Regulation of protein kinase C by ionizing radiation.
نویسندگان
چکیده
Members of the protein kinase C (PKC) gene family have been shown to play an important role in tumor promotion and regulation of cell growth. Experiments were designed to examine the effects of different qualities of ionizing radiation administered at a variety of doses and dose rates on the expression of PKC-specific mRNA in confluent Syrian hamster embryo cells. The results of these experiments showed that low-linear energy of transfer (LET) radiations (such as X-rays and gamma-rays) can induce increased expression of PKC mRNA within 1 h after radiation exposure. Levels of expression of PKC mRNA were increased 4- to 6-fold over unirradiated controls. Dose effects were evident, with increased accumulation of PKC mRNA at higher doses (ranging from 6 to 200 cGy). Induction of PKC mRNA occurred at a time when total cellular transcription was reduced following irradiation. Similar exposure of the cells to fission spectrum JANUS neutrons, however, had little effect on PKC mRNA expression. Modest induction (2-fold compared to untreated cells) occurred when irradiations were at very low dose rates (0.5 cGy/min). These results suggest that induction of PKC mRNA may be a step in the transformation process caused by ionizing radiation. In addition, they demonstrate that different qualities of radiation may regulate PKC differently.
منابع مشابه
Impact of Ionizing Radiation on the Expression of CDC25A Phosphatase (in vivo)
Background and Objective: The cell division cycle 25 (CDC25)is a familyof highly conserved dual-specificity phosphatases that activate cyclin-dependent kinase complexes. These complexes are the main cell cycle regulators. Mammalian cells ,exposure to DNA damaging radiations such as ionizing radiation and ultraviolet light, prevent cell cycle progression by activation of checkpoint pathways an...
متن کاملOpposing roles of c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinase in the cellular response to ionizing radiation in human cervical cancer cells.
Exposure of cells to ionizing radiation induces activation of multiple signaling pathways that play critical roles in determining cell fate. However, the molecular basis for cell death or survival signaling in response to radiation is unclear at present. Here, we show opposing roles of the c-jun NH(2)-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways in the mitochon...
متن کاملp53 stabilization in response to DNA damage requires Akt/PKB and DNA-PK.
The p53 protein is one of the major tumor suppressor proteins. In response to DNA damage, p53 is prevented from degradation and accumulates to high levels. Ionizing radiation leads to hypophosphorylation of the p53 ubiquitin ligase Mdm2 at sites where phosphorylation is critical for p53 degradation and to the phosphorylation and activation of Akt/PKB, a kinase that phosphorylates and inhibits G...
متن کاملIonizing radiation acts on cellular membranes to generate ceramide and initiate apoptosis
Recent investigations provided evidence that the sphingomyelin signal transduction pathway mediates apoptosis for tumor necrosis factor alpha (TNF-alpha) in several hematopoietic and nonhematopoietic cells. In this pathway, TNF-receptor interaction initiates sphingomyelin hydrolysis to ceramide by a sphingomyelinase. Ceramide acts as a second messenger stimulating a ceramide-activated serine/th...
متن کاملDifferential activation of the phosphatidylinositol 3'-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells.
Ionizing radiation induces an intracellular stress response via activation of the phosphatidylinositol 3'-kinase (PI3K)/Akt survival pathway. In tumor cells, the PI3K/Akt pathway is induced through activation of members of ErbB receptor tyrosine kinases. Here, we investigated the receptor dependence of radiation-induced PI3K/Akt activation in tumor cells and in endothelial cells. The integrity ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Cancer research
دوره 50 13 شماره
صفحات -
تاریخ انتشار 1990