PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25275439-1 2014 Butanol (C4H10OH) has been used both to dissect the molecular targets of alcohols/general anesthetics and to implicate phospholipase D (PLD) signaling in a variety of cellular functions including neurotransmitter and hormone exocytosis. Butanols 0-7 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 119-134 25275439-1 2014 Butanol (C4H10OH) has been used both to dissect the molecular targets of alcohols/general anesthetics and to implicate phospholipase D (PLD) signaling in a variety of cellular functions including neurotransmitter and hormone exocytosis. Butanols 0-7 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 136-139 20348036-10 2010 However, ropivacaine showed no effect on the fMLP-induced CD11b expression in the presence of butan-1-ol, a blocker of phospholipase D (PLD) pathway, which completely inhibited the fMLP-induced CD11b expression in neutrophils. Butanols 94-104 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 119-134 22178154-7 2012 Inhibition of Phosphatidic Acid (PA) formation by PLD using butan-1-ol, inhibited actin polymerization and motility, as well as in vitro fertilization (IVF) and the ability of the sperm to undergo the AR. Butanols 60-70 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 50-53 22178154-8 2012 The inhibition of sperm HAM by low concentration of butan-1-ol is completely restored by adding PA, further indicating the involvement of PLD in these processes. Butanols 52-62 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 138-141 20348036-10 2010 However, ropivacaine showed no effect on the fMLP-induced CD11b expression in the presence of butan-1-ol, a blocker of phospholipase D (PLD) pathway, which completely inhibited the fMLP-induced CD11b expression in neutrophils. Butanols 94-104 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 136-139 19032951-7 2009 This histamine-induced non-CCE was partially reduced by U73122, a phospholipase C (PLC) inhibitor, and by butan-1-ol, a phospholipase D (PLD) inhibitor. Butanols 106-116 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 120-135 19032951-7 2009 This histamine-induced non-CCE was partially reduced by U73122, a phospholipase C (PLC) inhibitor, and by butan-1-ol, a phospholipase D (PLD) inhibitor. Butanols 106-116 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 137-140 18218859-4 2008 Tertiary-butanol, a rather poor inhibitor of PLD, caused only moderate suppression of 5-LO and hardly inhibited 5-LO translocation. Butanols 9-16 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 45-48 15194005-6 2004 LPA-induced early gene induction was completely blocked by normal butanol (n-butanol) but not by t-butanol, suggesting that PLD activity is essentially required for the process. Butanols 66-73 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 124-127 15194005-6 2004 LPA-induced early gene induction was completely blocked by normal butanol (n-butanol) but not by t-butanol, suggesting that PLD activity is essentially required for the process. Butanols 75-84 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 124-127 12890682-8 2003 Butan-1-ol, which acts as an acceptor of phosphatidate generated by the PLD pathway, blocked LPA-mediated transactivation of PDGF-R beta. Butanols 0-10 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 72-75 11744730-7 2002 To examine the role of PLD in the regulation of PI(4,5)P(2) synthesis, we used butanol to diminish the PLD-derived PA. Butanols 79-86 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 103-106 11744730-10 2002 In contrast, 1.5% butanol was found to inhibit the activation of PLD by ARF1 and also decrease PIP levels by 50%. Butanols 18-25 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 65-68 11749856-5 2001 RESULTS: Treatment of A-549 cells with propranolol in the presence of butanol, resulted in the rapid activation of PLD. Butanols 70-77 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 115-118 1323272-6 1992 Experiments involving agonist preincubation with subsequent addition of butanol confirmed that vasopressin-stimulated PLD activity was desensitized. Butanols 72-79 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 118-121 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. Butanols 127-136 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 67-70 2186929-1 1990 A novel and sensitive assay for phospholipase D (PLD) that measures the incorporation of high specific activity [3H]butan-1-ol into [3H]phosphatidylbutanol has been developed. Butanols 116-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 32-47 2186929-1 1990 A novel and sensitive assay for phospholipase D (PLD) that measures the incorporation of high specific activity [3H]butan-1-ol into [3H]phosphatidylbutanol has been developed. Butanols 116-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 49-52 15769249-3 2005 Cells in which PLD activity is inhibited by butan-1-ol show a complete loss of actin-based structures, accompanied by relocalization of F-actin into small clusters, and eventually the nucleus, without a visible fall in levels of F-actin. Butanols 44-54 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 15-18 15769249-4 2005 Addition of exogenous phosphatidic acid reverses the effects of butan-1-ol, confirming that these effects are caused by inhibition of PLD. Butanols 64-74 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 134-137 15087463-6 2004 Most importantly, blockade of PLD-catalyzed phosphatidic acid formation using butan-1-ol inhibited insulin secretion in both MIN6 cells and isolated pancreatic islets. Butanols 78-88 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 30-33 12149127-6 2002 Treatment of Beas-2B cells with butan-1-ol, but not butan-3-ol, abrogated the S1P-induced phosphorylation of Raf-1 and ERK, suggesting that PLD is involved in this activation. Butanols 32-42 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 140-143 12458339-2 2002 METHODS: Alterations in the activities of Src, extracellular signal-regulated kinase (ERK), and phospholipase D (PLD) were measured using [gamma-(32)P] ATP for autophosphorylation of Src, phospho-specific ERK antibody, and [9,10-(3)H] myristic acid, respectively, while herbimycin A, PD98059 and butan-1-ol were used to inhibit their activities. Butanols 296-306 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 113-116 11719383-6 2001 In addition, coupling of FcgammaRI to activation of the nicotinamide adenine dinucleotide phosphate (reduced form) (NADPH) oxidase burst was inhibited by pretreating cells with 0.3% butan-1-ol, indicating an absolute requirement for PLD. Butanols 182-192 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 233-236 11718730-6 2001 Pretreatment with butan-1-ol, a PLD inhibitor, attenuated both pervanadate-induced necrosis and increase of intracellular Ca(2+). Butanols 18-28 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 32-35 10683250-6 2000 In the presence of butan-1-ol, suppression of SPP-induced phosphatidic acid formation and production of phosphatidylbutanol were found, clearly indicating activation of phospholipase D (PLD). Butanols 19-29 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 169-184 10683250-6 2000 In the presence of butan-1-ol, suppression of SPP-induced phosphatidic acid formation and production of phosphatidylbutanol were found, clearly indicating activation of phospholipase D (PLD). Butanols 19-29 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 186-189 9111933-3 1997 PLD from peanut utilizes C1 to C8 primary alcohols and gives maximal reaction with butanol. Butanols 83-90 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 7583579-3 1995 In [14C]lyso-PC-labeled or [14C]choline (Cho)-labeled cells, a biphasic activation of PC-specific phospholipase D (PLD) with peak maxima 30 to 60 seconds and 5 to 7 minutes after stimulation with 20 micrograms/mL HDL3 was shown by (1) a 1.5- to 3-fold increase in Cho release, and (3) transphosphatidylation of PC to phosphatidylbutanol in the presence of 0.3% butanol. Butanols 329-336 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 115-118 7758577-1 1995 The molecular selectivity of PLD in PMA-stimulated HL60 granulocytes was determined by HPLC analysis of [3H]butanol incorporation into phosphatidyl[3H]butanol (Ptd[3H]But) molecular species. Butanols 108-115 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 29-32 7758577-1 1995 The molecular selectivity of PLD in PMA-stimulated HL60 granulocytes was determined by HPLC analysis of [3H]butanol incorporation into phosphatidyl[3H]butanol (Ptd[3H]But) molecular species. Butanols 151-158 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 29-32 8335105-3 1993 An enhancement of ET-1-stimulated Ins(1,4,5)P3 accumulation was also seen when the product of PLD activity was either diverted into phosphatidyl butanol in the presence of butanol, or phosphatidate phosphohydrolase (PPH) activity was inhibited by DL-propranolol. Butanols 145-152 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 94-97