Heat shock induces transient p53-dependent cell cycle arrest at G1/S

Nitta, Makoto; Okamura, Hitoshi; Aizawa, Shinichi; Yamaizumi, Masaru

doi:10.1038/sj.onc.1201210

Cited by 95 publications

(73 citation statements)

References 23 publications

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“…Genes affecting cell cycle that have been shown to be affected by heat shock include p53 and p21 ( Table 2). Induction of p53 after heat shock appears to be critical to this process in some cell lines, as no cell cycle arrest was noted in cells that were homozygous for a defective p53 gene (78).…”

Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

545

409

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This review examines the effects of thermal stress on gene expression, with special emphasis on changes in the expression of genes other than heat shock proteins (HSPs). There are ∼50 genes not traditionally considered to be HSPs that have been shown, by conventional techniques, to change expression as a result of heat stress, and there are <20 genes (including HSPs) that have been shown to be affected by cold. These numbers will likely become much larger as gene chip array and proteomic technologies are applied to the study of the cell stress response. Several mechanisms have been identified by which gene expression may be altered by heat and cold stress. The similarities and differences between the cellular responses to heat and cold may yield key insights into how cells, and by extension tissues and organisms, survive and adapt to stress.

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Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

545

409

View full text Add to dashboard Cite

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“…In addition, apoptotic cell death in post-mitotic neurons induced by exposure to either kainic acid or N-methyl-D-aspartate occurs where p53 protein induction precedes DNA fragmentation, suggesting that DNA damage is a consequence rather than a cause of p53 induction (Sakhi et al, 1994(Sakhi et al, , 1997Hughes et al, 1997). Cellular damaging agents as diverse as heat shock (Nitta et al, 1997), hypoxia (Graeber et al, 1996), perturbation of nucleotide metabolism (Linke et al, 1996), low extracellular pH , and TGF-b (Bellamy et al, 1997a) can also activate p53 function, thus suggesting either that the signalling lesions that target p53 protein are quite diverse and/or that strikingly di erent damaging agents function through identical signalling lesions.…”

Section: Introductionmentioning

confidence: 99%

Synergistic activation of p53-dependent transcription by two cooperating damage recognition pathways

et al. 2000

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High level activation of p53-dependent transcription occurs following cellular exposure to genotoxic damaging agents such as UV-C, while ionizing radiation damage does not induce a similarly potent induction of p53-dependent gene expression. Reasoning that one of the major di erences between UV-C and ionizing radiation damage is that the latter does not inhibit general transcription, we attempted to reconstitute p53-dependent gene expression in ionizing irradiated cells by co-treatment with selected transcription inhibitors that alone do not activate p53. p53-dependent transcription can be dramatically enhanced by the treatment of ionizing irradiated cells with low doses of DRB, which on its own does not induce p53 activity. The mechanism of ionizing radiationdependent activation of p53-dependent transcription using DRB is more likely due to inhibition of gene transcription rather than prolonged DNA damage, as the non-genotoxic and general transcription inhibitor Roscovitine also synergistically activates p53 function in ionizing irradiated cells. These results identify two distinct signal transduction pathways that cooperate to fully activate p53-dependent gene expression: one responding to lesions induced by ionizing radiation and the second being a kinase pathway that regulates general RNA Polymerase II activity.

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“…It is often regarded as the 'guardian of the cell' for conserving genome stability by prevention of mutations (Lane, 1992). It is important in multicellular organisms to activate DNA repair mechanism and arrest the cell cycle at the G1/S phase (Nitta et al, 1997;Keimling and Wiesmuller, 2009). p53 directly participates in the DNA repair process by recognizing DNA lesions and by binding with the proteins that are involved in the excision repair complex (Yoshida and Miki, 2010).…”

Section: Introductionmentioning

confidence: 99%