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1 early RNA phenotype of Eg101 was restored in BHK cells.
2 idly than did rM51R-M virus in both HeLa and BHK cells.
3 ptosis more slowly than did rM51R-M virus in BHK cells.
4 that can establish persistent replication in BHK cells.
5  SFT, we studied this human factor in rodent BHK cells.
6  muscle thick filament proteins expressed in BHK cells.
7 ectious virus or to support recombination in BHK cells.
8 n activity in ts13 cells but not in parental BHK cells.
9 uantitatively eliminated in SFVRz-transduced BHK cells.
10 arge, turbid-plaque virus that only grows in BHK cells.
11 r gene in both infection and transfection of BHK cells.
12 ding to heparin and increased replication in BHK cells.
13 ndogenous and overexpressed CFTR in HT29 and BHK cells.
14 along with the 70 kDa E211Q-mutated ABCG2 in BHK cells.
15         Phorbol esters are without effect in BHK cells.
16 ut only approximately 3-fold less in hamster BHK cells.
17 use will inspire similar research in CHO and BHK cells.
18 RC1 mutants Cys(132)/Ser and Cys(135)/Ser in BHK cells.
19 , but enhanced binding was only detected for BHK cells.
20 2.9-fold more functional r-hFIX than control BHK cells.
21 t M protein delays apoptosis in VSV-infected BHK cells.
22 complex is indeed detectable in VSV-infected BHK cells.
23  classes of Aura virus particles produced in BHK cells.
24 L-(N-Pmut)] complex in both insect cells and BHK cells.
25 roblastoma cell line (N18), but similarly in BHK cells.
26 er than mitochondria in baby hamster kidney (BHK) cells.
27 us life cycle in neural (N18) and nonneural (BHK) cells.
28 d in stably transfected baby hamster kidney (BHK) cells.
29  cycles was examined in baby hamster kidney (BHK) cells.
30 helper RNA (DH-BB) into baby hamster kidney (BHK) cells.
31 y VEGF was performed in baby hamster kidney (BHK) cells.
32  virus is propagated in baby hamster kidney (BHK) cells.
33 exhibited growth restriction in MDBK but not BHK cells, a slower induction of apoptosis, and lower vi
34 llowing transfection of baby hamster kidney (BHK) cells, a recombinant TGEV (TGEV-GFP2) was isolated
35 ariants with distinct plaque morphologies on BHK cells: a small, clear-plaque virus that replicates i
36                                 In one case, BHK cell adaptation resulted in a 238-nucleotide deletio
37 The high transfection efficiency seen in the BHK cells allows studies of the viral replication in the
38                         Baby hamster kidney (BHK) cells also produced viral capsid proteins when tran
39 apid coselection of high-affinity binding to BHK cells and attachment to heparin-agarose beads.
40 r deprivation of growth factors, both normal BHK cells and BHK cells expressing mutant PLA(2) underwe
41  the catalytic center) were transfected into BHK cells and cells stably expressing these constructs w
42 pable of persistent, noncytopathic growth in BHK cells and describe here a new generation of Sindbis
43 man TPO (332 residues) has been expressed in BHK cells and purified to homogeneity using conventional
44 al, and His1961Asp, were stably expressed in BHK cells and purified.
45 ein contributes to induction of apoptosis in BHK cells and that wt M protein acts to delay induction
46 of nonpermissive Syrian baby hamster kidney (BHK) cells and decreasing concentrations of permissive m
47 dly in the cytoplasm of baby hamster kidney (BHK) cells and expressed large quantities of antigenical
48 sly established line of baby hamster kidney (BHK) cells and three new lines of human embryonic kidney
49 of the wild-type (WT) A24 Cruzeiro strain in BHK cells, and both high- and low-fidelity variants reta
50 aired in their ability to produce plaques in BHK cells, and had a reduced capacity to cause host cell
51 uman astrovirus serotype 1 were expressed in BHK cells, and nsP1a-derived processing products were im
52 indbis virus (SIN) variants were isolated in BHK cells, and the mutations responsible were mapped to
53 ccessfully expressed in baby hamster kidney (BHK) cells, and the presence of the eukaryotic secretion
54 this study as it applies to SIN infection of BHK cells are as follows: i) the classical 19-nt 3'CSE o
55  fail to recognize expressed proteins unless BHK cells are solubilized with detergents.
56 esulting from propagation of the virus using BHK cells, as viruses propagated on Vero, C8161 (a human
57 le both viruses infected essentially 100% of BHK cells at an MOI of 5.
58                                              BHK cells bind neither XMRV nor GALV envelope proteins.
59   Both viruses induced apoptosis in cultured BHK cells but not in the cells of the adult mouse brain.
60         VWF Cys1149Arg was not secreted from BHK cells but was degraded intracellularly within about
61 ted virus that grows in baby hamster kidney (BHK) cells but cannot grow at all in mouse L-929 cells.
62 ed with recombinant fibrinogen purified from BHK cells, but did not adhere to wells coated with a pur
63 ormation on and binding of mutant viruses to BHK cells by >95%.
64  ClC-3 in the early endosomal compartment of BHK cells; by fluorescence ratio imaging of endocytosed
65                                              BHK cells can be infected by NZB-XMV(New Zealand Black m
66                          Addition of VEGF to BHK cells caused a time and dose-related upregulation of
67                                           In BHK cells co-transfected with guanylate cyclase and G-ki
68 imately 10-fold decrease in virus yield from BHK cells compared to the TE12 amount.
69 on, we measured whole-cell Cl(-) currents in BHK cells cotransfected with GPCRs and CFTR.
70 se was purified from recombinant carboxylase BHK cells cultured in the presence or absence of vitamin
71  was observed with carboxylase isolated from BHK cells cultured in vitamin K, and 3 mol gla/mol carbo
72 ultiplicity-of-infection passage of TR339 on BHK cell cultures resulted in rapid coselection of high-
73 gglutinin-tagged wild type RSK2 (HA-RSK2) in BHK cell cytosol.
74 ion production or SINV-induced cell death in BHK cells deficient in IFN production (and thus IFN sign
75 r IX (r-hFIX)-producing baby hamster kidney (BHK) cells, engineered to stably overexpress various com
76 ells, which cleave PE2 more efficiently than BHK cells, exhibited a reduction in cell attachment effi
77 terestingly, membrane vesicles prepared from BHK cells expressing both YFP/ABCG2 and E211Q-mutated AB
78 ed strongly CFTR-mediated iodide efflux from BHK cells expressing G551D-CFTR.
79 rental MHV strain A59 failed to replicate in BHK cells expressing human Bgp or CEA.
80                                           In BHK cells expressing M1 receptors, a muscarinic agonist
81 ecombinant viruses replicated efficiently in BHK cells expressing mCEACAM1(a).
82                                           In BHK cells expressing mCEACAM1(b), only viruses expressin
83 te having the MHV-4 RBD, S(4)R replicated in BHK cells expressing mCEACAM1(b); this is most probably
84 of growth factors, both normal BHK cells and BHK cells expressing mutant PLA(2) underwent massive apo
85                                              BHK cells expressing the appropriate receptors bind XMRV
86 nt PLA(2) underwent massive apoptosis, while BHK cells expressing wt PLA(2) showed considerable resis
87     Although membrane vesicles prepared from BHK cells expressing YFP/ABCG2 exert higher ATPase activ
88 th mobilities identical to those detected in BHK cell extracts with the WNV (-)3' SL RNA were found i
89 E replicons (VRP-NV2), but upon infection of BHK cells failed to confer VLP self-assembly.
90                In contrast, recipients of wt BHK cells failed to display any effects on kindling deve
91                The mutant FF391/392 grown in BHK cells formed virus particles containing extruded mat
92                                    Unlike in BHK cells, however, overexpressed ZAP exhibited antivira
93 r kidney cells (BHK) and adenosine releasing BHK cell implants (BHK-AK2), which were previously shown
94 adherin did not stimulate differentiation of BHK cells in monolayer cultures.
95                            Growth of N18 and BHK cells in sodium chlorate to eliminate all sulfation
96                  The results suggest that in BHK cells in the presence of bafilomycin A(1), virus RNA
97                            Cotransfection of BHK cells in vitro with the H(C)-replicon and two helper
98       Analysis of factor IX (fIX)-expressing BHK cells indicated that slow egress of fIX from the end
99  with rM51R-M virus and delayed apoptosis in BHK cells infected with rM51R-M virus, similar to the ef
100                                     Thus, in BHK cells, inhibition of cell growth by cGMP analogs is
101 rrin receptor (sTFR) by baby hamster kidney (BHK) cells is described, and the effect of glycosylation
102 hen full-length human Nup153 is expressed in BHK cells, it accumulates appropriately at the nucleopla
103 ause CVS-B2c can be reproducibly selected in BHK cells, it is likely to be a conserved minor subpopul
104                 These findings indicate that BHK cells lack a factor that is required for infection b
105 brary by complementation of a zinc-sensitive BHK cell line.
106     NCX3 was also expressed in the mammalian BHK cell line.
107 oned and expressed in normally nonpermissive BHK cell lines by using noncytopathic Sindbis virus repl
108                                  We obtained BHK cell lines expressing low levels of SATB1 by stable
109        We analyzed carboxylation in 293- and BHK cell lines expressing r-factor IX (fIX) and endogeno
110  replaced with either Ala or Val, and stable BHK cell lines expressing the B-domainless proteins were
111                                       Stable BHK cell lines inducibly expressing wild-type or dominan
112                                          All BHK cell lines secreted r-hFIX into serum-free medium.
113                          In both HEK 293 and BHK cell lines, expression of human hPIP5Ibeta kinase si
114 opus laevis oocytes and imaging of mammalian BHK cells loaded with Ca(2+)-sensitive dyes.
115 e of mutant virus protein in the transfected BHK cell lysate.
116                     Virus plaque purified on BHK cells (MHV/BHK) grew more slowly in murine cells tha
117 emia virus significantly allows infection of BHK cells not otherwise susceptible to infection with na
118  promising but had an EC(50) against DENV in BHK cells of 6.5 muM, which limited its use in in vivo.
119 endent fusion by L289A-F is not exhibited in BHK cells or in several other cell lines.
120 ut repeated passaging of the H230A mutant in BHK cells produced a second-site compensatory mutant (V2
121  from endogenous NO since we found that: (i) BHK cells produced high amounts of NO; (ii) CAT activity
122                                         Four BHK cell proteins with molecular masses of 108, 60, 50,
123                                           In BHK cells, recombinant viruses 633 (E255Q) and TE (E255H
124                                              BHK cells remain resistant to xenotropic murine retrovir
125                                        Using BHK cells, removal of extracellular potassium (K(+)) cau
126 blish nonlytic persistent infections (PI) of BHK cells, replicons derived from Sindbis (SIN) and Seml
127   Transfection of this plasmid into cultured BHK cells resulted in prolonged, autonomous FHV RNA repl
128     Transfection of these two fragments into BHK cells resulted in vivo RNA-RNA recombination and rel
129 4 (where CVS is challenge virus standard) in BHK cells results in the rapid selection of a dominant v
130                                           In BHK cells, SFV4 and SFV-RDR replicate to high titers, bu
131                                           In BHK cells, six different striated myosin heavy chain iso
132 g membranes from cell lines expressing ssts [BHK cells (sst4) and HEK 293 cells (sst2)] utilizing [12
133  Expression of the DPP4s of these species on BHK cells supported MERS-CoV replication.
134 ing the five human DPP4 amino acids rendered BHK cells susceptible to MERS-CoV, whereas expression of
135 generates anti-apoptotic survival signals in BHK cells targeting the secretory pathway, and suggests
136 plication in avian cells also grew better in BHK cells than the wild-type virus, whereas the remainin
137             Selection for zinc resistance in BHK cells that cannot synthesize either MT or ZnT1 is in
138 ealed numerous viable and mitotically active BHK cells that continued to secrete hCNTF.
139                            However, parental BHK cells that grow in high concentrations (>500 microM)
140                                              BHK cells that lack an active ABCA1 pathway markedly inc
141 ion of the Znt1 gene in baby hamster kidney (BHK) cells that do not express their Mt genes results in
142 ed on vesicles and allows the zinc-sensitive BHK cells to accumulate zinc to levels that are much hig
143 to mediate resistance of receptor-expressing BHK cells to GALV or XMRV, as shown by tunicamycin treat
144                         After 13 passages on BHK cells to produce a vaccine, a Cathay topotype isolat
145 er gene under control of the fos promoter in BHK cells transfected with an empty vector or in cells t
146                                           In BHK cells transfected with expression vectors for guanyl
147                                              BHK cells transfected with synthetic RNAs containing sub
148                                     However, BHK cells transfected with synthetic RNAs encoding Phe a
149                       Electron microscopy of BHK cells transfected with these mutants revealed assemb
150                                              BHK cells transfected with this plasmid produced virus,
151 f these pseudorevertant viral populations in BHK cells under competitive conditions yielded evolved,
152 treated cells was compared to virus grown in BHK cells under standard conditions.
153  virus, TR339, bound to baby hamster kidney (BHK) cells very poorly.
154 n type I interferon (IFN) response-deficient BHK cells, W956IC infection produces higher levels of "u
155                The mutant KK391/392 grown in BHK cells was defective in the final membrane fission re
156        Binding of TE and 633 to N18, but not BHK, cells was dependent on the medium used for virus bi
157                                         When BHK cells were analyzed by immunocytochemistry, BAP31 di
158                                         When BHK cells were cultured as three-dimensional aggregates,
159                                              BHK cells were either cotransfected with TGEV-Rep(AvrII)
160                             SFVRz-transduced BHK cells were found to produce large amounts of genomic
161  and MHV-H2) which replicated efficiently in BHK cells were isolated.
162                                      HeLa or BHK cells were transfected with M mRNA to determine whet
163                         Baby hamster kidney (BHK) cells were stably transfected with a human endostat
164                     PS1 was also detected in BHK cells, where it was also intracellular and colocaliz
165 nd MT genes contribute to zinc resistance in BHK cells, whereas ZnT1 plays a larger role in regulatin
166 The effects of 2 and 3 were also examined in BHK cells which expressed either mGluR1a or mGluR5a rece
167 to produce hGDNF (BHK-hGDNF) or encapsulated BHK cells which were not modified to produce hGDNF (BHK-
168                   Using baby hamster kidney (BHK) cells, which are deficient in cGMP-dependent protei
169                 We used baby hamster kidney (BHK) cells, which have very low soluble guanylate cyclas
170 ynthesis was similar in 633- and TE-infected BHK cells, while in N18 cells, structural protein synthe
171 ignificant inhibition of virus adsorption to BHK cells, while soluble alphaVbeta3 caused a low (20 to
172                              Transfection of BHK cells with RlucRep RNA yielded two distinctive Rluc
173                                 Third, using BHK cells with stable NCX1 expression, we increased PIP(
174                  Following cotransfection of BHK cells with the replicon RNAs carrying gfp, GFP expre
175 d-anchored probes revealed that treatment of BHK cells with therapeutic levels of indomethacin enhanc
176 atitis virus (VSV) as a model, we coinfected BHK cells with VSV DIPs and recombinant helper virus car
177 ion assays performed in baby hamster kidney (BHK) cells with BETA2 and E47, but not USF.
178       Upon infection of baby hamster kidney (BHK) cells with VEE replicon particles (VRPs), the Norwa
179  E1s generation was strongly pH dependent in BHK cells, with optimal cleavage at a pH of < or =7.0, c
180 n production and virus-induced cell death in BHK cells, ZAP inhibited translation of the incoming vir

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