Please use this identifier to cite or link to this item:
|Title:||Isoform-specific activation of protein kinase c in irradiated human fibroblasts and their bystander cells|
|Authors:||Baskar, R. |
Protein kinase C
|Source:||Baskar, R., Balajee, A.S., Geard, C.R., Hande, M.P. (2008). Isoform-specific activation of protein kinase c in irradiated human fibroblasts and their bystander cells. International Journal of Biochemistry and Cell Biology 40 (1) : 125-134. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biocel.2007.07.002|
|Abstract:||Studies over the last several years have revealed the existence of a biological phenomenon known as "bystander effect", wherein cells that are not exposed to radiation elicit a similar response to that of irradiated cells. Understanding the mechanism(s) underlying the bystander effect is important not only for radiation risk assessment but also for evaluation of protocols for cancer radiotherapy. Evaluation of signaling pathways in bystander cells may provide an insight to understand the molecular mechanisms(s) responsible for this complex phenomenon. With this objective, the time course kinetics of intracellular distribution of protein kinase C (PKC isoforms PKC-βII, PKC-α/β, PKC-θ) was investigated in total and subcellular (cytosolic and nuclear) fractions of human lung fibroblast (MRC-5) cells. MRC-5 cells were either irradiated or treated with the irradiated conditioned medium collected 1 h after 1 or 10 Gy of γ-irradiation. The radiation dose selected was in the range of therapeutic usage of radiation for the human cancer treatment. Unexpectedly, bystander cells showed higher activation of protein kinase C isoforms as compared to irradiated and sham-treated control cells. Protein kinase C isoforms were more enriched in the nuclear fraction than the cytosolic fraction proteins. Induction of PKC isoforms in bystander cells are due to post-translational modifications as shown by the non-phosphorylated protein kinase C level in both irradiated and bystander cells did not differ from the sham-treated control cells. The specific activation of protein kinase C isoforms in bystander cells as demonstrated for the first time in this study may help to identify the effect of therapeutically used radiation exposure for the tumor destructions along with its implications for adjacent non-irradiated cells and organs. © 2007 Elsevier Ltd. All rights reserved.|
|Source Title:||International Journal of Biochemistry and Cell Biology|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Mar 8, 2018
WEB OF SCIENCETM
checked on Feb 12, 2018
checked on Mar 12, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.