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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Tyrosine kinase inhibitor-induced differentiation of K-562 cells: alterations of cell cycle and cell surface phenotype.

Protein tyrosine kinase ( PTK) inhibitor herbimycin A inhibited proliferation, induced accumulation of cells in the G0/ G1 phase of the cell cycle and a marked increae of hemoglobin-producing human leukemic K-562 cells in vitro. The isoflavonoid PTK- and topoisomerase II inhibitor genistein produced a similar effect with the accumulation of cells in the G2/M phase of cell cycle. Genistein potentiated the effect of herbimycin A on the cell cycle (i.e. decreased the proportion of S-phase cells) and induced an increased proportion of hemoglobin-producing cells. Genistein, but not herbimycin A induced a marked increase in cell surface expression of CD15 (LewisX) antigen. Both of these agents down-regulated CD45 (leukocyte common antigen) and monocyte- associated CD14 antigen on K-562 cells. Neither genistein nor herbimycin A induced increased cell surface expression of glycophorin.[1]

References

  1. Tyrosine kinase inhibitor-induced differentiation of K-562 cells: alterations of cell cycle and cell surface phenotype. Hunáková, L., Sedlák, J., Klobusická, M., Duraj, J., Chorváth, B. Cancer Lett. (1994) [Pubmed]
 
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