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热诱导的G1期阻滞依赖于p53功能,而非RB去磷酸化。

Heat-induced G1 arrest is dependent on p53 function but not on RB dephosphorylation.

作者信息

Miyakoda M, Nakahata K, Suzuki K, Kodama S, Watanabe M

机构信息

School of Pharmaceutical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan.

出版信息

Biochem Biophys Res Commun. 1999 Dec 20;266(2):377-81. doi: 10.1006/bbrc.1999.1829.

Abstract

Normal human cells were heat shocked at 43 degrees C for 2 hr and recovered at 37 degrees C. The levels of p53 and p21 reached a maximum approximately 2 and 6 hr after the heat shock, respectively, and these levels were higher than the control level even at 24 hr. The fraction of S phase cells decreased significantly 8 hr after heat shock, and gradually thereafter. Heat-induced G1 arrest was not found in NCI-H1299 and HeLa cells, which are deficient in p53 function, indicating that p53 function is essential for G1 arrest after heat shock. We found little or no change in phosphorylation of retinoblastoma (RB) protein until 12 hr after heat shock, and a significant change at about 24 hr. No change in phosphorylation of RB at serine-780 and serine-795 occurred within 12 hr after heat shock. These results suggest that heat shock induces G1 arrest mediated by p53, but that G1 arrest within 12 hr after heat shock does not require RB dephosphorylation.

摘要

将正常人细胞在43℃热激2小时,然后在37℃恢复。热激后约2小时和6小时,p53和p21的水平分别达到最高,甚至在24小时时这些水平仍高于对照水平。热激8小时后,S期细胞比例显著下降,此后逐渐下降。在p53功能缺陷的NCI-H1299和HeLa细胞中未发现热诱导的G1期阻滞,这表明p53功能对于热激后的G1期阻滞至关重要。我们发现,热激后12小时内视网膜母细胞瘤(RB)蛋白的磷酸化几乎没有变化,而在约24小时时有显著变化。热激后12小时内,RB蛋白丝氨酸780和丝氨酸795位点的磷酸化没有变化。这些结果表明,热激诱导由p53介导的G1期阻滞,但热激后12小时内的G1期阻滞不需要RB去磷酸化。

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