Nesic, Dobrila; Grumont, Raelene; Gerondakis, Steve (2008). The nuclear factor-kappaB and p53 pathways function independently in primary cells and transformed fibroblasts responding to genotoxic damage. Molecular cancer research, 6(7), pp. 1193-203. Philadelphia, Pa.: American Association for Cancer Research AACR 10.1158/1541-7786.MCR-07-2125
Full text not available from this repository.With nuclear factor-kappaB (NF-kappaB) and p53 functions generally having disparate outcomes for cell survival and cell division, understanding how these pathways are coordinated following a common activation signal such as DNA damage has important implications for cancer therapy. Conflicting reports concerning NF-kappaB and p53 interplay in different cell line models prompted a reexamination of this issue using mouse primary thymocytes and embryonic fibroblasts, plus fibroblasts transformed by E1A12S. Here, we report that following the treatment of these cells with a range of stress stimuli, p53 and NF-kappaB were found to regulate cell cycling and survival independently.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute of Pathology |
UniBE Contributor: |
Nesic, Dobrila |
ISSN: |
1541-7786 |
ISBN: |
18583526 |
Publisher: |
American Association for Cancer Research AACR |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:02 |
Last Modified: |
05 Dec 2022 14:19 |
Publisher DOI: |
10.1158/1541-7786.MCR-07-2125 |
PubMed ID: |
18583526 |
Web of Science ID: |
000257895900012 |
URI: |
https://boris.unibe.ch/id/eprint/27147 (FactScience: 104597) |