Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism by which the yeast form of Blastomyces dermatitidis resists killing by human peripheral blood polymorphonuclear neutrophils (PMN) was investigated. The metabolic products of the oxidative burst generated during the interaction of PMN and B. dermatitidis or Candida albicans were detected by lucigenin- or luminol-enhanced chemiluminescence (CL). Interaction of PMN and C. albicans resulted in luminol-enhanced CL 100-fold greater than that generated by PMN and B. dermatitidis. This correlated with killing of C. albicans and resistance of B. dermatitidis. Since B. dermatitidis and PMN interactions resulted in significant lucigenin-enhanced CL, deficient luminol CL was not due to a lack of products from the NADPH oxidase system. Killed B. dermatitidis cells at 37 degrees C were more efficient than live cells in stimulating PMN for luminol-enhanced CL; however, only fragmented B. dermatitidis cells elicited luminol-enhanced CL equivalent to that of C. albicans. Since lysates of PMN were active in a cell-free hydrogen peroxide-peroxidase-halide system, resistance of B. dermatitidis to PMN was not due to a defect in PMN peroxidase. Taken together, these findings indicate that resistance of B. dermatitidis to killing by PMN results from inefficient generation of products from the peroxidase-dependent PMN microbicidal system.
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PMID:A basis for resistance of Blastomyces dermatitidis killing by human neutrophils: inefficient generation of myeloperoxidase system products. 132 54

Plant responses to supplementary UV-B irradiation have been reported to include formation of reactive oxygen species (ROS), hydrogen peroxide, in particular, and regulation by mitogen-activated protein kinase (MAPK) cascades which in turn are fine-tuned by MAPK phosphatases (MKPs). Here we present direct genetic evidence for the involvement of plasma membrane NADPH oxidase, a source of superoxide and hydrogen peroxide in the apoplasts, in UV-B signalling in Arabidopsis thaliana, by analysis of gene expression of the UV-B molecular markers in NADPH oxidase (atrbohD, F and DF) and MAP kinase phosphatase 1 (MKP1) knockout mutants (mkp1). Whereas the NADPH oxidase mutants were affected in UV-B-dependent CHS, PYROA and MEB5.2 gene expression, the mkp1 mutant was affected in the general expression pattern of the pathogenesis-related (PR) and PDF1.2 genes. The results indicate involvement of MKP1 in repressive action on gene expression of more general stress response pathways, similar to those activated by pathogen attack, while NADPH oxidase is involved in quantitative (rather than absolute) regulation of more UV-B-specific genes. The expressions of the molecular markers in the knockout mutant mkp1 and in its complemented lines (lines 6 and 10) were similar, as opposed to the responses of the corresponding wild-type Wassilewskija-4 (Ws-4). Lines 6 and 10 showed much higher MKP1 mRNA than Ws-4 but did not complement the mutant. This suggests a complex dependency of the MAPK phosporylation level of the PR and PDF1.2 genes. Both NADPH oxidase mutants and the mkp1 mutant phenotypically responded to UV-B by growth retardation.
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PMID:The role of NADPH oxidase and MAP kinase phosphatase in UV-B-dependent gene expression in Arabidopsis. 1691 67

Vascular smooth muscle cell (VSMCs) proliferation is an essential factor in cardiovascular diseases, such as primary atherosclerosis and in-stent restenosis. In this study, we examined the effects of the novel synthetic naphthoquinone, 2-pyrrilidino-3-(p-hydroxyphenylamino)-1,4-naphthoquinone (TW-96), on cultured VSMCs and endothelial cells (ECs). Pharmacological concentrations of the derivative TW96 were found to induce VSMCs death, probably by increasing ROS levels while decreasing mitochondrial potential (DeltaPsi(m)) without affecting ECs. Treatment of tissue cultures with ROS is known to induce MAPK activity. Our observations showed prolonged phosphorylation and perinuclear accumulation of ERK1/2 and p38 simultaneously with an inhibition of MKP1. Increased expression of Bax found in TW96-stimulated VSMCs was inhibited by the NADPH oxidase inhibitor diphenyliodonium (DPI). An examination of the suppressive effects of TW96 on PDGF-BB-stimulated VSMCs cycle progression showed that TW96 leads to migration arrest at concentrations lower than LC(50). We hope that this prototype derivative will establish the basis for creating more specific naphthoquinone derivatives aimed at preventing the VSMCs proliferation associated with stenosis and restenosis.
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PMID:TW96, a synthetic 1,4-naphthoquinone, differentially regulates vascular and endothelial cells survival. 1957 4