Heat shock-mediated cell cycle arrest is accompanied by induction of p21 CKI.
Heat shock induces several events in cells including a series of gene expressions and cell cycle arrest. Recently, several types of cell cycle arrest have been related to the function of cyclin-dependent kinase inhibitors (CKI). Here we show that heat shock treatment up-regulates p21 CKI mRNA and protein in A172 glioma cells and arrests the cell cycle at the G1 phase, p53-deficient cell lines, MDAH041 and T98G, also showed a significant increase in p21 CKI expression after heat stress, indicating that the induction involves a p53-independent pathway. The kinetics of this transient induction, which is not affected by cycloheximide, demonstrate that p21 CKI is an immediate-early response gene.
Fuse
T
T
Department of Neurosurgery, Nagoya City University Medical School, Japan. tfuse@cmews2.med.nagoya-cu.ac.jp
Yamada
K
K
Asai
K
K
Kato
T
T
Nakanishi
M
M
D002453:Cell Cycle / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D018844:Cyclin-Dependent Kinases / Q000032:analysis*; D003513:Cycloheximide / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000378:metabolism*; D016193:G1 Phase / Q000235:genetics / Q000502:physiology; D017781:Genes, Immediate-Early; D006358:Hot Temperature; D006801:Humans; D007700:Kinetics; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D015854:Up-Regulation
D004791:Enzyme Inhibitors; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D003513:Cycloheximide; D018844:Cyclin-Dependent Kinases