کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2053062 | 1074254 | 2006 | 4 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Activation of p53 as a causal step for atherosclerosis induced by polycyclic aromatic hydrocarbons Activation of p53 as a causal step for atherosclerosis induced by polycyclic aromatic hydrocarbons](/preview/png/2053062.png)
This study was performed to prove our hypothesis that the metabolite(s) of polycyclic aromatic hydrocarbons (PAHs) caused the activation or phosphorylation of p53 via DNA damage to suppress the liver X receptor (LXR)-mediated signal transductions as a probably more direct mechanism. We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53. The exogenous expression of wild-type p53 suppressed the LXR-mediated trans-activation in Hep3B cells. The expression of mRNA for ATP binding cassette A1 was suppressed by MC and Dox in HepG2 cells. The protein expression of retinoid X receptor (RXR), a partner of LXR to form a heterodimer, was suppressed by MC and Dox in HepG2 cells.
Journal: FEBS Letters - Volume 580, Issue 3, 6 February 2006, Pages 890–893