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C Combadière J Hakim J P Giroud A Périanin 《Biochemical and biophysical research communications》1990,168(1):65-70
Staurosporine (STAR), a potent protein kinase C (PKC) antagonist, was found to modulate the chemoattractant-induced respiratory burst of human polymorphonuclear leukocytes (PMNs) according to drug concentration. Low STAR concentrations from 10 to 200 nM potentiated the N-formyl-methionyl-leucyl-phenylalanine (fMLP) and platelet activating factor (Paf)-induced respiratory burst, affecting both the initial rate and the total amount of superoxide anion generated. The maximal increase occurred in the presence of 100 nM STAR and optimal fMLP concentration and reached 60-100% of control values. Above 250 nM, STAR inhibited the respiratory burst with an IC50 of 360 and 320 nM for fMLP and Paf, respectively. The respiratory burst induced by PKC activators such as phorbol myristate acetate or phorbol 12, 13 dibutyrate was inhibited effectively by STAR, with a low IC50 (25 nM) for both stimuli. Thus, the use of low STAR concentrations points to two possible roles of PKC in the regulation of NADPH oxidase activity, i.e. a positive regulation in phorbol ester-treated cells and a negative regulation in chemoattractant-stimulated PMNs. 相似文献
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Mark Russell Daniel J. West Marc A. Briggs Richard M. Bracken Christian J. Cook Thibault Giroud Nicholas Gill Liam P. Kilduff 《PloS one》2015,10(3)
Reduced physical performance has been observed following the half-time period in team sports players, likely due to a decrease in muscle temperature during this period. We examined the effects of a passive heat maintenance strategy employed between successive exercise bouts on core temperature (Tcore) and subsequent exercise performance. Eighteen professional Rugby Union players completed this randomised and counter-balanced study. After a standardised warm-up (WU) and 15 min of rest, players completed a repeated sprint test (RSSA 1) and countermovement jumps (CMJ). Thereafter, in normal training attire (Control) or a survival jacket (Passive), players rested for a further 15 min (simulating a typical half-time) before performing a second RSSA (RSSA 2) and CMJ’s. Measurements of Tcore were taken at baseline, post-WU, pre-RSSA 1, post-RSSA 1 and pre-RSSA 2. Peak power output (PPO) and repeated sprint ability was assessed before and after the simulated half-time. Similar Tcore responses were observed between conditions at baseline (Control: 37.06±0.05°C; Passive: 37.03±0.05°C) and for all other Tcore measurements taken before half-time. After the simulated half-time, the decline in Tcore was lower (-0.74±0.08% vs. -1.54±0.06%, p<0.001) and PPO was higher (5610±105 W vs. 5440±105 W, p<0.001) in the Passive versus Control condition. The decline in PPO over half-time was related to the decline in Tcore (r = 0.632, p = 0.005). In RSSA 2, best, mean and total sprint times were 1.39±0.17% (p<0.001), 0.55±0.06% (p<0.001) and 0.55±0.06% (p<0.001) faster for Passive versus Control. Passive heat maintenance reduced declines in Tcore that were observed during a simulated half-time period and improved subsequent PPO and repeated sprint ability in professional Rugby Union players. 相似文献
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The cross-reacting antigenic determinant in the variant surface glycoproteins (VSGs) of Trypanosoma equiperdum was studied by testing the ability of VSG glycopeptides to bind heterologous anti-VSG sera. VSG glycopeptide purification revealed the presence of 3 oligosaccharide sidechains on the mature VSG. These consist of two sidechains containing only mannose and glucosamine and a third containing galactose and mannose (in a 5:1 ratio) as well as phosphorous and ethanolamine. This phosphorylated fragment completely blocked the binding of VSG to heterologous anti-VSG and therefore contained the cross-reacting determinants. 相似文献
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Claire Giroud Ikuko Sagami Yves Frapart Jean-Luc Boucher 《Journal of inorganic biochemistry》2010,104(10):1043-10081
Crystal structures of nitric oxide synthases (NOS) isoforms have shown the presence of a strongly conserved heme active-site residue, Tyr588 (numbering for rat neuronal NOS, nNOS). Preliminary biochemical studies have highlighted its importance in the binding and oxidation to NO of natural substrates L-Arg and Nω-hydroxy-l-arginine (NOHA) and suggested its involvement in mechanism. We have used UV-visible and EPR spectroscopy to investigate the effects of the Tyr588 to Phe mutation on the heme-distal environment, on the binding of a large series of guanidines and N-hydroxyguanidines that differ from L-Arg and NOHA by the nature of their alkyl- or aryl-side chain, and on the abilities of wild type (WT) and mutant to oxidize these analogues with formation of NO. Our EPR experiments show that the heme environment of the Tyr588Phe mutant differs from that of WT nNOS. However, the addition of L-Arg to this mutant results in EPR spectra similar to that of WT nNOS. Tyr588Phe mutant binds L-Arg and NOHA with much weaker affinities than WT nNOS but both proteins bind non α-amino acid guanidines and N-hydroxyguanidines with close affinities. WT nNOS and mutant do not form NO from the tested guanidines but oxidize several N-hydroxyguanidines with formation of NO in almost identical rates. Our results show that the Tyr588Phe mutation induces structural modifications of the H-bonds network in the heme-distal site that alter the reactivity of the heme. They support recent spectroscopic and mechanistic studies that involve two distinct heme-based active species in the two steps of NOS mechanism. 相似文献
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