ライフサイエンスコーパス: M-MuLV

1 M-MuLV IN exhibited greater activity with the heterologo

2 M-MuLV normally induces T-lymphoid tumors in all infecte

3 M-MuLV nucleocapsid protein increases the rates of RNA a

4 M-MuLV-induced tumors were screened for expression of th

5 an RNA 5' end recessed by 1 (HIV-1) or 2-3 (M-MuLV) bases on a longer DNA could accommodate both typ

6 An M-MuLV IN mutant without the HHCC domain (Ndelta105) cat

7 a cleavage site recognized by both HIV-1 and M-MuLV enzymes was introduced into a sequence that was o

8 otide positions -1 and +1) for the HIV-1 and M-MuLV enzymes were introduced into model hybrid substra

9 -processing activities of HIV-1, HTLV-2, and M-MuLV integrases (INs) with their corresponding U5 end

10 oculation, immunohistochemistry with an anti-M-MuLV CA antibody was performed.

11 magenesis identified for other MuLVs such as M-MuLV and SL3-3 MuLV.

12 Previous comparative studies between M-MuLV and an enhancer variant, Mo+PyF101 MuLV, suggeste

13 In both M-MuLV and HIV-1 IN, regions are identified which functi

14 l/NF-kappaB transcription factor activity by M-MuLV infection may prove relevant to the mechanism of

15 Reactions catalyzed by M-MuLV IN were additionally influenced by upstream regio

16 studies, we show that infection of cells by M-MuLV activates expression of Rel family transcription

17 the crossbone substrate were coordinated by M-MuLV IN, indicating a reliance on both LTR and target

18 on between the polytropic MuLVs generated by M-MuLV and other ecotropic MuLVs is the result of recomb

19 t sheath (ORS), were extensively infected by M-MuLV after s.c. inoculation.

20 ine the nature of the cell types infected by M-MuLV and Mo+PyF101 M-MuLV in the skin after a s.c. ino

21 Virus encoding the C209A M-MuLV IN mutation exhibited delayed virion production a

22 Double-positive (DP; CD4(+) CD8(+)) M-MuLV-induced tumor cells fell into two categories: tho

23 ction in vivo, since a replication defective M-MuLV-based vector expressing beta-galactosidase also i

24 ice with a helper-free replication-defective M-MuLV-based retroviral vector was carried out.

25 fection composed of the inoculated ecotropic M-MuLV and polytropic MuLVs generated by recombination o

26 g the first 28 amino acids (aa) of ecotropic M-MuLV resulted in Env expression and binding to the rec

27 crease in thymocytes that released ecotropic M-MuLV packaged within polytropic virions was also obser

28 The C and D elements, encompassing M-MuLV viral nucleotides 310 to 374, facilitate encapsid

29 suggests that unlike the other INs examined, M-MuLV IN has evolved with an IN-LTR interaction that is

30 introduced into BALB/c-3T3 cells expressing M-MuLV or cotransfected into BALB/c-3T3 cells with a vec

31 itions -14 to +1 for HIV-1 and -11 to +1 for M-MuLV.

32 for HIV-1 and positions -4, -9, and -11 for M-MuLV had more modest effects.

33 r HIV-1 and positions +1, -2, -6, and -7 for M-MuLV significantly affected RNase H cleavage efficienc

34 r HIV-1 and positions +1, -2, -6, and -7 for M-MuLV.

35 rked decrease in thymic size is apparent for M-MuLV-inoculated mice in comparison to age-matched unin

36 ults indicate that gPr80gag is important for M-MuLV replication in vivo and in vitro and that the pro

37 nd between the 17th and 20th nucleotides for M-MuLV.

38 end did not affect sequence preferences for M-MuLV reverse transcriptase.

39 trovirus-like element Ty3 can substitute for M-MuLV IN sequences in the C-terminal domain and contrib

40 at (LTR) did not alter the target tissue for M-MuLV transformation but significantly altered the patt

41 lasmids showed transcriptional activation in M-MuLV-infected cells relative to uninfected cells.

42 al pathways of apoptotic death are active in M-MuLV-induced tumors and that they must be modulated to

43 for higher levels of thymocyte apoptosis in M-MuLV leukemogenesis.

44 arked decrease in thymic size is apparent in M-MuLV-inoculated mice.

45 ocyte apoptosis were significantly higher in M-MuLV-inoculated mice than in uninoculated control anim

46 ssor inactivation is generally infrequent in M-MuLV-induced tumors but that a subset of these tumors

47 among the polytropic and ecotropic MuLVs in M-MuLV-infected mice.

48 A total of 178 individual M-MuLV constructs were analyzed; 40 in-frame insertions

49 oney murine leukemia virus (M-MuLV) RNA into M-MuLV virus particles.

50 ated by using a panel of chemically modified M-MuLV IN proteins.

51 of activity catalyzed by the IN on modified M-MuLV LTRs.

52 Moreover, M-MuLV induces disease efficiently following both intrap

53 ne sarcoma and leukemia virus complex (M-MSV/M-MuLV), and the induced immune response was monitored b

54 When M-MSV/M-MuLV-challenged mice were treated with the immunosuppr

55 eneration in the animal during Moloney MuLV (M-MuLV) infection is unknown, and the exact roles of MCF

56 clear, since gPr80gag-negative Moloney MuLV (M-MuLV) mutants are replication competent in vitro and p

57 a single group of proviruses, Moloney MuLV (M-MuLV) recombines with at least two distinct groups.

58 The enhancer elements of the Moloney MuLV (M-MuLV) were replaced by the 170-bp enhancers of SRS 19-

59 alent sequences from ecotropic Moloney MuLV (M-MuLV).

60 Mutant M-MuLV integrases were constructed to define the functio

61 , p12, or nucleocapsid domains of the mutant M-MuLV Gag protein lacking the PPPY motif.

62 rough lipid rafts, because gPr80gag-negative M-MuLV has a lower cholesterol content, is less sensitiv

63 econstruction of two-dimensional crystals of M-MuLV CA.

64 The C-terminal domain of M-MuLV integrase (IN) was replaced with the C-terminal d

65 The isolated RNase H domain of M-MuLV reverse transcriptase retained sequence preferenc

66 es of recombination between the env genes of M-MuLV and endogenous proviruses were confined to a shor

67 ly propagation following i.p. inoculation of M-MuLV.

68 ediated by the long terminal repeat (LTR) of M-MuLV, and we show here that the gene activation respon

69 ction may prove relevant to the mechanism of M-MuLV-induced leukemia.

70 These data suggest that the PPPY motif of M-MuLV acts in a partially position-independent manner a

71 A panel of M-MuLV IN mutants and substrate alterations highlighted

72 lytropic MuLVs generated by recombination of M-MuLV with endogenous retroviral sequences.

73 tudy, we investigated the apoptotic state of M-MuLV-induced tumors.

74 rate of thymocyte apoptosis in the thymi of M-MuLV-inoculated mice.

75 tumors were of T-lymphoid origin, typical of M-MuLV rather than SRS 19-6 MuLV.

76 previously shown that an enhancer variant of M-MuLV, Mo+PyF101 M-MuLV, is poorly leukemogenic when us

77 lated with the Mo+PyF101 enhancer variant of M-MuLV.

78 These results provide evidence for primary M-MuLV infection of osteoclasts or osteoclast progenitor

79 d in the skin by wild-type but not Mo+PyF101 M-MuLV after s.c. inoculation and that this infection is

80 pleen, and thymus of wild-type and Mo+PyF101 M-MuLV i.p.- and s.c.-inoculated mice were carried out b

81 cell types infected by M-MuLV and Mo+PyF101 M-MuLV in the skin after a s.c. inoculation, immunohisto

82 inoculation but leukemogenicity by Mo+PyF101 M-MuLV is efficient following i.p. inoculation but atten

83 MCFs were detected in tumors from Mo+PyF101 M-MuLV s. c.-inoculated mice even though they were large

84 is correlated with an inability of Mo+PyF101 M-MuLV to establish infection in the bone marrow of mice

85 The Mo+PyF101 M-MuLV variant also infected cells of the ORS but the le

86 the level of infection in skin by Mo+PyF101 M-MuLV was approximately 4- to 10-fold less than that of

87 Also, when Mo+PyF101 M-MuLV was inoculated i.p., MCF generation appeared to o

88 hat an enhancer variant of M-MuLV, Mo+PyF101 M-MuLV, is poorly leukemogenic when used to inoculate mi

89 ic mice inoculated with M-MuLV and Mo+PyF101 M-MuLV.

90 ase (RT) as well as the structurally related M-MuLV and human immunodeficiency virus type 1 (HIV-1) i

91 HIV-1) could also fully or partially restore M-MuLV assembly when introduced into matrix, p12, or nuc

92 However, all tumors contained DeltaMo+SRS M-MuLV proviruses with common enhancer alterations.

93 ulated with DeltaMo+SRS(+) or DeltaMo+SRS(-) M-MuLV, all tumors were of T-lymphoid origin, typical of

94 combinants DeltaMo+SRS(+) and DeltaMo+SRS(-) M-MuLV.

95 Our results indicate that M-MuLV motifs C and D are necessary for efficient encaps

96 bstitution of FeLV-945 U3 sequences into the M-MuLV long terminal repeat (LTR) did not alter the targ

97 , we carried out in vivo footprinting of the M-MuLV enhancer in infected cells by in vivo treatment w

98 uccessfully carry out the early phase of the M-MuLV life cycle.

99 D stem-and-loop sequences contribute to the M-MuLV cis-acting site for encapsidation.

100 al in vivo binding of nuclear factors to the M-MuLV enhancers in different cell types.

101 We studied the loci into which the M-MuLV had inserted, and found that in 73% of animals, e

102 Mutations within the M-MuLV proviral vectors were Tn7 based and resulted in 1

103 Of the 40 in-frame insertions within the M-MuLV RT connection-RNase H domains, only the three C-t

104 nuclear factors that can potentially bind to M-MuLV enhancer DNA in vitro, it has not been made clear

105 examined: stem structure A, corresponding to M-MuLV viral nucleotides 211 to 224; stem-loop B, nucleo

106 road disease specificity of SRS 19-6 MuLV to M-MuLV.

107 culated subcutaneously (s.c.) with wild-type M-MuLV (approximately 10(5) XC PFU).

108 itoneally, a route that results in wild-type M-MuLV leukemogenesis, mice displayed levels of enhanced

109 e of RNA displacement synthesis by wild-type M-MuLV RT is significantly greater than that of the RNas

110 arallel with replication-competent wild-type M-MuLV showed detectable infection in small cells positi

111 osis comparable to those seen with wild-type M-MuLV.

112 ly 4- to 10-fold less than that of wild-type M-MuLV.

113 scriptases of Moloney murine leukemia virus (M-MuLV) and human immunodeficiency virus type 1 (HIV-1).

114 sted that the Moloney murine leukemia virus (M-MuLV) CA protein may assemble differently.

115 al His-tagged Moloney murine leukemia virus (M-MuLV) capsid (CA) protein, His-MoCA, and in vivo studi

116 tidine-tagged Moloney murine leukemia virus (M-MuLV) capsid protein (his-MoCA) arrays.

117 of cells with Moloney murine leukemia virus (M-MuLV) causes an increase in specific cellular gene pro

118 ' part of the Moloney murine leukemia virus (M-MuLV) encapsidation domain (Psi region) with regard to

119 es release of Moloney murine leukemia virus (M-MuLV) from cells along an IFN-sensitive pathway.

120 region of the Moloney murine leukemia virus (M-MuLV) Gag protein contains a PPPY motif important for

121 Moloney murine leukemia virus (M-MuLV) IN-IN protein interactions important for catalys

122 The nature of Moloney murine leukemia virus (M-MuLV) infection after a subcutaneous (s.c.) inoculatio

123 alyzed by the Moloney murine leukemia virus (M-MuLV) integrase (IN) was used to investigate the bindi

124 Moloney murine leukemia virus (M-MuLV) is a replication-competent, simple retrovirus th

125 Moloney murine leukemia virus (M-MuLV) is a replication-competent, simple retrovirus th

126 uences in the Moloney murine leukemia virus (M-MuLV) long terminal repeat (LTR) are of considerable i

127 epeats of the Moloney murine leukemia virus (M-MuLV) LTR were synthesized, and their effects on integ

128 y of immature Moloney murine leukemia virus (M-MuLV) particles to examine how viral structural (Gag)

129 rminus of the Moloney murine leukemia virus (M-MuLV) pol gene encoding the connection-RNase H domains

130 apsidation of Moloney murine leukemia virus (M-MuLV) RNA into M-MuLV virus particles.

131 H- mutant of Moloney murine leukemia virus (M-MuLV) RT, we demonstrate that the polymerase can displ

132 Neo(r)-marked Moloney murine leukemia virus (M-MuLV) was constructed.

133 n (MA) of the Moloney murine leukemia virus (M-MuLV) was found to interact with IQGAP1, a prominent r

134 N) protein of Moloney murine leukemia virus (M-MuLV) were investigated by using a coordinated-disinte

135 1 (HIV-1) and Moloney murine leukemia virus (M-MuLV) were shown to require components of the cellular

136 U3 region of Moloney murine leukemia virus (M-MuLV) with homologous sequences from the FeLV-945 LTR.

137 emogenesis by Moloney murine leukemia virus (M-MuLV), a genome-wide scan for loss of heterozygosity (

138 uses, such as Moloney murine leukemia virus (M-MuLV), differ from transforming viruses in their mecha

139 pe 1 (HIV-1), Moloney murine leukemia virus (M-MuLV), human T-cell leukemia virus type 1 (HTLV-1), an

140 1 (HIV-1) and Moloney murine leukemia virus (M-MuLV), we determined the effects of sequence, distance

141 s type 1) and Moloney murine leukemia virus (M-MuLV), we evaluated how individual base preferences at

142 on of mice by Moloney murine leukemia virus (M-MuLV), which induces lymphocytic leukemia, results in

143 infection of Moloney murine leukemia virus (M-MuLV)-infected mice was studied.

144 IV-1) and the Moloney murine leukemia virus (M-MuLV).

145 eplication of Moloney murine leukemia virus (M-MuLV).

146 nic mice with Moloney murine leukemia virus (M-MuLV).

147 ia virus, and a Friend erythroleukemia virus-M-MuLV chimeric virus suggested that the appearance of p

148 cts of the insertions were examined in vivo (M-MuLV) and in vitro (HIV-1).

149 Examination of mice infected with M-MuLV, Friend erythroleukemia virus, and a Friend eryth

150 In murine cells chronically infected with M-MuLV, gel shift analyses with kappaB DNA-binding motif

151 ocytes from preleukemic mice inoculated with M-MuLV and Mo+PyF101 M-MuLV.

152 tious units of a BAG vector pseudotyped with M-MuLV proteins, and bone marrow cells were recovered 2

153 uences that is excluded in recombinants with M-MuLV.

154 are major participants in recombination with M-MuLV.

155 vivo inoculation of a gPr80gag mutant, Ab-X-M-MuLV, showed substantially lower (2 log) initial infec

156 Atomic force microscopy of Ab-X-M-MuLV-infected producer cells or of the PA317 amphotrop