Mild heat shock induces cyclin D1 synthesis through multiple Ras signal pathways

FEBS Letters

Han, Song Iy²  Jeon, Won Je²  Kang, Ho Sung²  Kim, Jung Mo²  Choi, Yung Hyun¹  Lee, Jun Hyuk²  Yoo, Mi Ae²  Chung, Hae Young³  Kim, Han Do²  Oh, Su Young² 

[1]Department of Biochemistry, College of Oriental Medicine, Dong-Eui University, Pusan 614-714, South Korea

[2]Department of Molecular Biology, College of Natural Sciences, and Research Institute of Genetic Engineering, Pusan National University, Pusan 609-735, South Korea

[3]Department of Pharmacy, College of Pharmacy, Pusan National University, Pusan 609-735, South Korea

关键词: Heat shock;    Cyclin D1;    Ras;    Rac1;    ERK;    extracellular signal-regulated kinase;    PI 3-kinase;    phosphatidylinositol 3-kinase;    CDK;    cyclin-dependent kinase;    GSK-3β;    glycogen synthase kinase-3β;    MAPK;    mitogen-activated protein kinase;    HSP;    heat shock protein;   

DOI  :  10.1016/S0014-5793(02)02459-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Hyperthermia such as that occurring during fever may improve cell survival during infection, although its mechanism of action is largely unknown. Here we show that acute exposure to mild, but not severe, heat shock induces the synthesis of cyclin D1 that plays a critical role(s) in G1 progression of the cell cycle. This induction seemed to be regulated through multiple Ras signal pathways involving extracellular signal-regulated kinase, phosphatidylinositol 3-kinase, and Rac1/NADPH oxidase, all of which have well been documented to be responsible for growth factor-induced cyclin D1 expression. In a physiological sense, mild heat shock may regulate cell proliferation through inducing cyclin D1 along with growth factors.

【 授权许可】

Unknown