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1 The study of the interactions of subgroup A avian sarcoma and leucosis viruses [ASLV(A)] with the TV
2 ystem, a well established model for studying avian sarcoma and leukemia oncogenes, we probed the tran
5 better elucidated the viral entry process of avian sarcoma and leukosis virus (ASLV) and human immuno
7 imaged fusion between single virions bearing avian sarcoma and leukosis virus (ASLV) envelope glycopr
10 distribution of avian retroviruses, we found avian sarcoma and leukosis virus (ASLV) gag genes in 26
11 hic effect (CPE) seen with some subgroups of avian sarcoma and leukosis virus (ASLV) is associated wi
12 f Tva-expressing avian or mammalian cells by avian sarcoma and leukosis virus (ASLV) or EnvA-pseudoty
13 "priming" model for entry of the retrovirus avian sarcoma and leukosis virus (ASLV) predicts that up
14 cterization of the defect associated with an avian sarcoma and leukosis virus (ASLV) receptor resista
17 el entry mechanism has been proposed for the avian sarcoma and leukosis virus (ASLV), whereby interac
18 e efficiency of acid-dependent fusion of the avian sarcoma and leukosis virus (ASLV), with endosomes.
19 of Tva, the cellular receptor for subgroup A avian sarcoma and leukosis virus (ASLV-A), in viral entr
20 ration that Tva, the receptor for subgroup A avian sarcoma and leukosis virus (ASLV-A), induces confo
21 d to express the TVA receptor for subgroup A avian sarcoma and leukosis virus (ASLV-A), the five cell
25 rly steps of retroviral replication by using avian sarcoma and leukosis virus as a model retrovirus.
27 tor of a model retrovirus, subgroup A of the Avian Sarcoma and Leukosis Virus genus (ASLV-A), was stu
31 ding to the two heptad repeat domains of the avian sarcoma and leukosis virus subgroup A (ASLV-A) TM
32 tages at which the envelope protein (Env) of avian sarcoma and leukosis virus subgroup A folds into a
35 gene conferring susceptibility to subgroup A avian sarcoma and leukosis viruses (ASLV-A) was recently
36 The TVB receptor for subgroup B, D, and E avian sarcoma and leukosis viruses (ASLVs) is a tumor ne
38 ified and cloned the receptor for subgroup C avian sarcoma and leukosis viruses [ASLV(C)], i.e., Tvc,
39 f the extracellular region of the subgroup A avian sarcoma and leukosis viruses envelope glycoprotein
40 HTLV-1, HIV-1, murine leukaemia virus (MLV), avian sarcoma leucosis virus (ASLV) and prototype foamy
41 ion of the mature carboxyl terminus of CA in avian sarcoma/leukemia virus is the result of a sequence
44 the Vps4 protein does not associate with the avian sarcoma leukosis virus or the HIV-1 budding comple
45 e glycoprotein and its specific receptor for avian sarcoma leukosis virus subgroup A or B) system all
47 on proteins of human immunodeficiency virus, avian sarcoma leukosis virus, and influenza virus was in
48 ndogenous avian virus (EAV) family or to the avian sarcoma-leukosis virus (ALV)-related subgroup E en
49 al substrate sequence of 5'-ACGACAACA-3' for avian sarcoma-leukosis virus (ASLV) and 5'-AACA(A/C)AGCA
50 zed the placement of sites of integration of avian sarcoma-leukosis virus (ASLV) and human immunodefi
52 te that retroviral infection mediated by the avian sarcoma-leukosis virus (ASLV-A) envelope glycoprot
53 n leukosis virus RCAS (replication-competent avian sarcoma-leukosis virus LTR splice acceptor)-mediat
54 ratory described selection from a subgroup B avian sarcoma-leukosis virus of an extended-host-range v
55 deficiency virus, murine leukemia virus, and avian sarcoma-leukosis virus, and found that a statistic
56 to test this model for the avian retrovirus avian sarcoma/leukosis virus (ASLV) and the filovirus eb
57 envelope glycoprotein (Env) of the oncovirus avian sarcoma/leukosis virus (ASLV) contains an internal
61 ous attempts to extend the host range of the avian sarcoma/leukosis virus (ASLV)-based RCASBP vectors
62 integration reaction was found for HIV-1 and avian sarcoma/leukosis virus but not murine leukemia vir
64 wed that the envelope glycoprotein (EnvA) of avian sarcoma/leukosis virus subtype A (ASLV-A) binds to
65 flanking the internal fusion peptide of the avian sarcoma/leukosis virus subtype A (ASLV-A) Env (Env
67 m amphotropic murine leukemia virus (A-MLV), avian sarcoma/leukosis virus type A (ASLV-A), and influe
68 P-M2C is a retroviral vector derived from an avian sarcoma/leukosis virus which has been modified so
69 characterized two new replication-competent avian sarcoma/leukosis virus-based retroviral vectors wi
72 (MYC) through the direct activation of v-src avian sarcoma viral oncogene homolog (SRC) and suppressi
73 etected independently of catalysis with both avian sarcoma virus (ASV) and human immunodeficiency vir
74 es of the core domain of integrase (IN) from avian sarcoma virus (ASV) and its active-site derivative
76 human immunodeficiency virus type 1 (HIV-1), avian sarcoma virus (ASV) and their close orthologs from
80 of E3 ubiquitin ligases bind the L domain in avian sarcoma virus (ASV) Gag and facilitate viral parti
82 nt of HIV-1, simian sarcoma virus (SIV), and avian sarcoma virus (ASV) INs predicted which of these r
83 in Daxx was identified as an interactor with avian sarcoma virus (ASV) integrase (IN) in a yeast two-
84 determined the size and shape of full-length avian sarcoma virus (ASV) integrase (IN) monomers and di
85 (aa) in the C-terminal region of the 286-aa avian sarcoma virus (ASV) integrase (IN) protein has bee
89 s comparable to one previously described for avian sarcoma virus (ASV) that was stimulated by the pre
90 the integrase protein of an oncoretrovirus, avian sarcoma virus (ASV), suggesting an active import m
91 netic repression and silencing of integrated avian sarcoma virus (ASV)-based vector DNAs in human HeL
95 ne is a cell-derived insert in the genome of avian sarcoma virus 31 (ASV 31) and functions as the onc
97 hly preferred in vitro integration sites for avian sarcoma virus and human immunodeficiency virus-1 i
98 tion as seen in the integrase core domain of avian sarcoma virus as well as human immunodeficiency vi
99 of integration catalyzed by HIV-1 to that of avian sarcoma virus by analyzing the effect of defined m
100 f chicken embryos with replication-competent avian sarcoma virus expressing either FgfR2(C278F), a re
101 es have indicated that in the context of the avian sarcoma virus genome, precise deletion of both ASV
102 m permanganate modification to show that the avian sarcoma virus IN catalytic domain is able to disto
103 he metal preference for in vitro activity of avian sarcoma virus IN is Mn2+ > Mg2+ and that a single
104 at the putative dimer-dimer interface of the avian sarcoma virus IN with its analogue, loop188-194, f
105 ar strategy, the unique amino acids found in avian sarcoma virus IN, rather than HIV-1 or Mason-Pfize
107 phic studies of the catalytic core domain of avian sarcoma virus integrase (ASV IN) have provided the
108 itor complex of the catalytic core domain of avian sarcoma virus integrase (ASV IN) were solved at 1.
109 of human immunodeficiency virus-1 integrase, avian sarcoma virus integrase, and bacteriophage Mu tran
113 in human (HeLa) cells, mediated by either an avian sarcoma virus or a human immune deficiency virus t
114 lected were substrates of HIV protease or of avian sarcoma virus protease, both of which have been re
115 t reduction in the total amount of HIV-1 and avian sarcoma virus retroviral vector DNA that is joined
118 n embryo fibroblasts (CEF) infected with the avian sarcoma virus UR2, encoding the oncogenic receptor
120 d HeLa cell populations that harbored silent avian sarcoma virus-based green fluorescent protein (GFP
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