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
Jiang et al., Nature 1995 : Involvement of Ral GTPase in v-Src induced phospholipase D activation ... An early response to the tyrosine kinase activity of v-Src is an increase in phospholipase D ( PLD ) activity, which leads to the generation of biologically active lipid second messengers, including phosphatidic acid, lysophosphatidic acid and diacylglycerol ... We have recently demonstrated that v-Src induced PLD activity is mediated by Ras, although Ras involvement was indirect, requiring a cytosolic factor for PLD activation ... Here we report that this newly identified Ras/Ral signalling pathway mediates PLD activation by v-Src ... Overexpression of RalA potentiated PLD activation by v-Src, and expression of dominant negative RalA mutants inhibited both v-Src- and v-Ras induced PLD activity
Jiang et al., J Biol Chem 1995 : We demonstrated previously that v-Src activates a phospholipase D ( PLD ) activity ( Song, J., Pfeffer, L.M., and Foster, D.A. ( 1991 ) Mol. Cell ... An in vitro PLD assay was developed to study G protein involvement in v-Src induced PLD activity ... In this report, we present three lines of evidence demonstrating that v-Src induced PLD activity is mediated by Ras
Jiang et al., Mol Cell Biol 1994 : Evidence that v-Src induced phospholipase D activity is mediated by a G protein ... v-Src induced PLD activity, as measured by PLD catalyzed transphosphatidylation of phosphatidylcholine to phosphatidylethanol, is inhibited by GDP beta S, which inhibits G-protein mediated intracellular signals ... In contrast to the PLD activity induced by v-Src, PLD activity induced by the protein kinase C agonist, 12-O-tetradecanoylphorbol-13-acetate ( TPA ), was insensitive to GDP beta S. Consistent with the involvement of a G protein in the activation of PLD activity by v-Src , GTP gamma S, a nonhydrolyzable analog of GTP that potentiates G-protein mediated signals, strongly enhanced PLD activity in v-Src transformed cells relative to that in parental BALB/c 3T3 cells ... The effect of GTP gamma S on PLD activity in v-Src transformed cells was observed only when cells were prelabeled with [ 3H ] myristate, which is incorporated exclusively into phosphatidylcholine, the substrate for the v-Src induced PLD ... There was no difference in the effect of GTP gamma S-induced PLD activity on v-Src transformed and BALB/c 3T3 cells when the cells were prelabeled with [ 3H ] arachidonate, which is not incorporated into phospholipids that are substrates for the v-Src induced PLD ... The GTP dependent activation of PLD by v-Src was dependent upon the presence of ATP but was unaffected by either cholera or pertussis toxin ... These data suggest that v-Src induces PLD activity through a phosphorylation event and is mediated by a cholera and pertussis toxin-insensitive G protein
Song et al., Biochem J 1993 (Cell Transformation, Viral) : v-Src activates a unique phospholipase D activity that can be distinguished from the phospholipase D activity activated by phorbol esters ... v-Src induced PLD activity could be distinguished from phorbol ester induced PLD activity by differential radiolabelling of phospholipids, which are the substrates of PLD ... As both arachidonic acid and alkyl-lysoPC are incorporated into phosphatidylcholine ( PC ), the substrate for v-Src induced PLD activity, these data suggest that the PLD activated by v-Src can distinguish PCs lacking arachidonic acid and ether linkages ... Consistent with v-Src activating a PLD activity that is distinct from that activated by phorbol esters that activate PKC directly, neither depleting cells of PKC nor treatment with the protein kinase inhibitor, staurosporine, had any effect on v-Src induced PLD activity, whereas both PKC depletion and staurosporine inhibited phorbol ester induced PLD activity ... Taken together, these data suggest that v-Src activates a PKC independent PLD activity that is specific for a subpopulation of PC and distinct from the PLD activity induced by PKC activity induced by phorbol esters ... The diacylglycerol produced from PC by the action of the v-Src induced PLD may therefore be responsible for the activation of PKC by v-Src
Luo et al., Proc Natl Acad Sci U S A 1998 : Brefeldin A, which inhibits Arf GDP-GTP exchange, inhibited PLD activity in v-Src- and v-Ras transformed cells but not in the nontransformed cells, suggesting that the association of Arf with RalA is required for the increased PLD activity induced by v-Src and v-Ras
Ushio-Fukai et al., Mol Pharmacol 1999 : This effect may be mediated by pp60(c-src) , because in beta-adrenergic receptor kinase1 overexpressing cells, pp60(c-src) activation was inhibited, and in normal cells anti-pp60(c-src) antibody inhibited Ang II-stimulated PLD activity