کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2601156 | 1133303 | 2009 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice](/preview/png/2601156.png)
چکیده انگلیسی
BPOZ2 is a tumor suppressive mediator in PTEN signaling pathway and plays an important role in cell proliferation. In this study, we investigated the physiology functions of BPOZ2 in CCl4-induced liver injury and hepatocyte proliferation afterwards. After acute CCl4 administration, BPOZ2 null mice exhibited delayed liver injury and impaired hepatocyte proliferation, which was accompanied by altered kinetics of CYP2E1 protein expression, compromised cyclin D1 expression and shortened duration of ERK activation. These results for the first time define that BPOZ2 is an important regulator involved in the injury and repair process induced by acute CC14 administration in mouse liver.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 188, Issue 3, 10 August 2009, Pages 201–207
Journal: Toxicology Letters - Volume 188, Issue 3, 10 August 2009, Pages 201–207
نویسندگان
Feng Zhang, Runzhe Shu, Xiaolin Wu, Xiaoping Zhao, Dechun Feng, Long Wang, Shunyuan Lu, Qiaoling Liu, Yougui Xiang, Jian Fei, Lei Huang, Zhugang Wang,