Often in karyotyping and cell cycle research it is desirable to increase the yield of mitotic cells in a particular phase of the cell cycle. This can be achieved in a variety of ways with the most popular being the use of a cell cycle synchronizing agent such as demecolcine. Demecolcine will arrest cells in metaphase with no remarkable effect on the biochemical events in mitotic cells or in synchronized G1 and S phase cells. White blood cells are often treated with demecolcine to arrest cells in metaphase.
Otras notas
Binds tubulin hence interfering with microtubule-dependent cell function[1]
European journal of biochemistry, 142(3), 577-581 (1984-08-01)
Colcemid binds tubulin rapidly and reversibly in contrast to colchicine which binds tubulin relatively slowly and essentially irreversibly. At 37 degrees C the association rate constant for colcemid binding is 1.88 X 10(6) M-1 h-1, about 10 times higher than
Biology of reproduction, 80(3), 464-472 (2008-12-17)
New techniques to boost male and female fertility are being pioneered at a rapid pace in fertility clinics to increase the efficiency of assisted reproduction methods in couples in which natural conception has not been achieved. This study investigates the
The Journal of biological chemistry, 285(42), 32242-32250 (2010-08-11)
Drugs that target microtubules are thought to inhibit cell division and cell migration by suppressing dynamic instability, a "search and capture" behavior that allows microtubules to probe their environment. Here, we report that subtoxic drug concentrations are sufficient to inhibit
Journal of cellular physiology, 225(2), 454-465 (2010-05-12)
When CHO cells are arrested in S-phase, they undergo repeated rounds of centrosome duplication without cell-cycle progression. While the increase is slow and asynchronous, the number of centrosomes in these cells does rise with time. To investigate mechanisms controlling this
Previous research showed that mutations in β1-tubulin are frequently involved in paclitaxel resistance but the question of whether the mutations are restricted by cell-type specific differences remains obscure. To circumvent cellular constraints, we randomly mutagenized β-tubulin cDNA, transfected it into
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