PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2037586-7 1991 In the presence of ethanol or n-butanol, transphosphatidylation by PLD resulted in the formation of [3H]phosphatidylethanol or - butanol, respectively, at the cost of PA and DG formation. 1-Butanol 30-39 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 67-70 8640350-5 1995 In the presence of 2% n-butanol, mastoparan (3-100 microM) induced phosphatidylbutanol (PBut) accumulation in a concentration- and time-dependent manner, suggesting that mastoparan activates phospholipase D (PLD). 1-Butanol 22-31 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 191-206 7882615-5 1995 Laminin-induced production of MMP-2 is attenuated by 1-butanol, a competitive substrate of PLD that reduces PLD-catalyzed production of PA. 1-Butanol 53-62 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 91-94 7882615-5 1995 Laminin-induced production of MMP-2 is attenuated by 1-butanol, a competitive substrate of PLD that reduces PLD-catalyzed production of PA. 1-Butanol 53-62 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 108-111 28490713-6 2017 However, inhibition of hydrolytic activity of PLD by 1-butanol treatment showed little or no effect on agonist-induced chemotaxis. 1-Butanol 53-62 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 46-49 25523098-6 2014 PLD induction of HIF-1alpha was significantly attenuated by 1-butanol which blocks PA production by PLD, and PA per se was able to elevate HIF-1alpha protein level. 1-Butanol 60-69 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 26089893-8 2015 Inhibition of PLD by a general antagonist (1-butanol) or specific inhibitor, halopemide, or N-hexanoylsphingosine, or by cellular ceramides accumulated in doxorubicin-treated hepatocytes decreased insulin-stimulated glucose metabolism. 1-Butanol 43-52 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 14-17 25523098-6 2014 PLD induction of HIF-1alpha was significantly attenuated by 1-butanol which blocks PA production by PLD, and PA per se was able to elevate HIF-1alpha protein level. 1-Butanol 60-69 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 100-103 19064628-2 2009 PLD production of PA is inhibited by the primary alcohol 1-butanol, which has thus been widely employed to identify PLD/PA-driven processes. 1-Butanol 57-66 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 25275439-2 2014 Like other primary alcohols, 1-butanol is a substrate for PLD and thereby disrupts formation of the intracellular signaling lipid phosphatidic acid. 1-Butanol 29-38 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 58-61 24618697-6 2014 Treatment of cells with the primary alcohol 1-butanol inhibits the hydrolysis of phosphatidylcoline by PLD thereby suppressing phosphatidic acid (PA) production. 1-Butanol 44-53 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 103-106 24618697-8 2014 When HSY cells were incubated with 1-butanol the total number of clathrin coated vesicles increased, especially in the juxtanuclear region and the co-localization of PLD with the clathrin coated vesicles was augmented. 1-Butanol 35-44 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 166-169 23681537-4 2013 The protocol takes advantage of a unique property of PLD, i.e., its ability to substitute a primary alcohol, such as 1-butanol, for water in the hydrolytic reaction. 1-Butanol 117-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 53-56 23662182-5 2013 1-Butanol, the quencher of PLD, generated PA leading to the formation of physiologically inactive phosphatidyl butanol but not its biologically inactive analog, 2-butanol, blocked the H2O2-mediated barrier dysfunction. 1-Butanol 0-9 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 27-30 22392280-6 2012 ABA-induced stomatal closure in both pldalpha1 and plddelta single mutants was inhibited by a PLD inhibitor (1-butanol ), suggesting that both PLDalpha1 and PLDdelta function in ABA-induced stomatal closure. 1-Butanol 109-118 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 94-97 20158570-5 2011 Using 1-butanol, a PLD substrate, to block phosphatidic acid (PA) generation, the PMA-stimulated neutrophil respiratory burst was also partially inhibited, further indicating that PLD activation, possibly its hydrolytic product PA and diacylglycerol (DAG), is involved in PMA-stimulated respiratory burst. 1-Butanol 6-15 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 19-22 20158570-5 2011 Using 1-butanol, a PLD substrate, to block phosphatidic acid (PA) generation, the PMA-stimulated neutrophil respiratory burst was also partially inhibited, further indicating that PLD activation, possibly its hydrolytic product PA and diacylglycerol (DAG), is involved in PMA-stimulated respiratory burst. 1-Butanol 6-15 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 180-183 23500715-5 2013 Adding of primary alcohol (1-butanol) to the incubation medium led to phosphatidylbutanol accumulation as a result of phospholipase D (PLD) action in wild-type and NADPH-oxidase RbohD deficient plants. 1-Butanol 27-36 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 118-133 23500715-5 2013 Adding of primary alcohol (1-butanol) to the incubation medium led to phosphatidylbutanol accumulation as a result of phospholipase D (PLD) action in wild-type and NADPH-oxidase RbohD deficient plants. 1-Butanol 27-36 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 135-138 20417698-2 2010 n-Butanol (0.5%) inhibited PLD activation, attenuated cell injury at 5 min of H(2)O(2) exposure, but enhanced injury at 3h of exposure. 1-Butanol 0-9 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 27-30 19064628-2 2009 PLD production of PA is inhibited by the primary alcohol 1-butanol, which has thus been widely employed to identify PLD/PA-driven processes. 1-Butanol 57-66 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 116-119 18358832-6 2008 Blocking the PLD signal by 1-butanol suppresses the proliferation. 1-Butanol 27-36 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 13-16 18498667-7 2008 PLD activity was assessed by measuring the formation of [3H]phosphatidylbutanol, the product of PLD-mediated transphosphatidylation, in the presence of n-butanol. 1-Butanol 152-161 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 18423386-6 2008 This response was inhibited by 1-butanol, a well known distracter of PLD activity, or upon overexpression of a dominant negative PLD2, and it was concomitant with a boost of PA/DAG production. 1-Butanol 31-40 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 69-72 17936375-4 2008 Here, we show that the inhibition of phospholipase D (PLD)-mediated phosphatidic acid (PA) formation by 1-butanol inhibited the maturation and export of CFTR from the ER. 1-Butanol 104-113 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 37-52 18218859-3 2008 Preincubation of PMNL with the phospholipase D (PLD) inhibitor 1-butanol potently suppressed 5-LO product synthesis induced by the Ca(2)(+) ionophore A23187 or thapsigargin (TG) and blocked A23187-evoked translocation of 5-LO from the cytosol to the nuclear membrane, analyzed by subcellular fractionation as well as by indirect immunofluorescence microscopy. 1-Butanol 63-72 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 31-46 18218859-3 2008 Preincubation of PMNL with the phospholipase D (PLD) inhibitor 1-butanol potently suppressed 5-LO product synthesis induced by the Ca(2)(+) ionophore A23187 or thapsigargin (TG) and blocked A23187-evoked translocation of 5-LO from the cytosol to the nuclear membrane, analyzed by subcellular fractionation as well as by indirect immunofluorescence microscopy. 1-Butanol 63-72 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 48-51 17936375-4 2008 Here, we show that the inhibition of phospholipase D (PLD)-mediated phosphatidic acid (PA) formation by 1-butanol inhibited the maturation and export of CFTR from the ER. 1-Butanol 104-113 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 54-57 16118212-6 2005 Unsaturated but not saturated fatty acids stimulated phospholipase D (PLD) activity, the PLD inhibitor 1-butanol prevented the unsaturated fatty acid-induced reduction in ABCA1 levels, and the PLD2 activator mastoparan markedly reduced ABCA1 protein levels, implicating a role for PLD2 in the ABCA1 destabilizing effects of fatty acids. 1-Butanol 103-112 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 89-92 17724165-5 2007 This up-regulation was dose-dependently prevented by incubation of neutrophils in 1-butanol, an inhibitor of PLD activity. 1-Butanol 82-91 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 109-112 17724165-7 2007 Incubation in 1-butanol did inhibit fMLP but not C5a-mediated migration across intestinal epithelial cell monolayers, showing that transepithelial migration to fMLP but not C5a is dependent on PLD. 1-Butanol 14-23 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 193-196 17724165-8 2007 The addition of phosphatidic acid, a reaction product of PLD, partially restored fMLP-mediated transepithelial migration in the presence of 1-butanol but not the migration of Mac-1-deficient neutrophil-differentiated HL-60 cells. 1-Butanol 140-149 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 57-60 16882041-6 2006 We show that blocking PLD activity, by expressing Y112-LMP2A, treating cells with the PLD inhibitor 1-butanol or reducing PLD expression by siRNA, blocked BCR trafficking to class II-containing compartments. 1-Butanol 100-109 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 22-25 16882041-6 2006 We show that blocking PLD activity, by expressing Y112-LMP2A, treating cells with the PLD inhibitor 1-butanol or reducing PLD expression by siRNA, blocked BCR trafficking to class II-containing compartments. 1-Butanol 100-109 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 86-89 16882041-6 2006 We show that blocking PLD activity, by expressing Y112-LMP2A, treating cells with the PLD inhibitor 1-butanol or reducing PLD expression by siRNA, blocked BCR trafficking to class II-containing compartments. 1-Butanol 100-109 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 86-89 16113073-8 2006 ANG II-induced PLD activity was inhibited by the primary alcohol n-butanol but not the tertiary alcohol t-butanol. 1-Butanol 65-74 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 15-18 16716806-5 2006 To examine the regulation mechanism of PMA and Se-MSC on CD11c gene expression through the activation of PLD1, we analyzed changes in the CD11c mRNA level and the promoter activity following treatment of a selective PLD inhibitor n-butanol. 1-Butanol 230-239 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 105-108 16280360-4 2006 Remarkably, all of these phenotypes, including accumulated tubular endosomes, blocked recycling, and failure to make protrusions and recruit ACAP effectively, could be recreated in either untransfected cells or cells expressing wild-type Arf6 by treatment with 1-butanol to inhibit the formation of phosphatidic acid (PA), the product of PLD. 1-Butanol 261-270 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 338-341 15843515-8 2005 Phorbol ester, which did not stimulate degranulation by itself, restored degranulation when used in combination with thapsigargin whether PLD function was disrupted with 1-butanol or the small inhibitory RNAs. 1-Butanol 170-179 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 138-141 15255942-4 2004 1-Butanol, which is a substrate for PLD and inhibits PA formation, inhibited carbachol-induced cell proliferation and the underlying intracellular signaling, whereas its analog tert-butanol, which is a poor substrate for PLD, was much less effective. 1-Butanol 0-9 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 36-39 15294123-6 2004 In 1-butanol+LPS+fMLP group, PLD activity of preoperative neutrophils was lower than that in LPS+fMLP group (P<0.01), besides the release of elastase and MPO decreased sharply below both LPS+fMLP and fMLP groups (P<0.01). 1-Butanol 3-12 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 29-32 15147910-2 2004 To investigate the role of PLD during the regulatory volume decrease, cells were treated with 1-butanol resulting in a depletion of PLD substrates. 1-Butanol 94-103 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 27-30 15147910-2 2004 To investigate the role of PLD during the regulatory volume decrease, cells were treated with 1-butanol resulting in a depletion of PLD substrates. 1-Butanol 94-103 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 132-135 14704231-4 2004 A PLD inhibitor, 1-butanol, almost completely suppressed VEGF-induced ERK phosphorylation and cellular proliferation, whereas the negative control for 1-butanol, 3-butanol, did not produce significant changes. 1-Butanol 17-26 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 2-5 15294123-11 2004 Notably, PLD activity was even nonstatistically lower in 1-butanol+LPS+fMLP group than that in LPS or fMLP group. 1-Butanol 57-66 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 9-12 12890486-7 2003 Moreover, PLD inhibitor, 1-butanol, inhibited Ang1-induced endothelial cell migration. 1-Butanol 25-34 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 10-13 12935885-7 2003 Incubation of cells with 1-butanol to inhibit PLD signaling attenuated PE-induced phosphorylation of mTOR, 4E-BP1 and p70 S6 kinase. 1-Butanol 25-34 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 46-49 11154852-9 2000 Taken together, our results suggest that ethanol and 1-butanol exert a specific inhibitory effect on PKC-dependent astroglial cell proliferation by synergistically inhibiting PKC activity and the PLD signaling pathway. 1-Butanol 53-62 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 196-199 11906165-4 2002 During established [Ca(2+)](i) oscillations induced by 1 microM histamine, 0.3% n-butanol, which "functionally" redirects phosphatidic acid formed by PLD to PBt, decreased [Ca(2+)](i) oscillation frequency by approximately 50% and produced a similar reduction in NF-kappaB activity. 1-Butanol 80-89 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 150-153 11854442-4 2002 Moreover, the treatment of [(3)H]myristate-labeled cells in the presence of 1-butanol caused the dose-dependent formation of [(3)H]phosphatidylbutanol (PBt), a product specific to PLD activity. 1-Butanol 76-85 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 180-183 11245595-6 2001 The transphosphatidylation reaction in the presence of the primary alcohol 1-butanol [leading to stable phosphatidylbutanol (Pbut) formation] was used to measure activity of PLD. 1-Butanol 75-84 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 174-177 10518598-6 1999 Application of 1-butanol (1-buOH), a selective inhibitor of PtdOH production by PLD, inhibited the increase in PtdOH production elicited by ABA. 1-Butanol 15-24 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 80-83 10088607-6 1999 The peptide-induced bacteria killing activity shares regulatory mechanisms for PLD activation with the superoxide generation, which is inhibited in the presence of 1-butanol. 1-Butanol 164-173 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 79-82 9245781-6 1997 The release of nascent secretory vesicles from the TGN was sensitive to 1% 1-butanol, a concentration that inhibited PLD-catalyzed formation of phosphatidic acid. 1-Butanol 75-84 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 117-120 10931844-8 2000 PLD inhibitors 1-butanol and 2, 3-diphosphoglycerate, or the ARF6(N48R) mutant assumed to be defective in PLD activation, blocked fMLP-elicited oxidase activity in transfected cells. 1-Butanol 15-24 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 10860542-9 2000 However, fMLP-mediated AA release was reduced by approximately 45% by Clostridium difficile toxin B (10 ng/ml) or by 1-butanol; both block phospholipase D (PLD) activity. 1-Butanol 117-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 156-159 9973503-8 1999 Phagocytosis of EIgG was reduced by two inhibitors of PLD-mediated signaling, 2,3-diphosphoglycerate or 1-butanol. 1-Butanol 104-113 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 54-57