Analysis of checkpoint responses to histone deacetylase inhibitors.
Cell cycle checkpoints respond to a wide range of stresses to prevent compromise to the integrity of the cell. The best studied checkpoints are those induced by genotoxic agents that cause DNA damage. Histone deacetylase inhibitors not only increase the acetylation state of chromatin histones, but they also perturb the cell cycle, causing both G1 and G2 phase arrests, the latter by initiating a checkpoint response. In this chapter we will describe the analysis of the histone deacetylase inhibitor-sensitive G2 checkpoint using synchronized cell populations.
Beamish
Heather
H
Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Australia.
Warrener
Robyn
R
Gabrielli
Brian G
BG
D001973:Bromodeoxyuridine; D018797:Cell Cycle Proteins / Q000378:metabolism; D002455:Cell Division; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005347:Fibroblasts / Q000166:cytology; D005434:Flow Cytometry; D016195:G2 Phase / Q000187:drug effects*; D006367:HeLa Cells; D056572:Histone Deacetylase Inhibitors; D006655:Histone Deacetylases / Q000378:metabolism; D006801:Humans; D015151:Immunoblotting; D007231:Infant, Newborn; D008938:Mitosis / Q000187:drug effects*; D011233:Precipitin Tests; D011838:Radiation-Sensitizing Agents; D008941:Spindle Apparatus / Q000187:drug effects*
D018797:Cell Cycle Proteins; D004791:Enzyme Inhibitors; D056572:Histone Deacetylase Inhibitors; D011838:Radiation-Sensitizing Agents; D006655:Histone Deacetylases; D001973:Bromodeoxyuridine