Cellular stress triggers the human topoisomerase I damage response independently of DNA damage in a p53 controlled manner
Rockstroh, Anja, Kleinert, A., Kramer, M., Grosse, F., & Søe, K. (2007) Cellular stress triggers the human topoisomerase I damage response independently of DNA damage in a p53 controlled manner. Oncogene, 26(1), pp. 123-131.
The 'human topoisomerase I (htopoI) damage response' was reported to be triggered by various kinds of DNA lesions. Also, a high and persistent level of htopoI cleavage complexes correlated with apoptosis. In the present study, we demonstrate that DNA damage-independent induction of cell death using colcemid and tumor necrosis factor is also accompanied by a strong htopoI response that correlates with the onset of apoptotic hallmarks. Consequently, these results suggest that htopoI cleavage complex formation may be caused by signaling pathways independent of the kind of cellular stress. Thus, protein interactions or signaling cascades induced by DNA damage or cellular stress might lead to the formation of stabilized cleavage complexes rather than the DNA lesion itself. Finally, we show that p53 not only plays a key role in the regulation of the htopoI response to UV-C irradiation but also to treatment with colcemid.
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|Item Type:||Journal Article|
|Keywords:||Apoptosis, Damage response, p53, topo-isomerase I, colcemid, TNFalpha|
|Subjects:||Australian and New Zealand Standard Research Classification > MEDICAL AND HEALTH SCIENCES (110000) > ONCOLOGY AND CARCINOGENESIS (111200)
Australian and New Zealand Standard Research Classification > MEDICAL AND HEALTH SCIENCES (110000) > ONCOLOGY AND CARCINOGENESIS (111200) > Cancer Cell Biology (111201)
|Divisions:||Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
|Copyright Owner:||Copyright 2007 Nature Publishing Group|
|Deposited On:||06 Feb 2014 05:08|
|Last Modified:||06 Feb 2014 05:08|
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