Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Teleocidin isolated from Streptomyces mediocidicus, its catalytically hydrogenated compound dihydroteleocidin B, and lyngbyatoxin A isolated from marine blue-green alga Lyngbya majuscula as well as its hydrogenated product, tetrahydrolyngbyatoxin A were tested for their ability to induce differentiation of human promyelocytic leukemia cells (HL-60 cells) in culture. All of these indole alkaloids induced differentiation of HL-60 cells, characterized by increased phagocytosis, increased release of lysozyme, and morphological changes resembling macrophages. The concentrations required for the induction were 1-5 ng/ml, showing similarity to those of 12-O-tetradecanoylphorbol-13-acetate (TPA). Teleocidin, lyngbyatoxin A, and tetrahydrolyngbyatoxin A are suggested to be tumor promoters, like TPA and dihydroteleocidin B. The HL-60 cell system might be useful for screening for environmental tumor promoters.
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PMID:Teleocidin, lyngbyatoxin A and their hydrogenated derivatives, possible tumor promoters, induce terminal differentiation in HL-60 cells. 679 52

Human promyelocytic leukemia cells (HL-60) were induced to differentiate into macrophage-like cells in a dose-dependent manner by the tumor promoters phorbol-12-myristate-13-acetate and teleocidin, a non-phorbol ester promoter. An HL-60 cell variant, designated as R-59, which is resistant to differentiation induction by phorbol-12-myristate-13-acetate was also resistant to differentiation induction by teleocidin. Differentiation was determined by increases in the percent of morphologically mature cells and in lysozyme and nonspecific esterase activities. Both compounds inhibited the growth of HL-60 cells by blocking them from entering the synthesis phase of the cell cycle with an accumulation of cells after 48 h in G1 phase. No such effects were observed in the R-59 cells. They were, however, as susceptible as the parent HL-60 cells, to inducers which are not considered to be tumor promoters such as dimethylsulfoxide and retinoic acid. However, these inducers cause the HL-60 and R-59 cells to differentiate into granulocyte-like cells. These results indicate that teleocidin produces in both the HL-60 and R-59 cells effects which are similar to those cause by phorbol-12-myristate-13-acetate. The possibility that agents producing such effects in these two cell types may represent potential tumor promoters is discussed.
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PMID:Induction of differentiation of human promyelocytic leukemia (HL-60) cells by teleocidin and phorbol-12-myristate-13-acetate. 680 9

Polyamine levels were evaluated in human HL-60 promyelocytic leukemia cells after treatment with inducers of terminal differentiation. Differentiation in these cells was determined by increases in the percentage of morphologically mature cells and in lysozyme activity. Treatment of the HL-60 cells with phorbol 12-myristate-13-acetate (PMA), phorbol 12,13-didecanoate or other inducers of terminal differentiation such as dimethylsulfoxide and retinoic acid resulted in increased levels of putrescine. However, no increase in putrescine could be detected after PMA treatment of a HL-60 cell variant that exhibited a decreased susceptibility to PMA-induced terminal differentiation. Similarly, no increase in putrescine was observed with two non-tumor-promoters (phorbol 12,13-diacetate and 4-O-methyl-PMA) or with anthralin, a non-phorbol tumor promoter. In addition to enhancing putrescine levels, PMA also increased the amount of spermidine and decreased the amount of spermine. The increase in putrescine and spermidine preceded the expression of the various differentiation markers. Unlike the changes observed in the polyamine levels after PMA treatment, the activities of ornithine and S-adenosylmethionine decarboxylases, which are polyamine biosynthetic enzymes, did not significantly change. alpha-Methylornithine and alpha-difluoromethylornithine and methylglyoxal bis(guanylhydrazone), which are inhibitors of the polyamine biosynthetic enzymes, did not affect differentiation in control or PMA-treated cells. Because of these observations, we suggest that the change in polyamine levels involve biochemical pathways other than the known biosynthetic ones. By-products of these pathways may perhaps be the controlling factors involved in the induction of terminal differentiation in the HL-60 and other cell types as well.
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PMID:Alterations in polyamine levels induced by phorbol diesters and other agents that promote differentiation in human promyelocytic leukemia cells. 694 Jan 23

The effect of sodium dodecyl sulfate (SDS), an anionic amphiphilic detergent, on the function of human neutrophils and of the human promyelocytic leukemia cell line HL-60 was investigated. SDS modulated the respiratory burst in human neutrophils and HL-60 cells which were stimulated with phorbol 12-myristate 13-acetate (PMA). In concentrations above 1 X 10(-6) M it also caused release of lysosomal enzymes (beta-D-glucuronidase, myeloperoxidase and lysozyme) from neutrophils. Our results demonstrate that SDS at concentrations 1 X 10(-6) M-1 X 10(-4) M strongly affect properties of human phagocytic cells.
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PMID:Immunomodulatory effect of sodium dodecyl sulfate on human neutrophils and the human promyelocytic HL-60 cell line. 780 77

We have previously identified and cloned an alternatively spliced form of human interleukin-6 mRNA lacking exon II, which encodes amino acid residues known to be important in gp130-mediated signal transduction pathways. We expressed and purified the recombinant protein (rIL6-alt) resulting from this alternatively spliced mRNA and now report the initial characterization of its biologic activities with comparison to full length IL6 (rIL6-full). rIL6-alt was found to have 10(4) to 10(5) fold less activity in proliferation assays with 7TD1 murine plasmacytoma cells and did not competitively inhibit the stimulatory activity of rIL6-full. In addition, like rIL6-full, rIL6-alt had antiproliferative activity toward M1 murine myeloblast cells and was 10-200-fold less active than rIL6-full. In contrast, in assays with human HL60 promyelocytic leukemia cells, rIL6-alt had greater antiproliferative activity than rIL6-full and more strongly upregulated phagocytosis as well as surface expression of the differentiation antigen CD11b. rIL6-full and rIL6-alt upregulated the level of lysozyme mRNA in HL60 cells approximately equally. These findings suggest that IL6-alt, which lacks amino acid residues encoded by the second exon of the gene, is not a natural inhibitor of IL6-full but may be relatively tissue specific and may play a role in modulation of hematopoietic cell growth and differentiation.
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PMID:Hematopoietic differentiation activity of a recombinant human interleukin-6 (IL-6) isoform resulting from alternatively spliced deletion of the second exon. 1039 9


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