Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cross-reactivity of the human IgE receptor with mouse and rat IgE was studied. Using leukocytes from a patient with chronic myelogenous leukemia, in which the mononuclear fraction contained up to 75% basophils, both rat and mouse IgE were found to inhibit the binding of 125I-human IgE to the human basophilic leukemia (HBL cells). About 15-fold more rodent IgE was required for 50% inhibition of binding than unlabeled human IgE (hIgE). Dose-response studies using increasing amounts of rodent vs human 125I-IgE indicated that the HBL cells had about 8000 receptors per cell for hIgE and 5500 receptors per cell for rodent IgE. When the HBL cells were surface labeled with 125I and subsequently solubilized with non-ionic detergent, the labeled hIgE receptor could be isolated by either affinity chromatography on IgE-Sepharose (either human or rodent) or by immunoprecipitation with hIgE and anti-IgE. By SDS-PAGE on 10% gels, the receptor had a m.w. of 58,000 daltons. The solubilized receptors exhibited some rebinding to hIgE-Sepharose, and this rebinding could be inhibited by either human or rodent IgE but not by human IgG. Both the HBL cells and normal human basophils could be passively sensitized with murine IgE anti-DNP for antigen-induced histamine release. The minimum concentration of the mouse IgE antibody for sensitizing normal basophils was 20 to 200 ng/ml. Pretreatment of basophils with human IgE, but not human IgG, abrogated the capacity of the murine IgE antibody to sensitize the cells for histamine release, which indicated that the human and rodent IgE were interacting with the same receptor.
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PMID:The interaction of human and rodent IgE with the human basophil IgE receptor. 618 55

The bis-indole indirubin is the active ingredient of the Traditional Chinese Medicine recipe Danggui Longhui Wan used against chronic myelocytic leukemia. We have previously shown that indirubins are potent inhibitors of cyclin-dependent kinases and glycogen synthase kinase-3. We here investigated the anti-mitotic properties of this class of compounds using the cell permeable indirubin-3'-monoxime and the HBL-100 cell line. Indirubin-3'-monoxime reversibly arrests asynchronous HBL-100 cells in G2. This arrest is not accompanied by any significant change in expression of the major cell cycle regulators. However indirubin-3'-monoxime inhibits the phosphorylation of consensus CDK phosphorylation sites as well as of nucleolin at a specific CDK1/cyclin B phosphorylation site, suggesting a direct action on the mitotic CDK1/cyclin B. When indirubin-3'-monoxime is added to HBL-100 cells synchronized in M phase by nocodazole, cells undergo an endoreplication leading to an 8n DNA content. As soon as indirubin-3'-monoxime is washed away, these polyploid cells become aneuploid and later die from necrosis. This mechanism of endoreplication followed by cell death may contribute to the anti-tumour properties of indirubins.
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PMID:Anti-mitotic properties of indirubin-3'-monoxime, a CDK/GSK-3 inhibitor: induction of endoreplication following prophase arrest. 1143 42