ライフサイエンスコーパス: retroviral infection

1 dead-end circular products that arise during retroviral infection.

2 on and in imposing innate resistance against retroviral infection.

3 rip1-/- murine embryonic fibroblast cells by retroviral infection.

4 HR repair pathway per se does not influence retroviral infection.

5 issues and are independently able to inhibit retroviral infection.

6 kaged into virions and confers resistance to retroviral infection.

7 cells expressing a series of HER2 levels by retroviral infection.

8 d as a host protein conferring resistance to retroviral infection.

9 ty is separable from the ability to restrict retroviral infection.

10 ction factors that confer host resistance to retroviral infection.

11 study the impact of inflammatory pathways on retroviral infection.

12 ta represents a new model of proinflammatory retroviral infection.

13 ) were expressed in lens primary cultures by retroviral infection.

14 factors are host cell proteins that inhibit retroviral infection.

15 continuous HAART for the early treatment of retroviral infection.

16 orm important components of host defenses to retroviral infection.

17 arcinoma cell lines by both transfection and retroviral infection.

18 immune response in controlling a persistent retroviral infection.

19 e is generated during the course of a normal retroviral infection.

20 nctions associated with enzyme synthesis and retroviral infection.

21 ndary event, irrespective of the presence of retroviral infection.

22 generated using either DNA microinjection or retroviral infection.

23 r, we found that this does not hold true for retroviral infection.

24 ulates the innate immune response to DNA and retroviral infection.

25 ific CD8(+) T cells in a naturally contained retroviral infection.

26 oes not readily occur, with the exception of retroviral infection.

27 tralizing antibodies (Abs) to the control of retroviral infection.

28 ivo by innate sensing of the early stages of retroviral infection.

29 es are essential for full protection against retroviral infection.

30 be actively involved in host defense against retroviral infection.

31 nt of the cellular innate immune response to retroviral infection.

32 ne deaminases provides intrinsic immunity to retroviral infection.

33 ecific cytidine deaminases that can restrict retroviral infection.

34 ral capsid, thus potentiating restriction of retroviral infection.

35 ave developed diverse strategies to restrict retroviral infection.

36 le, into a lymphoid progenitor population by retroviral infection.

37 necessary for TRIM5-mediated restriction of retroviral infection.

38 ns XPB and XPD in a cellular defense against retroviral infection.

39 tural determinant of cellular sensitivity to retroviral infection.

40 ity facilitates chemotherapeutic efficacy in retroviral infections.

41 efficient antiviral response and to control retroviral infections.

42 the observed sequence diversity in untreated retroviral infections.

43 brates are the proviral remnants of previous retroviral infections.

44 ich the immune system can control persistent retroviral infections.

45 roviding deeper insight into pathogenesis of retroviral infections.

46 has not been extensively explored in murine retroviral infections.

47 eins have evolved as innate defenses against retroviral infections.

48 ave profound effects on the pathogenicity of retroviral infections.

49 herapeutic approaches to the cure of chronic retroviral infections.

50 e deaminases which help defend cells against retroviral infections.

51 ion that might extend to HIV and other human retroviral infections.

52 proteins that provide intrinsic immunity to retroviral infections.

53 us retroviruses (ERVs), derived from ancient retroviral infections.

54 l responses for effective protection against retroviral infections.

55 ue disorders; viral, spirochete, fungal, and retroviral infection; (2) Paraneoplastic disorders; (3)

56 cells overcomes their natural block to avian retroviral infection; 815 bp of human GPIIb regulatory s

57 re known to undergo apoptosis in response to retroviral infection, a response that we show requires r

58 BP-associated factor plays a central role in retroviral infection and cancer development, and the C-t

59 ritical to many disease processes, including retroviral infection and carcinogenesis, and to gene the

60 tibody responses essential for recovery from retroviral infection and highlight APOBEC3-mediated deam

61 disease that results from an interaction of retroviral infection and immune activation.

62 has been described as a potent inhibitor of retroviral infection and retrotransposition.

63 E6 was introduced into C127 cells (PBE6) by retroviral infection and stable clones were isolated.

64 ature indicates an irreversible component to retroviral infection and suggests the utility of CD anti

65 protein levels are increased in response to retroviral infection and that Daxx acts at the time of i

66 ecretion is a powerful positive regulator of retroviral infection and that FMLV-IL-1beta represents a

67 se myeloid cells, which serve as targets for retroviral infection and transformation, as evidenced by

68 roviral "fossils" represent a record of past retroviral infections and forms.

69 uman genome, but all are remnants of ancient retroviral infections and harbor inactivating mutations

70 grated viral DNA is a common feature of many retroviral infections and is thought to play a role in p

71 represent novel therapeutic agents to treat retroviral infections and neurodegenerative disease.

72 tors that may hold promise as treatments for retroviral infections and neurodegenerative disease.

73 persistence and pathogenesis of both natural retroviral infections and retroviral gene therapy vector

74 ses (ERVs) represent genomic fossils of past retroviral infections and, thus, can inform us on the di

75 antiretroviral therapies, assess the risk of retroviral infection, and generate effective antiretrovi

76 ns are the rule rather than the exception in retroviral infection, and the ability to examine them in

77 iversification of Ig genes and inhibition of retroviral infection, and thus, it would appear to be vi

78 retroviruses (ERVs) are remnants of ancient retroviral infections, and comprise nearly 8% of the hum

79 We propose that cellular restrictions to retroviral infections are themselves cell cycle dependen

80 esent a new therapeutic avenue to fight this retroviral infection, as it reestablishes the Th1/Th2 ba

81 t these regions pharmacologically to inhibit retroviral infection at additional stages.

82 ly when Hlx was introduced into the cells by retroviral infection at an early time point that led to

83 ression of mutant H-ras (by scrapeloading or retroviral infection) at levels which stimulated prolife

84 CypA fusion protein (TRIMCyp) that restricts retroviral infection based on the retroviral capsid-bind

85 eriods during which primates were exposed to retroviral infections, based on the appearance of partic

86 that PARP-1 cannot be strictly required for retroviral infection because replication steps, includin

87 rface proteoglycans on T cells contribute to retroviral infection, binding of chemokines and other pr

88 ributable to general effects associated with retroviral infection but rather is a specific consequenc

89 g in the mouse that is strongly activated in retroviral infection but weakly in nematode infection.

90 thought to be an innate immunity barrier to retroviral infection, but the mechanistic features of th

91 horylated on residue T592 is unable to block retroviral infection, but this modification does not aff

92 newly described form of innate resistance to retroviral infection by catalyzing the deamination of de

93 uman proteins APOBEC3F and APOBEC3G restrict retroviral infection by deaminating cytosine residues in

94 ols, we developed a murine model for in vivo retroviral infection by direct intrafemoral injection (D

95 TRIM5alpha inhibits retroviral infection by promoting the abortive disassemb

96 Instead, the mechanism of attenuation of retroviral infection by RAD52 appears to be based upon c

97 Thus, TRIM5alpha restricts retroviral infection by specifically recognizing the cap

98 on factors that protect mammalian cells from retroviral infections by binding incoming viral capsids,

99 proteins are restriction factors that block retroviral infections by binding viral capsids and preve

100 suggest that very early treatment following retroviral infection can have a significant effect on mo

101 s increased in these tumors, indicating that retroviral infection can induce expression of oncogenic

102 nly a subset of cells with a Cre history for retroviral infection, clones with a gene expression hist

103 Retroviral infection could be initiated by electroporati

104 FN11 has no effect on the early steps of the retroviral infection cycle, including reverse transcript

105 s by NEM blocks early postentry steps in the retroviral infection cycle, virus preparations with modi

106 mmunodeficiency virus type 1 (HIV-1)-related retroviral infections dating from 1959 have stirred inte

107 TRIM5alpha restricts retroviral infection early after viral entry, before the

108 Recent innovations in retroviral infection efficiency and expression control h

109 Retroviral infection experiments showed that expression

110 During retroviral infection, FBP1 binds to and mediates replica

111 Mixed retroviral infections frequently exhibit pseudotyping, i

112 ular myocardial wall in the quail embryo via retroviral infection from E2-2.5, thus abolishing the tr

113 ugh the susceptibility of murine EC cells to retroviral infection has been extensively analyzed, few

114 nctioning as another innate immunity against retroviral infection, has been identified.

115 For millions of years, retroviral infections have challenged vertebrates, occas

116 HGF can render stem cells viable targets for retroviral infection, HGFs can promote differentiation,

117 thogenesis of cardiac injury associated with retroviral infection in a relevant nonhuman primate mode

118 amined the ability of TRIM5alpha to restrict retroviral infection in cells depleted of the autophagic

119 y with enhanced green fluorescent protein by retroviral infection in developing and committed Th2 cel

120 Therefore, we reintroduced (PTEN) by retroviral infection in MDA-468 cells.

121 cate that the diverse TRIM5 proteins inhibit retroviral infection in multiple ways and that inhibitio

122 nt, we ectopically expressed mouse Lats2 via retroviral infection in NIH3T3/v-ras cells to examine wh

123 w further analyzed the basis of the block to retroviral infection in the R3-2 line.

124 eted gp70 SU may contribute to resistance to retroviral infection in these mice.

125 RNAi can block retroviral infection in vertebrates.

126 Here we show that A3 functions during retroviral infection in vivo and provides partial protec

127 that chemokine induction also occurs during retroviral infection in vivo.

128 RIM5alpha provides intrinsic defense against retroviral infections in mammalian cells.

129 ogenous retroviruses (ERVs), the remnants of retroviral infections in the germ line, occupy ~8% and ~

130 ident within 5-10 population doublings after retroviral infection, indicating a direct effect of T ex

131 pression of WT1 in NIH 3T3 fibroblasts after retroviral infection induced murine E-cadherin expressio

132 It was shown recently that retroviral infection induces integrase-dependent apoptos

133 Retroviral infection induces integrase-dependent apoptos

134 domain proteins that have been implicated in retroviral infection, inflammation pathways, and cancer

135 e p53 expression vector by microinjection or retroviral infection into primary normal human fibroblas

136 We have used retroviral infection into the SVZ of mice to label adult

137 Retroviral infection involves continued genetic variatio

138 This innate mechanism of resistance to retroviral infection is counteracted by the HIV-1 viral

139 Susceptibility to retroviral infection is determined, in part, by host gen

140 s reviewed and their role in protection from retroviral infection is discussed.

141 l and cell-mediated responses in restraining retroviral infection is not well understood.

142 munological role played by CD4(+) T cells in retroviral infections is poorly defined.

143 In FeLV infections, as in other retroviral infections, it is less clear how virus varian

144 vinca alkaloid vincristine (HL60 RV+) or by retroviral infection (K562/human MDR 1 cells) exhibited

145 ion of WT-p53 into AFP-positive HCC cells by retroviral infection markedly inhibited their clonal gro

146 HIV transmission, and treatment during acute retroviral infection may attenuate HIV disease.

147 infection and indicate that protection from retroviral infection may be achievable.

148 malignant epithelial cells, suggesting that retroviral infection may be directly linked to tumorigen

149 Here, we demonstrate that retroviral infection mediated by the avian sarcoma-leuko

150 monstrated that the murine AIDS model (LPBM5 retroviral infection) mimics human immunodeficiency viru

151 Retroviral infection of an antisense TRX cDNA suppressed

152 These results suggest that direct human retroviral infection of CD4(+)CD25(+) T cells may be ass

153 In this study we have demonstrated that retroviral infection of CD4+ lymphocytes from either aut

154 Ihh since ectopic expression of Ihh by RCAS retroviral infection of chicken embryo hindlimbs restore

155 nt beta-globin gene status can be rescued by retroviral infection of EKLF, we demonstrate the importa

156 Retroviral infection of immature granule cells with a do

157 Retroviral infection of mixed cultures of cortical neuro

158 Overexpression of wild type Six3 by in vivo retroviral infection of newborn rat retinae led to an al

159 put selection of the libraries via iterative retroviral infection of nondividing cells led to the ide

160 Furthermore, retroviral infection of NPM/ALK+ BaF3 cells with a domin

161 Retroviral infection of NPM/ALK+ cells with a dominant-n

162 ed whether abrogation of NK-TR expression by retroviral infection of primary human or mouse NK cells

163 Knockdown of ERK5 by retroviral infection of shRNA attenuates prolactin-stimu

164 er, function as restriction factors to block retroviral infection of target cells.

165 e mock-transfected cells was accomplished by retroviral infection of the cells with a bcl-xL sense cD

166 Stable retroviral infection of the ZIP8 cDNA in mouse fetal fib

167 ly deficient in PLC-gamma1 (Null cells), and retroviral infection of those cells was used to derive P

168 Avian retroviral infection of unfractionated bone marrow from

169 roviruses (ERVs) are the remnants of ancient retroviral infections of germ cells and have been mainta

170 Selecting the library via iterative retroviral infections of mammalian cells led to the iden

171 related to exogenous retroviruses, represent retroviral infections of the deep past, and their abunda

172 oviruses (HERVs), which are remnants of past retroviral infections of the germline cells of our ances

173 Early events during retroviral infection play a critical role in determining

174 for the build-up of extracellular matrices, retroviral infection, protein modification, and steroid

175 Using a single-step retroviral infection protocol, either wild-type or mutan

176 e requirements for control or elimination of retroviral infection remains an important aim.

177 As retroviral infection requires integrase-catalyzed DNA st

178 sion of PrP in PrP-null bone marrow cells by retroviral infection rescued the defective hematopoietic

179 y active chimeric DDR2 in DDR2(-/-) cells by retroviral infection restored cell proliferation, migrat

180 uction of CIITA into primary CD4 T cells via retroviral infection resulted in a reduction in the leve

181 Unlike retroviral infection, SB transposition can be controlled

182 Neonatal retroviral infection substantially reduced length of sur

183 icularly in non-dividing cells, can restrict retroviral infections such as HIV and simian immunodefic

184 v1 and TRIM5alpha provide dominant blocks to retroviral infection, targeting incoming capsids at a po

185 ovel mechanism for the resistance of mice to retroviral infection that could lead to a better underst

186 gs reveal a novel mechanism of resistance to retroviral infection that is based on a robust and susta

187 mune system is able to combat the underlying retroviral infection, the accumulation and widespread ac

188 g bridge protein can also function to target retroviral infection, the TVA-VEGF110 bridge protein was

189 ing rapid TLR7-dependent inhibition of early retroviral infection through nonneutralizing IgM and IL-

190 asive behavior we have used transfection and retroviral infection to create a panel of epithelial cel

191 The successful adaptation of retroviral infection to hematopoietic stem cells require

192 rfaces, suggesting an approach for targeting retroviral infection to specific cell types.

193 ic expression of either Pitx2c or Pitx2a via retroviral infection to the right LMP equally randomized

194 tion to serving as a block for cross-species retroviral infection, TRIM5 was recently shown to play a

195 We evaluated the function of PARP-1 in retroviral infection using the chicken B lymphoblastoid

196 bx1, a genetic screen consisting of neonatal retroviral infection was used to identify genes that acc

197 The potential to establish dual retroviral infections was investigated in this study.

198 By retroviral infection, we constitutively expressed an EGF

199 Using retroviral infection, we demonstrate that levels of FRNK

200 Using high titer retroviral infection, we demonstrate that WT1 triggers r

201 To identify cellular processes involved in retroviral infection, we employed a high-volume forward

202 ovarian surface epithelial cell line T80 and retroviral infection, we generated cell lines that const

203 fold increase in VEGF expression mediated by retroviral infection with constructs encoding either VEG

204 immortal, and occurred within one passage of retroviral infection with vectors expressing HPV-16 E6.

205 S9 cells were obtained by retroviral infection with virions containing a tetracycl

206 A4 cells were obtained by retroviral infection with virions containing a tetracycl

207 reconstitution in TGFBI(-/-) cells by either retroviral infection with WT TGFBI gene or supplement wi

208 Retroviral infections with FBR v-fos and G2A-R transform

209 ion modulates the ability of SAMHD1 to block retroviral infection without affecting its ability to de

210 ed the abilities of the proteins to restrict retroviral infection without affecting trimerization or