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1 ICP34.5 of herpes simplex virus and NL-S of avian sarcoma virus.
4 ne is a cell-derived insert in the genome of avian sarcoma virus 31 (ASV 31) and functions as the onc
6 hly preferred in vitro integration sites for avian sarcoma virus and human immunodeficiency virus-1 i
7 tion as seen in the integrase core domain of avian sarcoma virus as well as human immunodeficiency vi
8 etected independently of catalysis with both avian sarcoma virus (ASV) and human immunodeficiency vir
9 es of the core domain of integrase (IN) from avian sarcoma virus (ASV) and its active-site derivative
11 human immunodeficiency virus type 1 (HIV-1), avian sarcoma virus (ASV) and their close orthologs from
15 of E3 ubiquitin ligases bind the L domain in avian sarcoma virus (ASV) Gag and facilitate viral parti
17 nt of HIV-1, simian sarcoma virus (SIV), and avian sarcoma virus (ASV) INs predicted which of these r
18 in Daxx was identified as an interactor with avian sarcoma virus (ASV) integrase (IN) in a yeast two-
19 determined the size and shape of full-length avian sarcoma virus (ASV) integrase (IN) monomers and di
20 (aa) in the C-terminal region of the 286-aa avian sarcoma virus (ASV) integrase (IN) protein has bee
24 s comparable to one previously described for avian sarcoma virus (ASV) that was stimulated by the pre
25 the integrase protein of an oncoretrovirus, avian sarcoma virus (ASV), suggesting an active import m
26 netic repression and silencing of integrated avian sarcoma virus (ASV)-based vector DNAs in human HeL
28 d HeLa cell populations that harbored silent avian sarcoma virus-based green fluorescent protein (GFP
29 of integration catalyzed by HIV-1 to that of avian sarcoma virus by analyzing the effect of defined m
31 f chicken embryos with replication-competent avian sarcoma virus expressing either FgfR2(C278F), a re
32 es have indicated that in the context of the avian sarcoma virus genome, precise deletion of both ASV
33 m permanganate modification to show that the avian sarcoma virus IN catalytic domain is able to disto
34 he metal preference for in vitro activity of avian sarcoma virus IN is Mn2+ > Mg2+ and that a single
35 at the putative dimer-dimer interface of the avian sarcoma virus IN with its analogue, loop188-194, f
36 ar strategy, the unique amino acids found in avian sarcoma virus IN, rather than HIV-1 or Mason-Pfize
38 phic studies of the catalytic core domain of avian sarcoma virus integrase (ASV IN) have provided the
39 itor complex of the catalytic core domain of avian sarcoma virus integrase (ASV IN) were solved at 1.
40 of human immunodeficiency virus-1 integrase, avian sarcoma virus integrase, and bacteriophage Mu tran
44 in human (HeLa) cells, mediated by either an avian sarcoma virus or a human immune deficiency virus t
45 lected were substrates of HIV protease or of avian sarcoma virus protease, both of which have been re
46 t reduction in the total amount of HIV-1 and avian sarcoma virus retroviral vector DNA that is joined
49 n embryo fibroblasts (CEF) infected with the avian sarcoma virus UR2, encoding the oncogenic receptor
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