Gene interactions and pathways from curated databases and text-mining

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CA2 — PLD5

Text-mined interactions from Literome

Liu et al., J Vasc Res 1999 (Second Messenger Systems) : Removal of extracellular Ca2+ and addition of 0.1 or 2 mM EGTA completely inhibited ET-1 stimulated PLD activity
Khare et al., Am J Physiol 1999 : Removal of Ca2+ from the medium, as well as preincubation of cells with Gö-6976, an inhibitor of Ca2+ dependent PKC isoforms, significantly reduced the stimulation of PLD by 1,25 ( OH ) 2D3 or TPA
Sun et al., J Neurochem 1999 : Furthermore, removal of extracellular Mg2+ enhanced the ATP- and BzATP stimulated increases in [ Ca2+ ] i. BzATP stimulated PLD in a concentration- and time dependent manner that could be abolished by removal of extracellular Ca2+ and was inhibited by suramin, PPADS, and oxidized ATP ... Taken together, these data indicate that activation of the P2X7 receptors induces Ca2+ influx and stimulates a Ca2+ dependent PLD in RBA-2 astrocytes
Tang et al., Eur J Biochem 2002 : Characterization and regulation of yeast Ca2+ dependent phosphatidylethanolamine-phospholipase D activity
Yang et al., Protein Sci 2002 : Cloning, overexpression, and characterization of a bacterial Ca2+ dependent phospholipase D
Huang et al., Am J Physiol Cell Physiol 2004 : Overexpression of p115RhoGEF-RGS in the MDCK cells that overexpress CaRWT inhibited extracellular Ca2+ stimulated PLD activity, but pretreatment of cells with pertussis toxin and overexpression of RGS4 were without effect
Garcia et al., J Lab Clin Med 1992 : Both the increase in [Ca2+ ] i and PKC activation are required for thrombin stimulated PLA2 and PLD activity, PGI2 synthesis, and barrier dysfunction, the latter occurring as the result of Ca2+ and PKC effects on specific cytoskeletal protein elements and other contractile proteins ( Fig. 3 )
Purkiss et al., Biochem J 1992 : The stimulation of phospholipase D was dependent on extracellular Ca2+ and was mostly transient ( completed within 3 min ), whereas the initial stimulation of phospholipase C was independent of extracellular Ca2+, followed by a Ca ( 2+ ) -dependent phase
Park et al., Biochem Int 1992 : Fusion of phospholipid vesicles composed of various combination of phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid was induced by Ca2+ in the presence or absence of phospholipase D from Streptomyces chromofuscus
De Vito et al., Mol Cell Biochem 2003 : The involvement of PLD in pHi and [Ca2+ ] i changes was confirmed by calphostin-c treatment, a potent inhibitor of PLD, which abolished all AAPH induced effects
Nishida et al., Brain Res 1992 : Both Ca2+ and Mg2+ inhibited PLD activity in a dose dependent manner
Akhtar et al., Curr Eye Res 1992 : Incubation of BCEC with staurosporine resulted in significant inhibition of ionomycin induced production of [ 3H ] PEt, suggesting that in addition to direct activation of PLD by Ca2+ , the enzyme is probably stimulated by sequential activation of PLC ( producing diacylglycerol ) and PKC following the ionomycin addition
Rábano et al., Mol Cell Endocrinol 2004 : PLD activation was dependent upon extracellular Ca2+ , and was blocked by inhibition of protein kinase C ( PKC )
Geny et al., Biochem J 1992 : Phorbol 12-myristate 13-acetate or Ca2+ alone can also stimulate PLD , but to a limited extent
Kanaho et al., J Immunol 1992 : In the present study, we first investigated which of the factors, protein kinase C ( PKC ) or Ca2+ , plays an important role in activation of phospholipase D ( PLD ) of rabbit peritoneal neutrophils stimulated by the chemoattractant FMLP
Greco et al., Biochem Biophys Res Commun 2006 : CpG oligodeoxynucleotides induce Ca2+ dependent phospholipase D activity leading to phagolysosome maturation and intracellular mycobacterial growth inhibition in monocytes ... These results show the presence of an antimicrobial pathway in monocytes, mediated by Ca2+ dependent PLD which can be useful for the exploitation of novel anti-tuberculosis immunotherapy approaches
Oh et al., J Cell Biochem 2007 (Cell Transformation, Viral) : PLD activation and neurite outgrowth induced by bFGF was dependent on phospholipase C gamma (PLC-gamma) and Ca2+ , but not protein kinase C ( PKC )
Liscovitch et al., Cell Regul 1991 : Ca2+ inhibits guanine nucleotide activated phospholipase D in neural derived NG108-15 cells ... We have investigated the regulation of phospholipase D ( PLD ) activity by guanine nucleotides and Ca2+ in cells of the NG108-15 neuroblastoma X glioma line that were permeabilized with digitonin ... The activation of PLD by GTP gamma S did not require Ca2+ and was independent of free Ca2+ ions up to a concentration of 100 nM ( resting intracellular concentration )
Vorland et al., Platelets 2008 : Extracellular Ca2+ potentiated thrombin stimulated PLD , but did not stimulate PLD in the absence of thrombin
Xie et al., Biochem J 1991 : Ca2+ , at concentrations less than or equal to nM, had no effect on the GTP [ S ] -dependent PLD activity
Reinhold et al., FASEB J 1990 : Thus, increased cytosolic Ca2+ and activated protein kinase C can each lead to activation of phospholipase D , but neither is required for receptor mediated activation of phospholipase D activity
Van der Meulen et al., Biochem J 1990 : GTP [ S ] -stimulated PLD activity was observed in the absence of Ca2+, but was increased by 1 microM-Ca2+ ( 3.5 +/- 0.2-fold and 1.8 +/- 0.1-fold in membranes from control and PMA treated platelets respectively )
Halenda et al., Biochem J 1990 (Leukemia, Erythroblastic, Acute) : These result suggest that phosphatidic acid is generated in agonist stimulated HEL cells by two routes : phospholipase C/diacylglycerol kinase and phospholipase D. Activation of the HEL-cell phospholipase D in response to agonists may be mediated by a rise in intracellular Ca2+
Mori et al., Biochim Biophys Acta 1989 : When the membranes were incubated with Ca2+ alone, the three bases were liberated into the water-soluble fractions accompanied by accumulation of phosphatidic acid, suggesting the presence of Ca2+ dependent phospholipase D-like activity
Anthes et al., Biochem Biophys Res Commun 1989 : It is concluded that HL-60 granulocytes contain a PC-specific PLD that requires both Ca2+ and GTP for activation
Perkins et al., Biochem J 1995 : Collectively, these data suggest that LTB4 activates the NADPH oxidase in eosinophils by PLD- and PtdIns 3-kinase independent mechanisms that involve Ca2+ , PLC and PKC
Kozawa et al., Prostaglandins Leukot Essent Fatty Acids 1995 : In this study, we examined the relationship between the tyrosine kinase regulated Ca2+ influx by PGF2 alpha and the activation of phospholipase D in MC3T3-E1 cells ... These results strongly suggest that the phospholipase D activation by PGF2 alpha is dependent on extracellular Ca2+ in osteoblast-like cells and that protein tyrosine kinase is involved in the activation of phospholipase D
Murthy et al., Mol Pharmacol 1995 : PC-PLC and PLD are Ca2+ dependent and appear to be G protein coupled ; only PLD is PKC sensitive
Chen et al., J Pharmacol Exp Ther 1995 : The M2 receptors are linked to Ca2+ influx, activation of phospholipase D and protein kinase C-dependent pathway, whereas the M3 receptors are preferentially associated with the activation of phospholipase C, intracellular Ca2+ release and calmodulin dependent pathway
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
Suzuki et al., J Endocrinol 1995 : These results suggest that extracellular ATP stimulates phospholipase D in a Ca2+/calmodulin dependent manner in osteoblast-like cells, and that neither PKC activation nor GTP binding protein is involved in this mechanism
Natarajan et al., Biochim Biophys Acta 1994 : These results indicate that an increase in intracellular Ca2+ is necessary for LPS mediated PLD activation
Natarajan et al., Am J Respir Cell Mol Biol 1994 : The sphingosine induced stimulation of PLD activity was not affected by treatment with the protein kinase C ( PKC ) inhibitor staurosporine or by down-regulation of PKC with TPA and was independent of extracellular Ca2+, suggesting that the PLD activation was independent of PKC and Ca2+
Akhtar et al., Curr Eye Res 1994 : The activation of PLD by GTP gamma S in the microsomal fraction was absolutely dependent on the presence of Ca2+ > 0.5 microM ... Taken together, the data suggest that a GTP binding protein is involved in regulation of PLD in BCEC, and that maximal stimulation of PLD probably results from an interaction between Ca2+ , PKC and G-protein in BCEC
Pfeilschifter et al., Br J Pharmacol 1993 : However, chelation of cytosolic Ca2+ with high concentrations of Quin 2 did not attenuate ATP- and UTP induced phosphatidylethanol production, thus suggesting that Ca2+ is not crucially involved in agonist stimulated phospholipase D activation
Gustavsson et al., J Biol Chem 1994 : The role of cytosolic Ca2+ , protein kinase C, and protein kinase A in hormonal stimulation of phospholipase D in rat hepatocytes
Mullmann et al., J Leukoc Biol 1993 : Full activation of PLD by fMLP required the simultaneous presence of both Ca2+ and cytochalasin B, a condition that caused no further enhancement of PLC
Pfeilschifter et al., FEBS Lett 1993 : The role of Ca2+ and protein kinase C ( PKC ) in the regulation of phosphatidylcholine hydrolyzing phospholipase D ( PLD ) was investigated in angiotensin II-stimulated mesangial cells ... However, chelation of cytosolic Ca2+ with high concentrations of quin 2 did not attenuate angiotensin II-induced phosphatidylethanol production, thus suggesting that Ca2+ is not crucially involved in agonist stimulated PLD activation
Pyne et al., Biochem Pharmacol 1993 : Removal of extracellular Ca2+ markedly reduced the bradykinin stimulated phospholipase D response ( by 73 +/- 10 %, N = 3 experiments ) but had only a limited effect upon PMA stimulated phospholipase D activity ( by 23 +/- 6 %, N = 3 experiments )
Takahashi et al., J Immunol 1996 : Interestingly, ARF stimulated PLD activity was augmented by CaM in the presence of GTP gamma S and Ca2+
Horwitz et al., Neurochem Res 1995 : These experiments were designed to learn the role of bradykinin induced changes in intracellular Ca2+ in the activation of phospholipase D activity in PC12 cells ... These preincubations completely blocked the bradykinin induced increase in intracellular Ca2+ but only attenuated the bradykinin mediated activation of phospholipase D. Physiological increases in intracellular Ca2+ apparently do not mediate the effect of bradykinin on phospholipase D
Oiso et al., J Bone Miner Res 1995 : PGE2 induced PLD activity was markedly suppressed by either chelating extracellular Ca2+ by EGTA or pertussis toxin
Natarajan et al., Chem Phys Lipids 1996 (Second Messenger Systems) : Activation of PLD in response to an external stimulus may involve PKC, Ca2+ , G-proteins and/or tyrosine kinases
Adachi et al., Hepatology 1996 : These results suggest that PTK, PKC, and Ca2+ regulate HGF induced PLD activation, and that DG produced by PLD pathway may play a role in the induction of immediate early genes, which is activated in MAPK independent manner, in rat hepatocytes
Banno et al., J Lipid Mediat Cell Signal 1996 : These results indicate that Ca2+ may not directly activate PLD but through some Ca ( 2+ ) -dependent mechanism ( s ) in Cch stimulated cells
Bourgoin et al., J Bone Miner Res 1996 (Osteosarcoma) : A good correlation was found between the levels of intracellular free Ca2+ and the activation of PLD
Liu et al., Prostaglandins 1996 : Depletion of extracellular Ca2+ with EGTA suppressed PGF2 alpha induced PLD activation by 50 %
Ito et al., J Neurochem 1997 : A Ca2+ ionophore, A23187, caused PLD activation and tyrosine phosphorylation of four proteins of 111, 91, 84, and 65-70 kDa only in the presence of extracellular Ca2+
Zheng et al., Proc Natl Acad Sci U S A 1997 (Ion Channel Gating) : Consistent with the role of action potential-driven Ca2+ entry in this process, agonist induced PLD activity was also reduced by nifedipine and low extracellular Ca2+
Pappan et al., J Biol Chem 1997 : We have designated names of PLDbeta for this PIP2 dependent PLD and PLDalpha for the previously characterized PIP2 independent PLD that requires millimolar Ca2+ for optimal activity
Ito et al., J Neurochem 1997 : Extracellular Ca2+ potentiated H2O2 induced PLD activation in a concentration dependent manner
Kato et al., Prostaglandins 1997 : In digitonin permeabilized MC3T3-E1 cells, [ 3H ] P But formation was stimulated by guanosine 5'-O- ( 3-thiotriphosphate ) ( GTP gamma S ) or 4 beta-phorbol 12-myristate 13-acetate ( PMA ) in the presence of Ca2+ ( 1 microM ) and ATP ( 1 mM ), and phosphatidylinositol 4,5-bisphosphate ( PIP2 ) was also required for its full PLD activation
Madesh et al., FEBS Lett 1997 : In this study, we have shown that intestinal mitochondria contain an active phospholipase D ( PLD ) which is activated by oxidants, Ca2+ or polyamines and this results in degradation of phosphatidylethanolamine ( PE ) and formation of phosphatidic acid ( PA )
van Dijk et al., Curr Biol 1998 : Exogenous phospholipase D generates lysophosphatidic acid and activates Ras, Rho and Ca2+ signaling pathways
Hou et al., Biochim Biophys Acta 1998 (Glioblastoma) : The Ca2+-ATPase inhibitor, thapsigargin, did not affect NMB- or TPA stimulated PLD activities, although it blocked completely the NMB induced increase in [ Ca2+ ] i
Watson et al., Biochem Biophys Res Commun 1998 : Stimulation of primed neutrophils by soluble immune complexes : priming leads to enhanced intracellular Ca2+ elevations, activation of phospholipase D , and activation of the NADPH oxidase
Bosch et al., Eur J Pharmacol 1998 : effectively inhibited both TPA/Ca2+ stimulated phospholipase D activation and TPA/phosphatidylserine stimulated protein kinase C activation in a homogenate of CHO-CCK ( A ) cells
Bosch et al., Biochem J 1999 : PMA/Ca2+ stimulated PLD activity was absent in a homogenate of PKC downregulated cells but could be restored upon addition of purified rat brain PKC