ライフサイエンスコーパス: replication

1 tly reduced PGE2 production, as well as PSaV replication.

2 n in DENV-infected cells and decreases viral replication.

3 provide insights into its functions in HBoV1 replication.

4 specific CD8(+) T cells in controlling HIV-1 replication.

5 agy and cell cycle arrest and benefits virus replication.

6 r timely repair of genetic material prior to replication.

7 of the main systems maintaining fidelity of replication.

8 , increased nitrite, and decreased bacterial replication.

9 ination and is important for efficient virus replication.

10 was also observed as a sign of active viral replication.

11 tome, regulating pathways that control lytic replication.

12 ear, SupT1, and THP-1 cells diminishes HIV-1 replication.

13 s a consequence of disrupting processive DNA replication.

14 KR plays a critical role in controlling HCMV replication.

15 mbrane trafficking pathways to promote their replication.

16 /-) cells were highly permissive to L. major replication.

17 gammadelta T cells, without affecting viral replication.

18 mental cellular processes such as growth and replication.

19 ort to and from their intracellular sites of replication.

20 rinciple to coordinate growth and chromosome replication.

21 ed in lipid remodeling and scavenging during replication.

22 ranscribed genes are always co-oriented with replication.

23 ging-strand template-switch mechanism during replication.

24 ll clones with diverse permissiveness to HBV replication.

25 y at a concentration that prevents bacterial replication.

26 sistent with the observed block in viral DNA replication.

27 e support AAV2 replication and inhibit HSV-1 replication.

28 p treatments to safely promote human ss-cell replication.

29 ting a molecular understanding of chromosome replication.

30 ccur even in the absence of productive viral replication.

31 KS tumors support both latent and lytic KSHV replication.

32 e discovery of host proteins involved in HIV replication.

33 ire genome alterations during the act of DNA replication.

34 but it was dependent on the extent of viral replication.

35 amide decreases survival and increases viral replication.

36 nt gene product(s) associated with borrelial replication.

37 ated DNA synthesis, thereby inhibiting HIV-1 replication.

38 (CTC1-STN1-TEN1) also functions in telomere replication.

39 nt of latent EBV infection and enhance viral replication.

40 in viral capsid production and robust viral replication.

41 nhances LT stability and promotes MCV genome replication.

42 ing that this pathway is important for viral replication.

43 inase R (PKR), which potently inhibits virus replication.

44 igate the role of autophagy in avibirnavirus replication.

45 echanistic links to histone variants and DNA replication.

46 cantly reduced HCV infection but not HCV RNA replication.

47 s (RV) and respiratory syncytial virus (RSV) replication.

48 ducing more compartments with increased self-replication.

49 d as a template for genome transcription and replication.

50 iological processes including DNA repair and replication.

51 ociated with translation, transcription, and replication.

52 reticulum that could impact viral entry and replication.

53 pus and human MTBP to assess its role in DNA replication.

54 harness host innate immunity to enhance its replication.

55 both RECQL5 and WRN severely compromises DNA replication, accumulates genomic instability and ultimat

56 olymerase-iota (Poliota) promotes error-free replication across 1-MeA.

57 6 and the C domain of YLDV-97 supported VACV replication albeit at a reduced efficiency.

58 against TGF-beta, though did not inhibit HBV replication alone, enhanced the antiviral and antifibrot

59 hibited VEEV pathogenesis in mice, and viral replication analyses suggest that the TF protein is crit

60 ccinia virus infection by blocking viral DNA replication and abrogating postreplicative intermediate

61 The mechanics of DNA replication and cell cycling are well-characterized in m

62 ated, and preferentially associated with DNA replication and cell division.

63 Viral replication and cellular responses were measured using q

64 ses have crucial functions in transcription, replication and DNA repair and are hence implicated in d

65 Self-replication and evolution under selective pressure are i

66 sting infection are characterized by minimal replication and genetic changes.

67 IFN-inducible LY6E promotes HIV-1 entry and replication and highlight a positive regulatory role of

68 e the functions of NoV proteins during virus replication and highlight the conserved properties of th

69 Anti-IL-33 decreased rhinovirus replication and increased IFN-lambda levels at the gene

70 ep protein levels in S/G2 phase support AAV2 replication and inhibit HSV-1 replication.

71 of lineage-specifying TFs occurs soon after replication and is facilitated by a decondensed chromati

72 from the Coronary Artery Disease Genome-wide Replication and Meta-analysis Plus the Coronary Artery D

73 ge is associated with multiple rounds of DNA replication and nuclear division without cytokinesis, re

74 and JAK inhibitor I) strongly stimulate VSV replication and oncolysis in all resistant cell lines bu

75 We here report the study of the roles of replication and oxidative stresses in mediating cellular

76 protein substantially affected the systemic replication and pathogenicity of these H5N1 influenza vi

77 of a duplex HBoV1 genome initiates viral DNA replication and produces progeny virions that are infect

78 nificantly increased the levels of HSV-1 DNA replication and production of viral progeny in SCG neuro

79 arly remove those cells through active virus replication and resulting cytopathicity.

80 schizogony, with only the final round of DNA replication and segregation being synchronous and coordi

81 help coordinate its assembly with chromosome replication and segregation.

82 lles to access host machineries required for replication and spread.

83 way is critical for ehrlichial intracellular replication and survival.

84 of the host immune system to suppress viral replication and the ability of a virus to counteract the

85 e proteins were required for efficient virus replication and the ability of NS5A to spread throughout

86 ng these enzymes significantly reduced phage replication and the generation of infectious particles.

87 Conflicts between replication and transcription challenge chromosome dupli

88 lymerase complex, which is essential for the replication and transcription of influenza virus RNA.

89 provided evidence for a temporal coupling of replication and transcription.

90 the TAT peptide significantly inhibited IAV replication and transmission.

91 s and stabilizes LT, leading to enhanced MCV replication and transmission.

92 minolysis, but not FAS, inhibit viral genome replication and, interestingly, are required for differe

93 he E2 protein, which controls transcription, replication, and genome maintenance in infected cells.

94 oles in metabolism, tumor progression, viral replication, and skin barrier formation.

95 undergoes collision release upon completing replication, and we propose Pol delta-PCNA collides with

96 pendent coupled oscillators and identify DNA replication as a critical process in the circadian mecha

97 Loss of DONSON leads to severe replication-associated DNA damage arising from nucleolyt

98 tissue growth and repair, but can result in replication-associated genome damage.

99 ibitors of this kinase effectively block HRV replication at an early stage of the viral life cycle.

100 To determine the impact of abortive replication at different stages of the viral life cycle

101 y demonstrated that autophagy enhances viral replication at the late stage of infection, and the auto

102 rotic, providing a niche for M. tuberculosis replication before escaping into the extracellular milie

103 Strategies to resolve replication blocks are critical for the maintenance of g

104 cycle in detail, we show that directly after replication both chromosomal origin regions localize to

105 ed in Okazaki fragment processing during DNA replication but is thought to be dispensable for DNA end

106 croRNA-134-5p (miR-134) can regulate Sabin-1 replication but not Sabin-2 or Sabin-3 via direct intera

107 the essentiality of GAPDH1 in intracellular replication but we confirmed that glycolysis is not stri

108 gument proteins involved in regulating lytic replication, but lacked capsid proteins.

109 critical for the initiation of dengue virus replication, but quantitative analysis of the interactio

110 the lymphoreticular system, intranodal prion replication by B and follicular dendritic cells, and pot

111 persistence is thought to interfere with DNA replication by slowing or impeding replication fork prog

112 SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building block

113 In this study, we show that the replication capacity of viruses isolated during acute in

114 ve a significantly lower Gag-protease-driven replication capacity than that of viruses derived from t

115 rticle maturation, and significant levels of replication capacity.

116 n but at the same time markedly impair HIV-1 replication capacity.

117 optotic sensitivity to inhibitors of the DNA replication checkpoint and suggesting it as a candidate

118 osis share many processes, including the DNA replication, chromosome condensation and precisely regul

119 SMAD3 methylation in IIS (n = 60) and in 2 replication cohorts (the Manchester Asthma and Allergy S

120 ronic) and three independent, nonoverlapping replication cohorts: a second WB set (n = 448, acute) an

121 Here, we detect persistent EBOV replication coinciding with systematic inflammatory resp

122 enerates high levels of ATP within the viral replication compartment at the expense of a reduction in

123 rter cell-based assay to quantify inducible, replication-competent latent HIV-1.

124 s indicated by the quantity of HIV-1 DNA and replication-competent-virus-producing cells.

125 , and the autophagy pathway facilitates IBDV replication complex function and virus assembly, which i

126 embranous structures in the cytoplasm called replication complexes (RCs).

127 acilitates the formation of virus-associated replication complexes, which are required for the amplif

128 family samples, 215 genes spanning rare and replication copy number variations, 99 genes overlapping

129 a cellular protein that is important in the replication cycle of HCMV, we identified a novel target

130 ein (eNP) gene, with additional roles in the replication cycle such as viral assembly.

131 hronized diel coupling of viral and cellular replication cycles in both photoautotrophic and heterotr

132 tive military cohorts (one discovery and one replication data set).

133 red random mutations but often arise through replication defects; transcription can interfere with re

134 Our efforts uncover replication-dependent and -independent ICL repair networ

135 ment of longer-range interactions connecting replication-dependent histone genes on chromosome 6, pot

136 DNA replication depends on primase, the specialised polymera

137 The canonical model of DNA replication describes a highly-processive and largely co

138 n between TopBP1 and Treslin and promote DNA replication despite the presence of a Cdk2 inhibitor.

139 We show that this replication difference occurs in a single round of infec

140 depletion of FANCM dramatically reduces the replication efficiency at ALT telomeres.

141 inactivated, excessive RAD51 activity slows replication elongation and causes double-strand breaks.

142 We measured HCV replication, entry, spread, production, and release in h

143 n the mismatch repair gene MLH1 is driven by replication errors and accurately models the mutation pr

144 mechanism exploited by cells to correct DNA replication errors both in growing cells and under nongr

145 Piwil 2 (Hili) protein can also inhibit HIV replication, especially in activated CD4(+) T cells that

146 HPV replication factories formed in the nucleus are location

147 Eukaryotic DNA replication fidelity relies on the concerted action of D

148 ases survival of bees while decreasing viral replication following infection with FHV, whereas treatm

149 d by blocking the Chk1-dependent response to replication fork damage.

150 2 Mechanistically, cDKO HSPCs showed altered replication fork dynamics, massive accumulation of DNA d

151 Protection of the stalled replication fork is crucial for responding to replicatio

152 Reduced rate of DNA replication fork progression and chromosomal shattering

153 on defects; transcription can interfere with replication fork progression and stability, leading to i

154 with DNA replication by slowing or impeding replication fork progression.

155 however the architecture and dynamics of the replication fork remain only partially understood, preve

156 Human Timeless is involved in replication fork stabilization, S-phase checkpoint activ

157 the DnaB helicase associates stably with the replication fork, providing the molecular basis for how

158 enesis and composition of the eukaryotic DNA replication fork, with an emphasis on the enzymes that s

159 d Pol alpha-primase at the top of CMG at the replication fork.

160 essential for the formation of a functional replication fork.

161 discontinuities on the lagging strand of the replication fork.

162 nhibitor-induced origins generate additional replication forks that are targeted by subsequent exposu

163 mediating the restart of temporarily stalled replication forks thereby suppressing the firing of new

164 R-loops are known to interfere with replication forks, and sensitivity of the double rnhAB m

165 is much more competitive than XPA in binding replication forks, PCNA sequestration by progerin may sh

166 arising from nucleolytic cleavage of stalled replication forks.

167 progerin each significantly restored PCNA at replication forks.

168 Replication gaps that persist into mitosis likely repres

169 h the replicative DNA polymerases during DNA replication has suggested that DNA polymerase epsilon (P

170 roles of co-opted host proteins in RNA virus replication have been appreciated for a decade, the equa

171 ortant functions of cellular lipids in virus replication have been gaining full attention only recent

172 ce of cellular functions necessary for viral replication if continuous protein synthesis is required.

173 ers remain roughly constant over time, their replication implies that ongoing destruction likewise oc

174 nfluence of endogenous retroviruses on HIV-1 replication.IMPORTANCE Endogenous retroviruses inhabit b

175 Genome-wide association analysis and replication in 12,540 individuals identified no single v

176 Replication in AUD datasets confirmed PCSK9 hypomethylat

177 haracterize how these viruses evolved during replication in cell culture and in experimentally infect

178 In addition, we observed that prion replication in cell culture was inversely related to the

179 s draw a rich and realistic picture of ChHV5 replication in cells derived from its natural host and m

180 SAMHD1 potently blocks HIV-1 replication in DCs, although the underlying mechanism is

181 t that persistence involves continuous viral replication in fibrocytes (possibly including tissue mac

182 Furthermore, we have determined that JCV DNA replication in G144 cells is stimulated by myristoylated

183 hat occurs on functional telomeres following replication in G2.

184 4-CMdT on the efficiency and fidelity of DNA replication in HEK293T human embryonic kidney cells.

185 ntiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does not eli

186 or future studies to explore the role of DNA replication in immune cell generation and function.

187 These data suggest that replication in macrophages affects cellular function and

188 s with reduced enzymatic activity had slower replication in mammalian neuronal cells and reduced viru

189 ing impairment in some older adults warrants replication in other prospective cohort studies.

190 fically modified single-stranded vectors for replication in primate (COS7) or Escherichia coli cells.

191 omplexes, and that Lon may help regulate DNA replication in response to growth conditions.

192 and CXCL16 significantly inhibited SIVagmSab replication in sabaeus PBMC and had a greater impact tha

193 ry site for latent virus and low-level viral replication in the absence of neuro-disease.

194 rstanding the environment of M. tuberculosis replication in the host.

195 ot always have a strong correlation with the replication in the human upper respiratory tract.

196 d in Caucasian population showed evidence of replication in the Indian population mainly with respect

197 AEE788 treatment inhibits DNA replication in the kinetoplast (mitochondrial nucleoid)

198 while respiratory infection results in virus replication in the lung.

199 a role for NS1 and characteristics of viral replication in the URT that were associated with airborn

200 e draining lymph node had no impact on viral replication in this organ, suggesting that WNV may migra

201 t some plant virus RdRPs are able to perform replication in trans of genomic or DI RNAs in the yeast

202 tibody titer has been shown to enhance viral replication in vitro and severe disease in animal models

203 udy the novel molecular biology of ascovirus replication in vitro is lacking.

204 functional CTM domain are defective for DNA replication in Xenopus egg extracts.

205 s involved in cellular redox balance and DNA replication, including the Mcm replicative helicases.

206 can control both early and persistent viral replication independently of adaptive immune effector fu

207 ophage-tropic virus expression, and probably replication, indicates that antiretroviral drugs with op

208 ic DNA is not required in mammalian cell DNA replication, indicating that drugs targeting the termina

209 tal reorganization, resulted in reduced RVFV replication, indicating that this pathway is important f

210 KSHV lytic replication induces dynamic reprogramming of epitranscri

211 Eukaryotic DNA replication initiates from multiple discrete sites in th

212 ., constant growth increments) that start at replication initiation.

213 on of HR-mediated repair and that unresolved replication intermediates impair chromosome segregation.

214 tions to degrade double-stranded RNA (dsRNA) replication intermediates.

215 sue, Muller and Nieduszynski find that early replication is a requirement for the highest expression

216 ing in detail the processes involved in HCMV replication is important for developing novel treatments

217 Histone mRNAs are rapidly degraded when DNA replication is inhibited by a 3' to 5' pathway that requ

218 Because cellular resistance to viral replication is marked by expression of antiviral restric

219 more, fitness of S. aureus in these sites of replication is not compromised by the absence of transpo

220 f transcription, CTCF, and TERRA in telomere replication is not known.

221 us by relocating cellular resources to viral replication, it also poses a challenge to the maintenanc

222 stent with ORCA-bound origins initiating DNA replication late in S-phase.

223 restingly, the transient activation of viral replication led to HIV-1 reservoir reduction after virem

224 n factors have been shown to inhibit HIV/SIV replication, little is known about their expression in v

225 icance of the components of the rabies virus replication machinery is incomplete.

226 anism underlying HBoV1 helper-dependent AAV2 replication may also provide insights into its functions

227 present analysis suggests that, although the replication modules of at least some classes of viruses

228 In dividing cells, DNA replication occurs in a precise order, but many question

229 A (ssDNA) genome to the nucleus, where viral replication occurs.

230 We found that GYY4137 significantly reduced replication of all tested viruses.

231 nduced mitochondrial fragmentation prevented replication of C. trachomatis even in p53-deficient cell

232 ee increased replication stress due to under-replication of DNA.

233 t reporting to facilitate interpretation and replication of experiments.

234 d plasma iron; this is proposed to limit the replication of extracellular microbes, but could also pr

235 involving a total of 8643 women) to test for replication of genomic loci that had significant genomew

236 miR) 122/CD81 cells, which support entry and replication of HCV, were transfected these cells with sm

237 assay and TRIM6 knockout cells have reduced replication of infectious EBOV, suggesting that VP35 hij

238 ms of cell-autonomous immunity that restrict replication of intracellular pathogens.

239 a deletion in the p27-p55 operon impairs the replication of M. bovis in bovine macrophages.

240 twork with a critical role in regulating the replication of multiple virus families.

241 or antioxidants, attesting to intracellular replication of S. pneumoniae as a key first step in pneu

242 ation and appearance of SSPiM over time, and replication of SSPiM OCTA signal in an in vitro phantom.

243 sfer via this route can result in productive replication of the infectious agents in the recipient ce

244 nces in correction of errors produced during replication of the leading and the lagging DNA strands w

245 1 inhibition during MVM infection.IMPORTANCE Replication of the parvovirus minute virus of mice (MVM)

246 es a DDR that plays significant roles in the replication of the viral DNA and the production of proge

247 One of the proteins, VP35, is essential for replication of the viral genome and for evasion of host

248 e expression of viral proteins and regulates replication of viral DNA within the nucleus.

249 Delta20 IFITM2 suppresses replication of X4 HIV-1 strains by inhibiting their entr

250 stages of the viral life cycle or productive replication on macrophage function, we assessed cytotoxi

251 y to identify host proteins supporting virus replication or enhancing resistance to virus infection.

252 ere was no direct impact of the TBD on viral replication or virulence in mice.

253 s transcription factors yet are defective in replication origin timing control.

254 undaries separate regions of similarly timed replication origins connecting the long-known effect of

255 e majority of the ORCA-bound sites represent replication origins that also associate with the repress

256 forks thereby suppressing the firing of new replication origins.

257 crete sites in the genome, termed origins of replication (origins).

258 ddC treatment inhibited mtDNA replication, oxidative phosphorylation, and induced cyto

259 conformation, which enables error-prone DNA replication past the adduct.

260 st association with acute kidney injury in a replication patient population containing 206 cases with

261 oops and gamma-H2A at sites of Sgs1 binding, replication pausing regions, and long genes.

262 ual regulatory role for chromatin during DNA replication: promoting origin dependence and determining

263 In the presence of replication protein A (RPA), MRN acts as a processivity

264 oordinator of all DNA metabolic processes is Replication Protein A (RPA).

265 ic pathways are required for efficient lytic replication, providing novel therapeutic avenues for KS

266 At pH 5.3, the replication rate of species I is approximately 1.3-1.4 t

267 Low replication rates are a concern in most, if not all, sci

268 sible explanation for the exceptionally high replication rates of EEEV and suggest a new means of its

269 Our findings indicate that HIV infection and replication rely on a limited set of host-dispensable ge

270 DNA replication results in the doubling of the genome prior

271 ping in 7164 cases and 21005 controls, and a replication set of 1840 cases and 129016 controls of Eur

272 Therefore, the cooperative induction of DNA replication stress and damage by ATR inhibition and cyta

273 Replication stress and deregulated origin firing increas

274 eplication fork is crucial for responding to replication stress and minimizing its impact on chromoso

275 al shattering were also observed, suggesting replication stress as a root causative factor in CHKi hy

276 BRCA1 and BLM help to resolve the telomeric replication stress by stimulating DNA end resection and

277 ion of CKS proteins promotes override of the replication stress checkpoint.

278 ed human mammary cell line and see increased replication stress due to under-replication of DNA.

279 FANCD2 also functions during the replication stress response by mediating the restart of

280 lls displayed compromised proliferation, and replication stress that could be rescued with an antioxi

281 gnaling suppresses endogenous DNA damage and replication stress.

282 le-strand break repair and resolution of DNA replication stress.

283 Replication studies and understanding the roles of these

284 ting that VP35 hijacks TRIM6 to promote EBOV replication through ubiquitination.

285 questions remain regarding the mechanisms of replication timing establishment and regulation.

286 erent cell lineages and present whole-genome replication timing profiles from cells in early, mid, an

287 the long-known effect of genomic context on replication timing to genome architecture.

288 s, Fkh1 and Fkh2, previously associated with replication timing.

289 ecific interactions need to be dissolved for replication to proceed.

290 a cell lines leads to an upregulation of HBV replication, transcription, and antigen expression.

291 Head-on replication-transcription conflict is especially bitter

292 ls, which display a robust decrease in viral replication upon infection with Vpr-deficient HIV-1.

293 dinating the intercellular movement of viral replication vesicles.

294 Evidence of elevated lytic EBV replication was also found in EBV/KSHV dually infected l

295 ble of expressing reporter genes while viral replication was blocked.

296 e who developed LTI; no difference in B cell replication was observed.

297 (6)A in regulating viral gene expression and replication was previously unknown.

298 fected cell protein synthesis and productive replication were reduced compared to levels in cells inf

299 hogens manipulate host organelles to support replication within cells.

300 no terminus of gamma134.5 undergoes temporal replication without production of infectious virus.