PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9144502-4 1997 Several lines of evidence suggest that pleckstrin is phosphorylated in part by a nonconventional PKC following stimulation by FMLP: 1) chelation of intracellular Ca2+ had only a partial inhibitory effect; 2) diacylglycerol kinase inhibitors shortened the duration of phosphorylation, while the phosphatidic acid phosphohydrolase antagonist propranolol extended it; and 3) wortmannin and erbstatin blocked the phosphorylation of pleckstrin. Propranolol 340-351 formyl peptide receptor 1 Homo sapiens 126-130 18968085-9 2000 The interaction with propranolol, clonidine, phenylephrine, carbachol and tripeptide fMLP, which hinder adenylate cyclase (AdC) and activate Ca-polyphosphoinisitide (Ca-PPI) signaling system of a cell, initiates structural rearrangements similar to acidic transitions of albumin. Propranolol 21-32 formyl peptide receptor 1 Homo sapiens 85-89 11322936-6 2001 These effects of epinephrine on the clearance of Ca(2+) from the cytosol of FMLP-activated neutrophils were attenuated by propranolol, and are compatible with enhancement of the activity of the cAMP-dependent Ca(2+) sequestering/resequestering endo-membrane Ca(2+)-ATPase. Propranolol 122-133 formyl peptide receptor 1 Homo sapiens 76-80 9807240-7 1998 The interaction with propranolol, clonidine, phenylephrine, carbachol and tripeptide fMLP which hinder adenylate cyclase (AdC) and activate Ca-polyphosphoinositide (Ca-PPI) signaling system of a cell initiates structural rearrangements similar to acidic transitions. Propranolol 21-32 formyl peptide receptor 1 Homo sapiens 85-89 8440692-4 1993 Both fMLP-induced PAF production and the activation of lyso-PAF:acetyl-CoA acetyltransferase were diminished by propranolol. Propranolol 112-123 formyl peptide receptor 1 Homo sapiens 5-9 7931078-13 1994 Propranolol, an inhibitor of phosphatidate phosphohydrolase, and calyculin A, a phosphatase 1 and 2A inhibitor, blocked DAG production in response to FMLP but not to IL-4. Propranolol 0-11 formyl peptide receptor 1 Homo sapiens 150-154 1326583-6 1992 Propranolol, an inhibitor of diacylglycerol formation from phosphatidic acid, caused a prolonged transmembrane influx of Ca2+ and partially reversed the inhibitory effect of ethanol on FMLP-induced O2- production. Propranolol 0-11 formyl peptide receptor 1 Homo sapiens 185-189 1659906-3 1991 Propranolol (150 microM) enhanced the production of O2- in response to the receptor agonists n-formyl-methionyl-leucyl-phenylalanine (FMLP, 292 +/- 94% of controls), platelet-activating factor (PAF, 932 +/- 215%) and leukotriene B4 (LTB4, 1305 +/- 475%). Propranolol 0-11 formyl peptide receptor 1 Homo sapiens 134-138 1864964-7 1991 Propranolol was also observed to have a concentration-dependent enhancement of mass of 1,2-DG formed in PMN stimulated with FMLP. Propranolol 0-11 formyl peptide receptor 1 Homo sapiens 124-128 1864964-4 1991 Pretreatment of cells with various concentrations of propranolol enhanced (less than or equal to 200 microM) or inhibited (greater than 300 microM) PLD-induced production of PA (mass and radiolabel) in a manner that correlated with enhancement or inhibition of O2 consumption in PMN stimulated with 1 microM FMLP in the absence of cytochalasin B. Propranolol 53-64 formyl peptide receptor 1 Homo sapiens 308-312 1864964-5 1991 The concentration-dependent effects of propranolol on FMLP-induced NADPH oxidase activation was confirmed by direct assay of the enzyme in subcellular fractions. Propranolol 39-50 formyl peptide receptor 1 Homo sapiens 54-58 1864964-6 1991 In PA extracted from cells pretreated with 200 microM propranolol before stimulation with 1 microM FMLP, phospholipase A1 (PLA1)-digestion for 90 min, followed by quantitation of residual PA, showed that a minimum of 44% of PA in control (undigested) sample was diacyl-PA; alkylacyl-PA remained undigested by PLA1. Propranolol 54-65 formyl peptide receptor 1 Homo sapiens 99-103 1850243-5 1991 However, propranolol induced a similar dose-dependent inhibition of O2- generation in neutrophils stimulated with either FMLP + cytochalasin B or with 20.0 mM NaF. Propranolol 9-20 formyl peptide receptor 1 Homo sapiens 121-125 1850243-1 1991 Relatively high levels of propranolol (170 microM) markedly attenuated the generation of 1,2 diacylglycerol in neutrophils stimulated with either FMLP plus cytochalasin B or with 20.0 mM NaF. Propranolol 26-37 formyl peptide receptor 1 Homo sapiens 146-150 1850243-3 1991 Although propranolol enhanced phosphatidic acid levels in neutrophils treated with FMLP alone, the drug had only a slight inhibitory influence on diglyceride generation in these cells. Propranolol 9-20 formyl peptide receptor 1 Homo sapiens 83-87 1850243-4 1991 The effect of propranolol on enhancement of PA levels in neutrophils treated with FMLP alone strongly correlated with enhancement of FMLP-induced O2- generation. Propranolol 14-25 formyl peptide receptor 1 Homo sapiens 82-86 1850243-4 1991 The effect of propranolol on enhancement of PA levels in neutrophils treated with FMLP alone strongly correlated with enhancement of FMLP-induced O2- generation. Propranolol 14-25 formyl peptide receptor 1 Homo sapiens 133-137 2328008-4 1990 In fact: 1) in neutrophils treated with propranolol, an inhibitor of phosphatidate phosphohydrolase, FMLP plus cytochalasin B induces a respiratory burst associated with a stimulation of phospholipase D, formation of phosphatidic acid and complete inhibition of that of diacylglycerol. Propranolol 40-51 formyl peptide receptor 1 Homo sapiens 101-105 2328008-5 1990 2) The respiratory burst by FMLP plus cytochalasin B lasts a few minutes and may be restimulated by propranolol which induces an accumulation of phosphatidic acid. Propranolol 100-111 formyl peptide receptor 1 Homo sapiens 28-32