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1 -) mice with 2-acetylaminofluorene and NOH-2-acetylaminofluorene.
2 e, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.
3 itrosamine followed by a brief exposure to 2-acetylaminofluorene.
4 olved in rat liver regeneration induced by 2-acetylaminofluorene (2-AAF) and 70% partial hepatectomy
5 of the arylamine 2-aminofluorene (2-AF) to 2-acetylaminofluorene (2-AAF) by acetyl coenzyme A (AcCoA)
6                       The hepatocarcinogen 2-acetylaminofluorene (2-AAF) efficiently activates rat md
7                       The hepatocarcinogen 2-acetylaminofluorene (2-AAF) efficiently activates rat md
8                          Administration of 2-acetylaminofluorene (2-AAF) given before a two-thirds pa
9                          Administration of 2-acetylaminofluorene (2-AAF) given before partial hepatec
10 zed DNA to examine the earliest effects of 2-acetylaminofluorene (2-AAF) on the mitotic activation of
11 riductal cells after their activation with 2-acetylaminofluorene (2-AAF).
12  HOC can be induced to proliferate using a 2-acetylaminofluorene (2-AAF)/hepatic injury (i.e., CCl4,
13  is a hallmark of liver regeneration after 2-acetylaminofluorene (2-AAF)/partial hepatectomy (PHx) in
14 g oval cell differentiation during the rat 2-acetylaminofluorene (2AAF) and 2/3 partial hepatectomy (
15 one partial hepatectomy in the presence of 2-acetylaminofluorene (2AAF) or retrorsine, both of which
16 del system using the carcinogen, N-acetoxy-2-acetylaminofluorene (AAAF), was used to synthesize a N-a
17 arcinogens 2-aminofluorene (AF), N:-acetyl-2-acetylaminofluorene (AAF) and 1-nitropyrene (1-NP) in a
18 ations at G3 by aromatic amine carcinogens 2-acetylaminofluorene (AAF) and 2-aminofluorene (AF) that
19 tion of hepatocytes is inhibited, and to N-2-acetylaminofluorene (AAF) hepatocarcinogenesis; and 3) t
20 nd in an experimental cirrhosis induced by 2-acetylaminofluorene (AAF) with carbon tetrachloride (CCl
21  well-studied aromatic amine carcinogen, N-2-acetylaminofluorene (AAF), forms adducts at the C8 posit
22 a predominantly incorporated a G opposite an acetylaminofluorene (AAF)-adducted guanine.
23  role of Rev1 in translesion synthesis of an acetylaminofluorene (AAF)-dG DNA adduct.
24  rats fed a diet supplemented with 0.03% N-2-acetylaminofluorene (AAF).
25 y insert C opposite N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (AAF-dG).
26 ons reported on the alignment of the related acetylaminofluorene [AAF]dG adduct opposite a -2 deletio
27 frameshift (deletion) mutagenesis induced by acetylaminofluorene- (AAF-) derived DNA adducts.
28 ith either a cisplatin lesion (1,2-GG) or an acetylaminofluorene adduct (AAF-dG).
29 DNA adducts: the N-(2'-deoxyguanosin-8-yl)-2-acetylaminofluorene adduct (dG-C8-AAF) and its deacetyla
30                                           An acetylaminofluorene adduct located on the transcribed st
31 ofluorene adduct or the helix-distorting N-2-acetylaminofluorene adduct situated at a specific site d
32           Even bulky DNA adducts such as N-2-acetylaminofluorene-adducted guanine, (+)- and (-)-trans
33 nine adducts, very inefficiently opposite an acetylaminofluorene-adducted guanine, but was unresponsi
34 , we treated XPC mutant (XPC-/-) mice with 2-acetylaminofluorene and NOH-2-acetylaminofluorene.
35 6-methyldipyridol[1,2-a:3',2'-d]imidazole, 2-acetylaminofluorene, benzidine, 2-naphthylamine, aflatox
36 tation with the model arylamine derivative 2-acetylaminofluorene but G1 is not.
37 lation of repair synthesis by N:-acetoxy-N:- acetylaminofluorene, but are proficient in the stimulati
38 a plays a role in translesion synthesis past acetylaminofluorene-derived lesions in mammalian cells.
39 jor DNA adducts: N-(2'-deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-AAF) and its deacetylated deriva
40 nesis studies of N-(2'-deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-AAF) and N-(2'-deoxyguanosin-8-y
41 e-specifically with N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-AAF) and N-(deoxyguanosin-8-yl)-
42 agenic potential of N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-AAF) and N-(deoxyguanosin-8-yl)-
43 major groove adduct N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-AAF).
44 e (dG-C8-AF) and N-(2'-deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-C8-AAF) adducts that differ by a
45 ts with DNA to form N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-C8-AAF), N-(deoxyguanosin-8-yl)-
46 dG-C8-AF), and 3-(deoxyguanosin-N(2)()-yl)-2-acetylaminofluorene (dG-N(2)-AAF) DNA adducts.
47 guanosine (dG) and aminofluorene-dG (but not acetylaminofluorene-dG).
48  adduct N-(2'-deoxyguanosin-8-yl)-7-fluoro-2-acetylaminofluorene (FAAF) at G(1), G(2) or G(3) of NarI
49 obiphenyl (FABP), 2-aminofluorene (FAF) or 2-acetylaminofluorene (FAAF), and N is either dA or dT.
50                             The carcinogen 2-acetylaminofluorene forms two major DNA adducts: N-(2'-d
51 orene (G-AF) and N-2-(2'-deoxyguanosin-8-yl)-acetylaminofluorene (G-AAF) derivatives are the best stu
52 cleosomes with a 200-bp duplex containing an acetylaminofluorene-guanine (AAF-G) adduct at a single s
53 n, we prepared mononucleosomes containing an acetylaminofluorene-guanine adduct (AAF-G), a (6-4) phot
54                             The carcinogen 2-acetylaminofluorene is metabolically activated in cells
55 ever, pol kappa shows limited bypass of an 2-acetylaminofluorene lesion and can incorporate dCTP or d
56                    The 1,3 crosslink and the acetylaminofluorene lesion were repaired by normal cell
57 G, and 1,3-GTG cisplatin-crosslinks, and a 2-acetylaminofluorene lesion.
58         Human Polkappa was able to bypass an acetylaminofluorene-modified G in DNA, incorporating eit
59 ta) efficiently incorporated a C opposite an acetylaminofluorene-modified G, and efficiently inserted
60 ogenic hydroxyarylamines such as N-hydroxy-2-acetylaminofluorene (N-OH-2AAF) can be further activated
61  cultured human cells exposed to N-acetoxy-2-acetylaminofluorene (NA-AAF), which generates bulky DNA
62 ntaining bulky adducts formed by N-acetoxy-2-acetylaminofluorene or benzo(a)pyrene diol epoxide.
63 +)-trans-dG-N(2)-benzo[a]pyrene and dC*dG-C8-acetylaminofluorene pairs, respectively, suggesting that
64 stitution in rats of a diethylnitrosamine, 2-acetylaminofluorene, partial hepatectomy carcinogenesis
65 ell-mediated liver regeneration induced by 2-acetylaminofluorene/partial hepatectomy (AAF/PH) protoco
66   During the hepatic stem cell activation (2-acetylaminofluorene/partial hepatectomy [AAF/PH] model),
67 ur weeks later, rats were subjected to the 2-acetylaminofluorene/partial hepatectomy model of oval ce
68 xpression was knocked down in the liver of 2-acetylaminofluorene/partial hepatectomy-treated rats usi
69 tion during liver regeneration following N-2-acetylaminofluorene/partial hepatectomy.
70 nd ST1E2 mRNAs (corresponding to N-hydroxy-2-acetylaminofluorene ST and estrogen ST, respectively) in
71        Transplanted rats were treated with 2-acetylaminofluorene, to block hepatocyte proliferation,
72               Oval cells were activated in 2-acetylaminofluorene-treated rats subjected to partial he
73  markers in the liver of rats subjected to 2-acetylaminofluorene treatment followed by partial hepate
74 g OC activation, after the implantation of 2-acetylaminofluorene with partial hepatectomy in rats or
75  of miR-133b in DR/OC activation models of 2-acetylaminofluorene with partial hepatectomy in rats, an
76 duced in the rat DR/OC activation model of 2-acetylaminofluorene with partial hepatectomy.

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