PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10529371-1 1999 Phospholipase D (PLD) plays an important role in signaling through phosphatidylcholine (PC) and in the production of superoxide (respiratory burst) by polymorphonuclear leukocytes (PMN) stimulated by the chemoattractant fMet-Leu-Phe (fMLP). Superoxides 117-127 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 11927657-5 2002 On the basis of these results, we propose that upon chemoattractant stimulation, PLD activity is involved in induction of degranulation and O2*- production, but a BFA-sensitive ARF is only required to the activation of the NADPH oxidase. Superoxides 140-144 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 81-84 11830497-2 2002 Here it is postulated that increased PLD activity generating phosphatidic acid and diacylglycerol (DAG) is essential for superoxide release and degranulation and that ceramide, previously shown to be generated during PMN activation, inhibits PLD activation, thereby leading to inhibition of PMN function. Superoxides 121-131 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 37-40 11830497-8 2002 In conclusion, superoxide, gelatinase, and lactoferrin release require activation of the PLD pathway in primed PMNs and cytochalasin B-treated PMNs. Superoxides 15-25 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 89-92 11446714-0 2001 Increased generation of superoxide by angiotensin II in smooth muscle cells from resistance arteries of hypertensive patients: role of phospholipase D-dependent NAD(P)H oxidase-sensitive pathways. Superoxides 24-34 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 135-150 10660303-1 2000 The signalling pathway leading, for example, to actin cytoskeletal reorganisation, secretion or superoxide generation involves phospholipase D (PLD)-catalysed hydrolysis of phosphatidylcholine to generate phosphatidic acid, which appears to mediate the messenger functions of this pathway. Superoxides 96-106 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 127-142 10660303-1 2000 The signalling pathway leading, for example, to actin cytoskeletal reorganisation, secretion or superoxide generation involves phospholipase D (PLD)-catalysed hydrolysis of phosphatidylcholine to generate phosphatidic acid, which appears to mediate the messenger functions of this pathway. Superoxides 96-106 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 144-147 31090437-6 2019 Bleomycin stimulated mitochondrial (mt) superoxide production, mtDNA damage, and apoptosis in Beas2B cells, which was attenuated by the catalytically inactive mutants of PLD or PLD2 siRNA. Superoxides 40-50 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 170-173 11223870-0 2001 Roles of phosphatidylinositol 3-kinase and phospholipase D in temporal activation of superoxide production in FMLP-stimulated human neutrophils. Superoxides 85-95 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 43-58 11223870-7 2001 NADPH oxidase is activated in a PI3-kinase-dependent manner at the early phase, and PLD activity follows it and is related to superoxide production at the late phase in human neutrophils by stimulation with FMLP. Superoxides 126-136 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 84-87 10529371-1 1999 Phospholipase D (PLD) plays an important role in signaling through phosphatidylcholine (PC) and in the production of superoxide (respiratory burst) by polymorphonuclear leukocytes (PMN) stimulated by the chemoattractant fMet-Leu-Phe (fMLP). Superoxides 117-127 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 17-20 10529371-8 1999 They further indicate that PLD stimulation by fMLP receptors occurs through two pathways, dependent and independent on MAP kinase, the former pathway being linked to superoxide production. Superoxides 166-176 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 27-30 8911682-4 1996 One such function is neutrophil superoxide generation, which is induced when phosphatidic acid, generated by activated phospholipase D (PLD), facilitates the interaction of a cytoplasmic low-molecular-weight G-protein with dormant, membrane-bound reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Superoxides 32-42 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 119-134 10088607-3 1999 Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), a peptide that stimulates phosphoinositide (PI) hydrolysis in human leukocytes, including monocytes, binds to a unique cell surface receptor and stimulates superoxide generation, killing of Staphylococcus aureus, and activation of phospholipase D (PLD) in human monocytes. Superoxides 192-202 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 284-287 10088607-7 1999 We suggest that the peptide stimulates PLD downstream of PLC activation and PLD activation in turn is essential for the peptide-induced immunological functions such as the superoxide generation and killing of bacteria by human monocytes. Superoxides 172-182 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 39-42 10088607-7 1999 We suggest that the peptide stimulates PLD downstream of PLC activation and PLD activation in turn is essential for the peptide-induced immunological functions such as the superoxide generation and killing of bacteria by human monocytes. Superoxides 172-182 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 76-79 9663393-1 1998 Phospholipase D (PLD) activity has been implicated in the regulation of membrane trafficking [1,2], superoxide generation and cytoskeletal remodelling [3,4]. Superoxides 100-110 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 9663393-1 1998 Phospholipase D (PLD) activity has been implicated in the regulation of membrane trafficking [1,2], superoxide generation and cytoskeletal remodelling [3,4]. Superoxides 100-110 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 17-20 9199889-3 1997 Free radical exposure did not alter neutral lipids, but among the phospholipids, phosphatidylethanolamine (PE) content was decreased on exposure to superoxide anion, generated by xanthine-xanthine oxidase or menadione with a concomitant increase in the level of phosphatidic acid (PA), suggesting activation of phospholipase D (PLD). Superoxides 148-164 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 311-326 9199889-3 1997 Free radical exposure did not alter neutral lipids, but among the phospholipids, phosphatidylethanolamine (PE) content was decreased on exposure to superoxide anion, generated by xanthine-xanthine oxidase or menadione with a concomitant increase in the level of phosphatidic acid (PA), suggesting activation of phospholipase D (PLD). Superoxides 148-164 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 328-331 9199889-11 1997 These findings suggest that superoxide anion stimulates intestinal mitochondrial PLD resulting in PE degradation and PA formation. Superoxides 28-44 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 81-84 8911682-4 1996 One such function is neutrophil superoxide generation, which is induced when phosphatidic acid, generated by activated phospholipase D (PLD), facilitates the interaction of a cytoplasmic low-molecular-weight G-protein with dormant, membrane-bound reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Superoxides 32-42 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 136-139 8207217-4 1994 In the presence of propranolol (phosphatidic acid (PA) phosphohydrolase inhibitor), or ethanol, the activation of PLD results in the modulation of PA and/or diglyceride (DG) generation, producing an irregularity in O2- production. Superoxides 215-217 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 114-117 8699936-6 1996 These data show that decreased superoxide generation by neutrophils in insulin-dependent diabetics is, in part, due to impaired activation of phospholipase D and is solely due to high glucose concentrations. Superoxides 31-41 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 142-157 8207217-6 1994 These results suggest that PLD is a downstream effector of FMLP-induced tyrosine kinase activation that leads to activation of the PMN superoxide release but not to chemotactic migration. Superoxides 135-145 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 27-30 1659906-1 1991 Recent evidence suggests that the hydrolysis of phosphatidylcholine (PC) by phospholipase D (PLD) may mediate superoxide anion (O2-) production in human neutrophils. Superoxides 110-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 76-91 7683614-2 1993 The O2- production by the stimulants was completely inhibited by PKC inhibitors such as calphostin C and staurosporine and was not affected by 1% ethanol, a metabolic modulator of phospholipase D (PLD). Superoxides 4-6 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 180-195 7683614-2 1993 The O2- production by the stimulants was completely inhibited by PKC inhibitors such as calphostin C and staurosporine and was not affected by 1% ethanol, a metabolic modulator of phospholipase D (PLD). Superoxides 4-6 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 197-200 1659906-1 1991 Recent evidence suggests that the hydrolysis of phosphatidylcholine (PC) by phospholipase D (PLD) may mediate superoxide anion (O2-) production in human neutrophils. Superoxides 110-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 93-96 1659906-7 1991 These data are consistent with the hypothesis that PA produced through the hydrolysis of PC by PLD is an important mediator of O2- production in response to receptor-dependent agonists. Superoxides 127-129 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 95-98 1659906-1 1991 Recent evidence suggests that the hydrolysis of phosphatidylcholine (PC) by phospholipase D (PLD) may mediate superoxide anion (O2-) production in human neutrophils. Superoxides 128-130 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 76-91 1659906-1 1991 Recent evidence suggests that the hydrolysis of phosphatidylcholine (PC) by phospholipase D (PLD) may mediate superoxide anion (O2-) production in human neutrophils. Superoxides 128-130 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 93-96 1659906-2 1991 To define the role of the PC-specific PLD products phosphatidic acid (PA) and diacylglycerol (DAG) in O2- production in response to agonists which activate the PLD pathway, we blocked the metabolism of PA to DAG with propranolol, an inhibitor of PA phosphohydrolase. Superoxides 102-104 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 38-41