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.
Other Notes
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
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
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
Prolonged in vitro culture of human embryonic stem (hES) cells can result in chromosomal abnormalities believed to confer a selective advantage. This potential occurrence has crucial implications for the appropriate use of hES cells for research and therapeutic purposes. In
BioEssays : news and reviews in molecular, cellular and developmental biology, 34(9), 760-770 (2012-06-19)
Recent studies indicate that mammalian chromosomes contain discrete cis-acting loci that control replication timing, mitotic condensation, and stability of entire chromosomes. Disruption of the large non-coding RNA gene ASAR6 results in late replication, an under-condensed appearance during mitosis, and structural
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