ライフサイエンスコーパス: HVS

1 HVS encodes seven small RNAs (HSURs) of unknown function

2 HVS is an oncogenic gammaherpesvirus that causes acute T

3 HVS triggers a distinctive retinopathy with a central re

4 HVS-related retinopathy improved in all patients after p

5 hondrial DNA results of 213 individuals (151 HVS-I sequences) from the northeast, central, southeast

6 Only one HVS (US 708, HVS 2) is a compact helium star.

7 In addition, HVS Deltaorf14 was nononcogenic in common marmosets.

8 In addition, HVS deltaSTP/v-ras-immortalized T cells showed a high le

9 This allows HVS-based vectors to stably transduce a dividing cell po

10 ommon marmosets, while HVS deltaSTP-C488 and HVS deltaTip were nononcogenic.

11 to interact with cellular type D cyclins and HVS v-cyclin.

12 lead to a hyperviscosity syndrome (HVS) and HVS-related retinopathy.

13 Interaction between Integrator and HVS primary miRNA (pri-miRNA) substrates that contain on

14 Although KSHV and HVS are related members of the rhadinovirus subgroup of

15 The KSHV and HVS LANAs have also been shown to be required for mainte

16 Epstein-Barr virus membrane antigen p140 and HVS p160, (ii) HVS and cellular type D cyclins, (iii) HV

17 Finally, HVS deltaSTP/v-ras and HVS deltaSTP/c-ras each induced lymphoma in one of two c

18 itive T lymphocytes, HVS deltaSTP/c-ras- and HVS deltaSTP/v-ras-immortalized cells were principally C

19 these two functional domains of the TEAS and HVS genes resulted in a novel enzyme capable of synthesi

20 The relative ratio of the TEAS and HVS reaction products was also influenced by the source

21 he vitreous of the eye and is induced before HVS regression in the first postnatal week.

22 his cis-acting element is sufficient to bind HVS ORF73 from strains C488 and A11, and plasmids contai

23 ets resulted in fulminant lymphoma with both HVS/Tip mSH3B and wild-type HVS.

24 for TS and DHFR enzymes are also encoded by HVS (ORF70 and ORF2), both occur at different genomic lo

25 A protein encoded by HVS known as Tip-484 (for tyrosine kinase interacting pr

26 ate that, due to the sequestration of Lck by HVS Tip, T cell receptor (TCR) stimulation fails to acti

27 iri-immortalized primary CD4(+) T cells (CD4/HVS), which resemble activated primary T cells.

28 However, a TR-deleted HVS bacterial artificial chromosome can form replication

29 on the functions of the recently discovered HVS miRNAs, called miR-HSURs.

30 In the absence of Arf, failed HVS regression causes a pathological process that resemb

31 Finally, HVS deltaSTP/v-ras and HVS deltaSTP/c-ras each induced l

32 city experiments, the Michaelis constant for HVS was 3.5 microM, while CH3 and CH4 exhibited smaller

33 The patients were evaluated for HVS-related retinopathy, and hemodynamic changes in a ma

34 like sequence (miRNA 3' box) downstream from HVS pre-miRNAs that is essential for miRNA biogenesis.

35 for tyrosine kinase interacting protein from HVS strain 484) is required for this transformation.

36 ull-length form (residues 1-187) of Tip from HVS strain C484.

37 Furthermore, HVS terminal repeats (TRs) contain a cis-acting sequence

38 Analysis of the gammaHV68, HVS, EBV, and KSHV genomes demonstrated that each of the

39 However, HVS/Tip mSH3B produced greater infiltration of affected

40 We examined embryonic and fetal human HVS using a variety of techniques to gain new insights i

41 Our results support the view that the human HVS, like the choriocapillaris, develops by hemo-vasculo

42 f14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in the o

43 rus membrane antigen p140 and HVS p160, (ii) HVS and cellular type D cyclins, (iii) HVS and cellular

44 (ii) HVS and cellular type D cyclins, (iii) HVS and cellular G protein-coupled receptors, and (iv) H

45 Consistently, inhibition of miR-HSUR5-3p in HVS-infected cells decreases their proliferation.

46 Furthermore, the p56lck kinase activity in HVS-infected human peripheral blood T lymphocytes was at

47 ri U RNAs), that are abundantly expressed in HVS-transformed, latently infected marmoset T cells but

48 pesvirus type 4 and a similar motif found in HVS ORF12.

49 the ARE-binding proteins hnRNP D and HuR in HVS-transformed T cells using a new cross-linking assay.

50 ential for transformation and oncogenesis in HVS-infected cells.

51 f is degraded by an ARE-dependent pathway in HVS-transformed T cells, suggesting that HVS may take ad

52 8 TR element are maintained and replicate in HVS C488 ORF73-expressing cells.

53 ) are the most abundant viral transcripts in HVS-transformed, latently infected T cells but are not r

54 llular G protein-coupled receptors, and (iv) HVS.

55 pression from a range of both early and late HVS promoters, depending on the target gene.

56 zed CD4- CD8+ single-positive T lymphocytes, HVS deltaSTP/c-ras- and HVS deltaSTP/v-ras-immortalized

57 f infected marmosets for more than 5 months, HVS Deltaorf14 did not persist at a high level in vivo.

58 cells transformed with wild-type or a mutant HVS lacking the most highly conserved HSURs, HSURs 1 and

59 bits inoculated with Tip-484 deletion mutant HVS.

60 escued after transduction of deletion-mutant-HVS-transformed cells with a lentiviral vector carrying

61 In contrast to other nononcogenic HVS mutant viruses which were repeatedly isolated from p

62 The LYVE-1 expression was detected on normal HVS between E12.5 and P14.

63 oded by other gammaherpesviruses (gene 16 of HVS and KSHV and the BHRF1 gene of EBV).

64 stetraprolin induced following activation of HVS-transformed T cells, but even in such stimulated cel

65 at the signaling and targeting activities of HVS Tip rely on functionally and genetically separable m

66 stent with the lack of oncogenic activity of HVS subgroup B viruses, STP-B was deficient for transfor

67 Orf73, encoding the nuclear antigen of HVS, is the positional homolog of the LANA gene, and the

68 t sequence is a determinant of the degree of HVS STP transforming activity.

69 Despite the pronounced effects of HVS Tip on T cell signal transduction, the details of it

70 ng signal (3' box), generates the 5' ends of HVS pre-miRNA hairpins.

71 of orf14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in

72 We constructed a mutant form of HVS in which prolines in the SH3B motif of Tip were alte

73 us, the signaling and targeting functions of HVS Tip rely on two functionally and genetically separab

74 hat may contribute to the immunopathology of HVS infection.

75 t ras can substitute for the STP oncogene of HVS C488 to allow immortalized growth of primary lymphoi

76 ant herpesvirus in which the STP oncogene of HVS was replaced by R1 immortalized T lymphocytes to int

77 ant herpesvirus in which the STP oncogene of HVS was replaced with K1, immortalized primary T lymphoc

78 These results demonstrate that orf14 of HVS is not required for replication but is required for

79 However, the function of ORF73 of HVS has not been thoroughly investigated.

80 e below the level of detection in a panel of HVS-transformed CD8(+) cells with potent HIV-1 inhibitor

81 The transforming potential of HVS Deltaorf14 was tested in cell culture and in common

82 P is required for the oncogenic potential of HVS, we investigated the functional consequence of K1 ex

83 Here we assess the potential of HVS-based vectors for the generation of induced pluripot

84 ents confirmed that the 3' end processing of HVS pre-miRNAs also depends on Integrator activity.

85 ation, we constructed recombinant strains of HVS C488 in which the STP-C488 oncogene was replaced wit

86 A better understanding of HVS biology will help advance our knowledge of virus-ind

87 The spike component of HVSs was associated with fast field oscillations (400-60

88 rces determined the amplitude variability of HVSs and sleep spindles.

89 investigate the effects of plasmapheresis on HVS-related retinopathy and retinal hemodynamic paramete

90 ncer, viral miRNAs from the highly oncogenic HVS might also be important for transformation.

91 Only one HVS (US 708, HVS 2) is a compact helium star.

92 ion of p53 tetramerization by either LANA or HVS-encoded ORF73, suggesting that p53 inactivation may

93 ntrasts with the recent description of other HVS-transformed CD4+ T cells that provide B cell help pr

94 ost favored ejection mechanism for the other HVSs.

95 Through the interactions with Lck and p80, HVS Tip modulates diverse T-cell functions, which leads

96 Parental HVS subgroup C strain 488 immortalized common marmoset T

97 Parental HVS subgroup C strain 488 immortalized common marmoset T

98 es and high voltage spike-and-wave patterns (HVSs).

99 -2) knockout mice with abnormally persistent HVS were examined.

100 gly, in contrast to snRNA 3' end processing, HVS pre-miRNA 3' end processing by Integrator can be unc

101 lation or repress Vegf expression to promote HVS involution and prevent PHPV.

102 Recombinant HVS deltaSTP/v-ras immortalized primary common marmoset

103 ld-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras did so with low efficiency.

104 hat the RRV26-95 DHFR more closely resembles HVS DHFR (74% similarity) than KSHV DHFR (55% similarity

105 Plasmapheresis is effective in reversing HVS-related retinopathy and in reducing abnormal venous

106 acting protein (Tip) of Herpesvirus saimiri (HVS) activates the lymphoid-specific member of the Src f

107 ed cyclin (v-cyclin) of herpesvirus saimiri (HVS) and 31% identity and 53% similarity to human cellul

108 by the DNA tumor virus herpesvirus saimiri (HVS) and designated tyrosine kinase interacting protein

109 orming protein (STP) of herpesvirus saimiri (HVS) and of K1 of KSHV, other members of the gamma-2 or

110 The lymphotropic Herpesvirus saimiri (HVS) causes acute leukemia, T-cell lymphoma, and death i

111 Herpesvirus saimiri (HVS) encodes seven Sm-class small nuclear RNAs, called H

112 ing frame 14 (orf14) of herpesvirus saimiri (HVS) exhibits significant homology with mouse mammary tu

113 ected marmoset T cells, Herpesvirus saimiri (HVS) expresses six microRNAs (known as miR-HSURs [H. sai

114 th the right end of the herpesvirus saimiri (HVS) genome and more limited homology to the left end of

115 The herpesvirus saimiri (HVS) immediate-early gene product encoded by open readin

116 Herpesvirus saimiri (HVS) infects a range of human cell types with high effic

117 Herpesvirus saimiri (HVS) is a gamma-herpesvirus that expresses Sm class U RN

118 Herpesvirus saimiri (HVS) is a T-cell-specific transforming and oncogenic vir

119 Herpesvirus saimiri (HVS) is an oncogenic gamma-herpesvirus that produces mic

120 Herpesvirus saimiri (HVS) is an oncogenic, lymphotropic, gamma-herpesvirus th

121 ) of the T lymphotropic Herpesvirus saimiri (HVS) is constitutively present in lipid rafts and intera

122 Herpesvirus saimiri (HVS) is divided into three subgroups, A, B, and C, based

123 acting protein (Tip) of herpesvirus saimiri (HVS) is required for binding to the cellular Src family

124 , including the gamma-2 herpesvirus saimiri (HVS) of New World squirrel monkeys.

125 minal repeats (TR) from herpesvirus saimiri (HVS) renders it unable to produce infectious virus or ge

126 by the DNA tumor virus herpesvirus saimiri (HVS) strain 484, designated tyrosine kinase-interacting

127 ogene, called STP-A, of herpesvirus saimiri (HVS) subgroup A is not required for viral replication bu

128 STP oncoproteins of the herpesvirus saimiri (HVS) subgroup A strain 11 and subgroup C strain 488 are

129 Mutant forms of herpesvirus saimiri (HVS) subgroup C strain 488 with deletions in either STP-

130 The herpesvirus saimiri (HVS) tyrosine kinase-interacting protein (Tip), required

131 d by two herpesviruses, herpesvirus saimiri (HVS) which can transform blood lymphocytes and induce ma

132 Sm class are encoded by Herpesvirus saimiri (HVS), a gamma Herpesvirus that causes aggressive T cell

133 T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding (nc) RNA, HSUR 1, specifi

134 s human herpesvirus 8), herpesvirus saimiri (HVS), and Epstein-Barr virus (EBV).

135 Herpesvirus saimiri (HVS), another gamma-2-herpesvirus, primarily infects New

136 genome in RRV26-95 and herpesvirus saimiri (HVS), but in KSHV the DHFR gene is displaced 16,069 nucl

137 herpesvirus (KSHV) and herpesvirus saimiri (HVS), has been shown to encode a latency-associated nucl

138 orming protein (STP) of herpesvirus saimiri (HVS), Kaposi's sarcoma-associated herpesvirus (KSHV) con

139 onors by infection with Herpesvirus saimiri (HVS), to evaluate functional properties of these immorta

140 ded by the lymphotropic Herpesvirus saimiri (HVS), we determined the specific sequence and structural

141 The Tip protein of herpesvirus saimiri (HVS), which is a T-lymphotropic tumor virus, interacts w

142 emonstrated that Tip of herpesvirus saimiri (HVS), which is a T-lymphotropic tumor virus, is constitu

143 -1 and CAF derived from herpesvirus saimiri (HVS)-transformed CD8(+) cells inhibited HIV-1 infection

144 e 6 (ORF6) and ORF31 of herpesvirus saimiri (HVS).

145 eading frame (ORF) from herpesvirus saimiri (HVS).

146 elated gammaherpesvirus herpesvirus saimiri (HVS).

147 ymphotropic tumor virus herpesvirus saimiri (HVS).

148 STP-C488 (STP of herpesvirus saimiri [HVS] group C strain 488 [C488]) is the only virus-encode

149 tochondrial SNPs and hypervariable sequence (HVS) 1, Tamil castes have higher affinity to eastern Asi

150 By deep sequencing, we identified six HVS microRNAs (miRNAs) that are derived from three hairp

151 cellular currents underlying sleep spindles, HVSs, and evoked responses result from activation of int

152 sources were similar during sleep spindles, HVSs, and thalamic-evoked responses, although their rela

153 Hypervelocity stars (HVSs) travel with velocities so high that they exceed th

154 which can lead to a hyperviscosity syndrome (HVS) and HVS-related retinopathy.

155 Hyoscyamus muticus vetispiradiene synthase (HVS) gene and by characterization of the resulting chime

156 Hyoscyamus muticus vetispiradiene synthase (HVS), a chimeric 5-epi-aristolochene synthase (CH3), and

157 l regression of the hyaloid vascular system (HVS) in the mouse eye.

158 The hyaloid vascular system (HVS) is a transient network nourishing developing eyes a

159 cell biology in the hyaloid vascular system (HVS) of the developing eye.

160 opment of the human hyaloid vascular system (HVS) remains unclear.

161 These results demonstrate that HVS utilizes a novel signaling protein, ORF5, to activat

162 We demonstrate that HVS-based exogenous delivery of Oct4, Nanog, and Lin28 c

163 processing assays in vitro demonstrated that HVS does not utilize the Microprocessor complex that gen

164 These results indicate that HVS-immortalization of CD4+ lymphocytes may produce T ce

165 We show that HVS miRNA biogenesis relies on cis-acting elements speci

166 In this report, we show that HVS ORF73 may be important for episome persistence and c

167 in HVS-transformed T cells, suggesting that HVS may take advantage of the host ARE-mediated mRNA dec

168 The HVS STP-C488 P10-->R mutant was deficient in human T-lym

169 erentiation trials suggest that although the HVS-derived putative iPCs are capable of differentiation

170 mon marmoset lymphocytes immortalized by the HVS/Tip mSH3B mutant displayed increased expression of H

171 ns C488 and A11, and plasmids containing the HVS C488 TR element are maintained and replicate in HVS

172 vestigate whether LYVE-1 is expressed in the HVS and how it is associated with the vascular structure

173 s that map to the host genome but few in the HVS genome.

174 In the HVS, Arf expression in perivascular cells may block thei

175 there is no report on its expression in the HVS.

176 farther diverged from human DHFR than is the HVS version, implying that they were probably acquired a

177 Moreover, the HVS episome is able to persist and provide prolonged tra

178 roducts of the tobacco enzyme, exon 6 of the HVS gene conferred specificity for the predominant react

179 Nucleotide sequence analysis of the HVS genome revealed an open reading frame with 22% amino

180 The transforming potentials of the HVS mutants were tested in cell culture and in common ma

181 ng the embryogenesis and pathogenesis of the HVS, it also leads to a completely natural model in whic

182 Further analysis of the HVS-derived putative iPCs showed some degree of reprogra

183 ORF73, the HVS homologue of LANA, is shown to bind both p53 and pRb

184 s study provides the first evidence that the HVS contains a LYVE-1(+) cellular component in both phys

185 homologous to HVS and KSHV ORFs and used the HVS/KSHV numbering system to designate these ORFs.

186 interleukin-2-independent growth, while the HVS Deltaorf14 mutant did not produce such a growth tran

187 episome persistence and colocalizes with the HVS genomic DNA on metaphase chromosomes.

188 rf, perivascular cells accumulate within the HVS and prevent its involution.

189 Therefore, HVS Tip uniquely targets the retromer complex to impair

190 d that these activities likely contribute to HVS-mediated lymphoid cell immortalization in culture an

191 63 open reading frames (ORFs) homologous to HVS and KSHV ORFs and used the HVS/KSHV numbering system

192 he v-cyclin of the T-lymphocyte-transforming HVS in its specificity for association with cdk6 and in

193 dependent growth as efficiently as wild-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras

194 Wild-type HVS produced fatal lymphoma within 19 to 20 days of expe

195 mphoma with both HVS/Tip mSH3B and wild-type HVS.

196 erating lymphoid cells compared to wild-type HVS.

197 compared to cells immortalized by wild-type HVS.

198 The mutant virus, HVS/Tip mSH3B, retained its ability to immortalize commo

199 imental infection of common marmosets, while HVS deltaSTP-C488 and HVS deltaTip were nononcogenic.

200 Infection of T cells with HVS or expression of recombinant Tip-484 significantly i

201 ot altered in T cells latently infected with HVS mutants lacking HSURs 1 and 2.

202 lize with p53 in human T cells infected with HVS, and in cells overexpressing both ORF73 and p53, as

203 Nine patients with HVS due to WM were studied.

204 gammaHV68 shares with HVS and KSHV ORFs homologous to a complement regulatory

205 wth as efficiently as wild-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras did so with l

206 Whereas wt HVS immortalized CD4- CD8+ single-positive T lymphocytes