[The role of stress-kinase p38 in cell cycle blocking delay under osmotic stress].
Alteration in osmotic conditions leads to activation of some defensive mechanisms resulting in blocking the cell cycle progression. One of stress kinases, activated after osmotic stress, is p38 MAPK. In the present study the role of p38 both in intra-S-phase and G2/M checkpoint is shown. Besides, p38-dependent degradation of Cdc25A phosphatase after osmotic stress is demonstrated. Expression of stable form of Cdc25A results in a partial abrogation of G2/M block of the cell cycle, but has no effect on DNA synthesis arrest.
Goloudina
A R
AR
Pospelov
V A
VA
D002453:Cell Cycle / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D004247:DNA / Q000096:biosynthesis; D016195:G2 Phase / Q000502:physiology; D006367:HeLa Cells; D006801:Humans; D009997:Osmotic Pressure; D016196:S Phase / Q000502:physiology; D020687:cdc25 Phosphatases / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology*
D004247:DNA; D048051:p38 Mitogen-Activated Protein Kinases; D020687:cdc25 Phosphatases