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1                                              2-AAF activates IkappaB kinase (IKK), resulting in degra
2                                              2-AAF treatment led to the increase of intracellular rea
3 generation induced by 2-acetylaminofluorene (2-AAF) and 70% partial hepatectomy (PHx).
4 inofluorene (2-AF) to 2-acetylaminofluorene (2-AAF) by acetyl coenzyme A (AcCoA) dependent N-acetylat
5  The hepatocarcinogen 2-acetylaminofluorene (2-AAF) efficiently activates rat mdr1b expression in cul
6  The hepatocarcinogen 2-acetylaminofluorene (2-AAF) efficiently activates rat mdr1b expression.
7     Administration of 2-acetylaminofluorene (2-AAF) given before a two-thirds partial hepatectomy (PH
8     Administration of 2-acetylaminofluorene (2-AAF) given before partial hepatectomy (PHx) results in
9 e earliest effects of 2-acetylaminofluorene (2-AAF) on the mitotic activation of cells in the adult r
10 their activation with 2-acetylaminofluorene (2-AAF).
11 o proliferate using a 2-acetylaminofluorene (2-AAF)/hepatic injury (i.e., CCl4, partial hepatectomy [
12 er regeneration after 2-acetylaminofluorene (2-AAF)/partial hepatectomy (PHx) in rats.
13 mportant for robust oval cell response after 2-AAF/PHx treatment in rats.
14       Our results demonstrate that, although 2-AAF acts as a mitogenic stimulus for ductal and peridu
15 with the above two protocols (2-AAF/CCl4 and 2-AAF/PHx) as affected by previous bile ductular damage
16       Using the protocols of 2-AAF/ CCl4 and 2-AAF/PHx, when DAPM was given 24 hours before the hepat
17 sponse and AFP gene expression was ranked as 2-AAF/ CCl4 > or = 2-AAF/PHx > 2-AAF/AA.
18 he activation of MDR1 promoter activation by 2-AAF.
19 activation of rat mdr1b in cultured cells by 2-AAF involves a cis-activating element containing a NF-
20 cysteine inhibited the induction of mdr1b by 2-AAF.
21 anced the activation of the MDR1 promoter by 2-AAF.
22 nduction of mdr1b by the chemical carcinogen 2-AAF.
23 toprotein (AFP) gene expression by combining 2-AAF with selective damage of centrilobular regions (ca
24 toprotein (AFP) gene expression by combining 2-AAF with selective hepatic damage caused by either car
25 was ranked as 2-AAF/ CCl4 > or = 2-AAF/PHx > 2-AAF/AA.
26 e treatment followed by partial hepatectomy (2-AAF/PH) by using rat genome 230 2.0 Array chips and su
27                      CapLC-MS/MS analysis of 2-AAF/DNA reaction products was consistent with 2-AF-gua
28                                A low dose of 2-AAF (and its analogs, 2-AF [2-aminofluorene] and N-OH-
29                                 Low doses of 2-AAF were used to activate ductal and periductal cells,
30                       Using the protocols of 2-AAF/ CCl4 and 2-AAF/PHx, when DAPM was given 24 hours
31 its analogs, 2-AF [2-aminofluorene] and N-OH-2-AAF) elicited a mitogenic response in ductal cells and
32  expression was ranked as 2-AAF/ CCl4 > or = 2-AAF/PHx > 2-AAF/AA.
33  cell response with the above two protocols (2-AAF/CCl4 and 2-AAF/PHx) as affected by previous bile d
34 n addition to inducing a mitogenic response, 2-AAF resulted in increased numbers of apoptotic cells i
35     Based on these results, we conclude that 2-AAF up-regulates mdr1b through the generation of ROS,
36                 Our results demonstrate that 2-AAF and some of its analogs can elicit a specific mito
37              These results demonstrated that 2-AAF up-regulates MDR1 expression is mediated by the mu
38                In this study, we report that 2-AAF could also activate the human MDR1 gene in human h
39 eceived PHx only, while group B received the 2-AAF/PHx required for the oval cell activation.
40 little AFP gene expression compared with the 2-AAF/hepatic injury models.
41 TGF synthesis, Iloprost, was administered to 2-AAF/PHx treated rats to investigate the effect of Ilop
42                         Although exposure to 2-AAF alone or combined with infusion of HGF resulted in
43 of cells undergoing apoptosis in response to 2-AAF.
44 We then delineated the pathway through which 2-AAF activates NF-kappa B.
45                 Treating hepatoma cells with 2-AAF activated phosphoinositide 3-kinase (PI3K) and its
46             Treatment of hepatoma cells with 2-AAF also activated another PI3K downstream effector Ak
47 ntraportal bile duct epithelia was seen with 2-AAF/AA than with 2-AAF/CCl4.
48 t epithelia was seen with 2-AAF/AA than with 2-AAF/CCl4.
49  Subsequently, the animals were treated with 2-AAF/PHx.

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