Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tRNA methyltransferase activities of C57BL/6J, C57L/J, C58/J, AKR/J, and C3H/HeJ inbred mice were studied with the use of various amino acid-specific Escherichia coli tRNA's as substrates. Mice from two strains with high incidence of spontaneous leukemia (AKR/J and C58/J) exhibited levels of liver N2-guanine tRNA methyltransferase II (N2-MeGII) activity that were double those of two strains of mice with low incidence of spontaneous leukemia (C57BL/6J and C57L/J). Activities of liver and kidney N2-MeGII of the high spontaneous hepatoma strain C3H/HeJ were also found to be twice as high as those of C57BL/6J mice. The activities of other tRNA base-specific liver tRNA methyltransferases were very similar in all strains studied. The N2-MeGII activity of the F1 progeny of a cross between C57BL/6J and C3H/HeJ showed levels of activity intermediate to those of the parental strains. Activities of liver N2-MeGII of two inbred strains of mice that differ in their H-2 haplotype (C57BL/10SnJ and the congenic strain B10.BR/SgSnJ) were also compared. Both C57BL/10SnJ and B10.BR/SgSnJ strains exhibited low levels of liver N2-MeGII activity, indicating that H-2 does not directly control the activity of this enzyme.
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PMID:Differences in activity of N2-guanine tRNA methyltransferase II among several inbred strains of mice. 385 80

Variants of the rat basophilic leukemia (RBL) cell line were isolated and screened for phospholipid methyltransferase I and II activities, enzymes that convert phosphatidylethanolamine to phosphatidylcholine. Two variants were found that had decreased phospholipid methyltransferase enzyme levels and were unable to cause an influx of Ca2+ or release histamine in an IgE-mediated reaction. However, these cells were able to release histamine through an ionophore-induced reaction, indicating that the releasing mechanism distal to the Ca2+ channel was intact. One cell line, 1C1.B1, had low specific activity for phospholipid methyltransferase I. A second variant, 2H3.B6, had reduced phospholipid methyltransferase II activity. Although both variants were unable to incorporate label from [methyl-3H]methionine or [3H]serine into phosphatidylcholine, they were able to incorporate [methyl-3H]choline and myo-[2-3H(N)]inositol into phospholipids. Fusion of the two cell lines and isolation on selective media resulted in the growth of eight independent hybrids. All eight had an increased number of chromosomes and normal phospholipid methyltransferase activities. Stimulation of the hybrids with IgE resulted in CA2+ influx and histamine release. These results indicate that phospholipid methylation precedes and is necessary for Ca2+ influx, and they further support the hypothesis that methylation is a necessary early step in the IgE-mediated histamine release reaction in RBL cells.
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PMID:Rat basophilic leukemia cell lines defective in phospholipid methyltransferase enzymes, Ca2+ influx, and histamine release: reconstitution by hybridization. 617 12

Cloning of the rat basophilic leukemia (RBL) cell lines demonstrates variability in cell chromosome number (approximately 44-70) and in their capacity to release histamine following an IgE- or Ca2+-ionophore stimulus. After IgE activation there is increased phospholipid methylation, Ca2+ influx, arachidonic acid, and histamine release. On Ca2+ ionophore A23187 stimulation, phospholipid methylation is not increased, but Ca2+ influx, arachidonic acid, and histamine release occur. Variants of the RBL-cloned sublines defective at different stages in the release process were obtained and used to sequence the different events in the release process: IgE activation is followed by methylation, Ca2+ influx, arachidonic acid, and histamine release. However, there are other variants with defects in intermediate steps in the pathway, e.g., increased phospholipid methylation that is not followed by Ca2+ influx or arachidonic acid release not followed by histamine release. Isolating variants carrying drug-resistance markers made hybridization (reconstitution) experiments possible. Two variants were recognized, each of which was deficient in one of the two phospholipid methyltransferase enzymes. Neither of these two variants released histamine; hybrids formed by fusion of these two cell lines have both phospholipid methyltransferase enzymes and release histamine. By other complementation experiments, groups of variants with defects at different steps in the histamine release sequence were recognized. Clearly, these basophilic leukemia cell lines provide a unique system for the study of the mechanism of histamine release.
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PMID:Variants of the rat basophilic leukemia cell line for the study of histamine release. 617 65