Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To delineate the proximity and spatial arrangement of the major structural proteins of intact vesicular stomatitis (VS) virions, protein complexes formed by oxidation or by bivalent cross-linkers were analyzed by two-dimensional electrophoresis on polyacrylamide slab gels. H2O2 oxidation of VS virions produced an N-polypeptide dimer (molecular weight, approximately equal to 110,000) on a first dimension gel that could be reduced to N monomers (molecular weight, approximately equal to 50,000). Proteins extracted from unreduced and unoxidized VS virions contained dimeric and trimeric forms of M-protein complexes as well as a heterodimer of M and N protein. Qualitatively similar VS viral protein complexes were generated by exposing VS virions to the reversible protein cross-linkers methyl-4-mercaptobutyrimidate (MMB), tartryl diazide (TDA), and dithiobis(succinimidyl proprionate) (DTBSP); cross-linked complexes on first-dimension gels were cleaved by reduction with 2-mercaptoethanol (MMB or DTBSP cross-linked) or by periodate oxidation (TDA cross-linked). In addition to covalently linked homodiamers of M and N proteins and a protein M-N heterodimer, the protein cross-linkers also generated homo-oligomers of G protein and a G-M heterodimer. These data suggest that the glycoprotein spike of VS virus is composed of more than one G protein. The existence of N-M and G-M heterodimers is consistent with the hypothesis that the matrix (M) protein may serve as a bridge between the G and N proteins in assembly of the VS virion.
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PMID:Spatial relationships of the proteins of vesicular stomatitis virus: induction of reversible oligomers by cleavable protein cross-linkers and oxidation. 19 63

A 15-year-old girl, suffering from recurrent stomatitis since the age of 7 years, turned out to be heterozygous for x-linked cytochrome b558-negative chronic granulomatous disease. Two different populations of neutrophils were found in her peripheral blood: one normal (ca. 44%) and one cytochrome b558-negative (ca. 56%) subpopulation which was unable to produce H2O2. There was no history of chronic granulomatous disease in the maternal family line and the blood from the mother and from the grandmother contained a single normal population of neutrophils only. Therefore a recent mutation in one of the x-chromosomes of maternal or paternal origin is most likely. We wish to emphasize that the possibility of a carrier status for chronic granulomatous disease should be considered if recurrent aphthous stomatitis occurs (especially in context with discoid lupus). An easy flow cytometrical method for H2O2 measurement on the single cell level is advised as a screening test [5]. Genetic counselling is a most important consequence of the correct diagnosis.
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PMID:[Chronic recurrent aphthous stomatitis in a 15-year-old carrier of x-chromosome inherited cytochrome b558-negative septic granulomatosis]. 208 42

The role of oxygen metabolites in mediating virucidal activity was studied in two cloned macrophage-like cell lines. The parental cell line, J774.16, upon appropriate stimulation with either phorbol myristate acetate (PMA) or aggregated immunoglobulin, is induced to oxidize glucose via the hexose monophosphate shunt and produce O2- and H2O2. A variant derived from it, clone C3C, is defective in oxidative metabolism and cannot be stimulated to produce O2- or H2O2. Significant differences in yields of vesicular stomatitis virus (VSV) between stimulated clone 16 cells and unstimulated cells could be obtained only when low multiplicities were used for infection. Under the same conditions, PMA stimulation of the variant clone C3C produced no reduction in yields. The effect of PMA on virus yields in clone 16 was short-lived and dose dependent. PMA stimulation of either cell line had no effect on the number of infectious centers, suggesting that the antiviral effect was likely to be an extracellular, rather than an intracellular, one. Using glucose oxidase plus aglucose to generate H2O2 in solution, we observed that H2O2 alone is capable of killing limited amounts of VSV. The inactivation of VSV, both by H2O2 in solution and by activated clone 16 cells, could be inhibited by catalase. We conclude that intracellular resistance to VSV is primarily mediated through nonoxidative mechanisms, since activated macrophages can kill only a limited number of infectious virus particles extracellularly by means of secreted H2O2.
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PMID:Role of macrophage oxidative metabolism in resistance to vesicular stomatitis virus infection. 628 44