Cellular stress triggers the human topoisomerase I damage response independently of DNA damage in a p53 controlled manner
Data(s) |
01/01/2007
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Resumo |
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. |
Identificador | |
Publicador |
Nature Publishing Group |
Relação |
http://www.nature.com/onc/journal/v26/n1/full/1209766a.html DOI:10.1038/sj.onc.1209766 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. |
Direitos |
Copyright 2007 Nature Publishing Group |
Fonte |
School of Biomedical Sciences; Faculty of Health; Institute of Health and Biomedical Innovation |
Palavras-Chave | #111200 ONCOLOGY AND CARCINOGENESIS #111201 Cancer Cell Biology #Apoptosis #Damage response #p53 #topo-isomerase I #colcemid #TNFalpha |
Tipo |
Journal Article |