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aspartic acid/nekros
Länken sparas på Urklipp
Sida 1 från 142 resultat
Aspartic acid 50 and tyrosine 108 are essential for receptor binding and cytotoxic activity of tumour necrosis factor beta (lymphotoxin).
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Single amino acid substitutions were generated in predicted hydrophilic loop regions of the human tumour necrosis factor beta (TNF-beta) molecule, and the mutant proteins were expressed in Escherichia coli and purified. Mutants with single amino acid changes at either of two distinct loop regions,
Alteration in folding efficiency and conformation of recombinant human tumor necrosis factor-alpha by replacing cysteines 69 and 101 with aspartic acid 69 and arginine 101.
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An analog of human tumor necrosis factor-alpha (TNF-alpha) was created involving the replacement of Cys69 with Asp and Cys101 with Arg. The solution structure and behavior of this analog were compared with the native protein. The analog exhibited a greatly decreased folding efficiency following
Monocytic U937 adhesion, tumor necrosis factor-alpha and interleukin-1 beta expression in response to gelatin-based networks grafted with arginine-glycine-aspartic acid and proline-histidine-serine-arginine-asparagine oligopeptides.
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In this study we synthesized gelatin-based, tissue-engineering, interpenetrating network (IPN) scaffolds immobilized with fibronectin (FN)-derived peptides to assess monocyte-biomaterial interaction. Human promonocytic U937 cells were seeded onto peptide-grafted IPN or tissue-culture polystyrene
[The effect of L-aspartic acid in isoproterenol necrosis of cardiac muscle].
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Simvastatin prevents neuroinflammation by inhibiting N-methyl-D-aspartic acid receptor 1 in 6-hydroxydopamine-treated PC12 cells.
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This study investigates the impact of simvastatin on neuroinflammation in experimental parkinsonian cell models. 6-Hydroxydopamine (6-OHDA)-treated pheochromocytoma-12 (PC12) cells were used to investigate the neuroprotective nature of simvastatin. After incubation with 6-OHDA, simvastatin, and/or
Replacing the 238th aspartic acid with an arginine impaired the oligomerization activity and inflammation-inducing property of pyolysin.
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Trueperella pyogenes (T. pyogenes) is an important opportunistic pathogen. Pyolysin (PLO) importantly contributes to the pathogenicity of T. pyogenes. However, the relationship between the structure and function and the virulence of PLO is not well documented. In the current study, recombinant PLO
Non-NMDA and NMDA receptor-mediated excitotoxic neuronal deaths in adult brain are morphologically distinct: further evidence for an apoptosis-necrosis continuum.
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Apoptosis and necrosis are generally recognized as two distinct pathways of cell death, based on biochemical and morphological characteristics. Despite rapid advances in elucidating molecular mechanisms of cell death, little is known about the morphological progression of death in neurons and the
Toxicity assessment of repeated intravenous injections of arginine-glycine-aspartic acid peptide conjugated CdSeTe/ZnS quantum dots in mice.
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BACKGROUND
Nanotechnology-based near-infrared quantum dots (NIR QDs) have many excellent optical properties, such as high fluorescence intensity, good fluorescence stability, and strong tissue-penetrating ability. Integrin αvβ3 is highly and specifically expressed in tumor angiogenic vessel
Inactivation of cystein-aspartic acid protease (caspase)-1 by saikosaponin A.
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This work investigates the anti-inflammatory mechanism of saikosaponin A (SA), a major component of Bupleurum falcatum LINNE. SA significantly inhibited phorbol myristate acetate (PMA) plus A23187-induced the production and expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in human
Excitotoxin-induced myocardial necrosis.
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The excitotoxins, kainic acid and N-methyl-D-aspartic acid (NMDA), were injected bilaterally into the paraventricular hypothalamus of rats. Kainic acid elicited pressor responses, tachycardia and sudden cardiac death in Nembutal-anesthetized rats. Injections of NMDA caused cardiovascular stimulation
Nicotine-induced neuroprotection against N-methyl-D-aspartic acid or beta-amyloid peptide occur through independent mechanisms distinguished by pro-inflammatory cytokines.
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Nicotine, the causative agent of addiction to tobacco, can also be a neuroprotectant. Nicotine-induced neuroprotection against different toxins is imparted through pharmacologically distinct neuronal nicotinic acetylcholine receptors (nAChR) where protection against chronic N-methyl-d-aspartic acid
Inhibition of in vitro RNA binding and replicase activity by phosphorylation of the p33 replication protein of Cucumber necrosis tombusvirus.
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Tombusviruses, which are small plus-strand RNA viruses of plants, require the viral-coded p33 replication co-factor for template selection and recruitment into replication in infected cells. As presented in the accompanying paper [Shapka, N., Stork, J., Nagy, P.D., 2005. Phosphorylation of the p33
A mutational analysis of the cytosolic domain of the tomato Cf-9 disease-resistance protein shows that membrane-proximal residues are important for Avr9-dependent necrosis.
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The tomato Cf-9 gene encodes a membrane-anchored glycoprotein that imparts race-specific resistance against the tomato leaf mould fungus Cladosporium fulvum in response to the avirulence protein Avr9. Although the N-terminal half of the extracellular leucine-rich repeat (eLRR) domain of the Cf-9
Effect of a novel tetrapeptide derivative in a model of isoproterenol induced myocardial necrosis.
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Isoproterenol hydrochloride (ISO), a beta adrenergic agonist, is known to cause ischemic necrosis in rats. Cardiotoxicity of three different doses of ISO were studied using physiological, biochemical and histopathological parameters. The effects of single and double dose of ISO were analysed, which
Mutational analysis of structure--activity relationships in human tumor necrosis factor-alpha.
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To determine the region of human tumor necrosis factor-alpha (TNF-alpha), essential for cytotoxic activity against mouse L-M cells, single amino-acid-substituted TNF-alpha mutant proteins (muteins) were produced in Escherichia coli by protein engineering techniques. An expression plasmid for
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