Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.biocel.2007.07.002
DC FieldValue
dc.titleIsoform-specific activation of protein kinase c in irradiated human fibroblasts and their bystander cells
dc.contributor.authorBaskar, R.
dc.contributor.authorBalajee, A.S.
dc.contributor.authorGeard, C.R.
dc.contributor.authorHande, M.P.
dc.date.accessioned2011-08-01T03:04:30Z
dc.date.available2011-08-01T03:04:30Z
dc.date.issued2008
dc.identifier.citationBaskar, 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
dc.identifier.issn13572725
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/25084
dc.description.abstractStudies 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.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.biocel.2007.07.002
dc.sourceScopus
dc.subjectBystander effects
dc.subjectFibroblasts
dc.subjectIonizing radiation
dc.subjectProtein kinase C
dc.subjectSubcellular fractions
dc.typeArticle
dc.contributor.departmentPHYSIOLOGY
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/j.biocel.2007.07.002
dc.description.sourcetitleInternational Journal of Biochemistry and Cell Biology
dc.description.volume40
dc.description.issue1
dc.description.page125-134
dc.identifier.isiut000251461800012
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