Aflatoxin genotoxicity is associated with a defective DNA damage response bypassing p53 activation
Article first published online: 15 FEB 2011
© 2011 John Wiley & Sons A/S
Volume 31, Issue 4, pages 561–571, April 2011
How to Cite
Gursoy-Yuzugullu, O., Yuzugullu, H., Yilmaz, M. and Ozturk, M. (2011), Aflatoxin genotoxicity is associated with a defective DNA damage response bypassing p53 activation. Liver International, 31: 561–571. doi: 10.1111/j.1478-3231.2011.02474.x
- Issue published online: 8 MAR 2011
- Article first published online: 15 FEB 2011
- Received 14 September 2010, Accepted 10 January 2011
Figure S1. Induction of DNA adducts and 8-hydroxy-deoxyguanosine lesions following AFB1 exposure in HepG2.
Figure S2. Induction of senescence arrest and apoptosis in HepG2 cells by Adriamycin, but not AFB1 in HepG2.
Figure S3. Time-dependent increase in 53BP1 foci-positive HepG2 cells under AFB1 exposure.
Figure S4. The duration of 53BP1 foci after 24 h of exposure to AFB1 in HepG2.
Figure S5. Incomplete DNA damage checkpoint response of Huh7 hepatoma cells to AFB1.
Figure S6. Induction of 8-hydroxy-deoxyguanosine lesions and double-strand breaks in HCT116 isogenic clones following AFB1 exposure.
Figure S7. Increased DNA damage-induced foci detection after exposure of HCT116 isogenic clones to AFB1.
Figure S8. Incomplete DNA damage checkpoint response of wild-type p53 HCT116 cells to AFB1.
Figure S9. p53-dependent and p53-independent cell cycle arrest in HCT116 isogenic clones after Adriamycin treatment.
Figure S10. Lack of cell cycle arrest of HCT116 isogenic clones in response to AFB1-induced DNA damage.
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