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1  thus helps suppress their interference with replication.
2 s a cellular factor required for enterovirus replication.
3  during vacuole biogenesis and intracellular replication.
4 d the consequences of PDS5 depletion for DNA replication.
5 longation activities and essential for viral replication.
6 ty began their evolutionary path toward self-replication.
7 ukaryotic cell-cycle kinases controlling DNA replication.
8 ve a direct inhibitory effect on C. burnetii replication.
9  by interacting with the EBV lytic origin of replication.
10 ing RT maturation and interfering with viral replication.
11 the template of ribosomes to allow efficient replication.
12 ic leukemia (PML) protein, which limits ZIKV replication.
13 ell motility, signal transduction, and virus replication.
14  3CL protease, an enzyme essential for viral replication.
15 docytosis, genome assembly, translation, and replication.
16 rmed on day four to confirm absence of virus replication.
17  augmented AMPK activity and attenuated ZIKV replication.
18   Here, we report its activity against viral replication.
19 he phosphoprotein (P), for transcription and replication.
20 ated Bro1 proteins are dispensable for HSV-1 replication.
21 ating pathways the virus manipulates for its replication.
22 of the helicase DnaB onto the DNA to restart replication.
23 ble strand breaks (DSBs) that interfere with replication.
24 tionary history and certain aspects of viral replication.
25 iation with PMA, supported an enhanced viral replication.
26  efficient HIV-1 transcription, release, and replication.
27 hase causes an early switch and inhibits DNA replication.
28 strand as it exits the polymerase during RNA replication.
29 d, providing a second opportunity to inhibit replication.
30 s required for restricting influenza A virus replication.
31 ly affects ZIKV protein expression and viral replication.
32 ucing type I interferons, which limits virus replication.
33 ron response in cells undergoing lytic virus replication.
34 e PEL cell viability and regulate productive replication.
35 ALSPAC birth cohort was used for independent replication.
36 sing cell death prior to completion of phage replication.
37  complex with Brd4 does not support episomal replication.
38  the susceptibility of CD4+ T cells to HIV-1 replication.
39 targeting of USP7 regulates HHV-8 productive replication.
40 on interferes with the response to perturbed replication.
41 s, of which experiment 2 was a preregistered replication, 160 toddlers (aged 25 to 32 months) identif
42                               Based on their replication ability in G3BP-deleted cells, Old World alp
43 istically, 6-4PPs, but not CPDs, impeded DNA replication across the genome as revealed by microfluidi
44    Here, we investigated whether reduced HCV replication after pregnancy is associated with recovery
45 nction of Nef has a positive effect on HIV-1 replication, allowing for more efficient replication whi
46     We also expanded these observations with replication analyses in a large biorepository database.
47                                              Replication analyses were conducted using a large biorep
48                                              Replication analysis using genetic instruments from a di
49 ein (pH 5.5-5.6) was necessary for efficient replication and airborne transmission.
50 d composition results in a complete cycle of replication and asymmetrical RNA synthesis, which is a h
51 een monkeys (AGMs) support robust SARS-CoV-2 replication and develop pronounced respiratory disease,
52  sarcoma-associated herpesvirus (KSHV) lytic replication and directly activate viral interleukin-6 (v
53  required host factor for both DENV and ZIKV replication and further contribute to our understanding
54  that is broadly effective in limiting virus replication and in suppressing the pro-inflammatory resp
55 hages with LVS-immune lymphocytes halted LVS replication and inhibited the spread of LVS infection be
56 in several cellular processes, including DNA replication and metabolism.
57  into a murine coronavirus and evaluated the replication and pathogenesis of the DUB mutant virus (DU
58 amics in neurons, thereby facilitating viral replication and pathogenesis.
59 3p miRNA as a strong inhibitor of Salmonella replication and performing in-depth analysis of its mech
60 increasing NR4A1 expression and allowing VZV replication and propagation.
61  DNA2 is an essential enzyme involved in DNA replication and repair in eukaryotes.
62 ctions in both nuclear and mitochondrial DNA replication and repair processes, preferentially unwindi
63 he presence of cycloheximide to block genome replication and secondary transcription.
64 urb host cellular metabolism to enable their replication and spread.
65 ion, A. baumannii must acquire nutrients for replication and survival.
66 y on the strand-specific role of Pole in DNA replication and the action of extrinsic correction syste
67 M helicase protein plays a vital role in DNA replication and the maintenance of genomic integrity.
68 fe cycle to provide favorable conditions for replication and to avoid the litany of antiviral detecti
69   We demonstrate that SMARCB1 regulates both replication and transcription activator (RTA) activity a
70 driver of this phenotype and that both viral replication and transcription are affected.
71 -1 (RPS6KB1) was shown to play a role in MuV replication and transcription.
72  population by interfering with normal virus replication and/or by stimulating the innate immune resp
73 er, the host factors critical for its entry, replication, and assembly are poorly understood.
74 ls that regulate cell cycle progression, DNA replication, and cell survival.
75 oplasmic proteins involved in DNA packaging, replication, and protein synthesis were detected at lowe
76  nuclease family are crucial for DNA repair, replication, and recombination.
77 osome linkage, advances the timing of genome replication, and reduces reproductive fitness by 45%.
78 id therapeutic tools to control virus entry, replication, and spread as well as to impair its lethal
79 letion of Mdm4 and Mdm2 further impaired DNA replication, and the overexpression of each partially co
80 ed to guide chemical analysis, to improve de-replication, and to identify ecosystems with promising c
81 In conclusion, both HBsAg production and HDV replication are effectively inhibited by REP 2139-Ca.
82 ed recovering BLBCs to AZD1775 by abrogating replication arrest, allowing replication despite DNA dam
83  positive and negative effects on KSHV lytic replication as well as effects on the host cell that enh
84  of the BBB, its ability to potentiate viral replication, as well as current therapies and insufficie
85 ays a key role in gene regulation and genome replication, as well as maintaining genome integrity.
86 phorylation of DNA-PK, protecting cells from replication-associated DNA damage and promoting cellular
87 d that the acquired G mutations improved VSV replication, at least in part due to improved virus atta
88 unction can be used as an indicator of viral replication before detectable plasma viremia.
89  Here, we show that cells survive retroviral replication, both in vitro and in vivo in SIVmac-infecte
90 retroviral therapies efficiently block HIV-1 replication but need to be maintained for life.
91 ese results indicate that PARP1 promotes IAV replication by controlling viral HA-induced degradation
92 ion of the MCM6 gene that is involved in DNA replication by directly binding to specific motifs withi
93                                        Viral replication can be blocked by antiretroviral therapy.
94 rrant RNA products of influenza virus genome replication can trigger retinoic acid-inducible gene I (
95 d PTEN and DNA-PK as essential regulators of replication checkpoint arrest in response to AZD1775 and
96                                        For a replication cohort, we meta-analyzed data from 36 cohort
97 ort, two of which were weakly supported in a replication cohort.
98                                       In the replication cohorts, multiple SNPs in strong linkage dis
99 nd co-opted host proteins within large viral replication compartments in the cytosol of infected cell
100 essing gibberellin production to condition a replication competent state.
101 nces, suggestive of a cell clone harboring a replication-competent provirus.
102                         Plasma virus matched replication-competent virus cultured from CD4+ T cells.
103 mitochondrial genomes and sets the stage for replication competition.
104 pment of specialized domains harboring viral replication complexes, replication organelles.
105 hat inhibition of BRD4 induces transcription-replication conflicts, DNA damage, and cell death in onc
106 icate only once in coordination with the DNA replication cycle and have an important role in segregat
107 e essential for multiple phases of the viral replication cycle.
108 ides in the context of the entire nairovirus replication cycle.
109 sociated with ADHD risk in the discovery and replication data sets.
110 (adjusted OR = 2.61, P = 7.98 x 10(-22)) and replication datasets (adjusted OR = 1.55, P = 0.06) with
111 sly showed that maternal immunization with a replication-defective HSV vaccine candidate, dl5-29, lea
112            Most of them were generated using replication-deficient lentiviruses, a technique that pre
113                                              Replication-dependent histones (RDH) are required for pa
114 5 by abrogating replication arrest, allowing replication despite DNA damage.
115  By regulating DNA access for transcription, replication, DNA repair, and epigenetic modification, ch
116 ps of conjugative transfer, DNA transfer and replication (Dtr) proteins assemble at the origin-of-tra
117 mary macrophages and one that inhibits virus replication during reverse transcription.
118 y analysis can be used to reveal the average replication dynamics using copy-number analysis in any p
119 own mutational mechanisms - CpG deamination, replication error by polymerase zeta, and polymerase sli
120 urveilles the DNA, and upon recognition of a replication error it undergoes adenosine triphosphate-de
121           RNA-protein interfaces control key replication events during the HIV-1 life cycle.
122 endonuclease Mus81 from cleaving the stalled replication fork inappropriately.
123 work of interactions important for efficient replication fork pausing.
124 nly full-length Mdm4 was able to support DNA replication fork progression.
125 s CtBP interacting protein (CtIP) to promote replication fork restart while suppressing new origin fi
126 ve sister chromatid cohesion and reduced DNA replication fork speed.
127 ia pathway of ICL repair is activated when a replication fork stalls at an ICL(2); this triggers mono
128             Instead of utilizing a canonical replication fork, BIR is driven by a migrating D-loop an
129 itment of error-prone DNA polymerases to the replication fork.
130 n in BRCA2-deficient cells protected stalled replication forks (RFs).
131  pathway protein, FANCD2, locates to stalled replication forks and recruits homologous recombination
132 iously found that LSD1 associates with HSV-1 replication forks and replicating viral DNA, suggesting
133               In this Review, we discuss how replication forks are actively stalled, remodelled, proc
134               Without this response, stalled replication forks are not stabilized, and new origin fir
135                                      Stalled replication forks can be restarted and repaired by RAD51
136             FAM111A, but not SPRTN, protects replication forks from stalling at poly(ADP-ribose) poly
137 pression on hydroxyurea (HU)-induced stalled replication forks in the setting of BRCA1 deficiency.
138 PriA can recognize and remodel abandoned DNA replication forks, unwind DNA in the 3'-to-5' direction,
139 ficient cells by acetylating H4K8 at stalled replication forks, which recruits MRE11 and EXO1.
140 itigating the effect of protein obstacles on replication forks.
141 and tight nucleoprotein complexes, can block replication forks.
142 catalytic activity and symmetric movement of replication forks.
143 ase RECQ1, which promotes restart of stalled replication forks.
144 ion in transfected cells, with initiation of replication from the upstream genome copy.
145 smic sites of nucleocapsid formation and RNA replication, housing key steps in the virus life cycle t
146                        Instead, we show that replication hurdles, including secondary structures in t
147 t lipids for structural support, metabolism, replication, immune evasion, and disease severity.
148 e is an urgent need for information on virus replication, immunity and infectivity in specific sites
149 ntiviral effects and promote efficient viral replication.IMPORTANCE Host cells mount a response to cu
150 ation of viral mRNA processing and viral DNA replication.IMPORTANCE Human bocavirus 1 (HBoV1) is one
151 ively regulates autophagy to facilitate ZIKV replication.IMPORTANCE The re-emergence of Zika virus (Z
152 haped helicase unwinds DNA during chromosome replication in all organisms.
153  in the RV-A16 2C protein allowed for robust replication in cells expressing mSTING, suggesting a rol
154 , defines the localization of the origins of replication in eukaryotes.
155 licate this, these viruses are restricted to replication in human cells and tissues, making them diff
156 16/B22 and C12 proteins together promote MVA replication in human cells to levels that are comparable
157 V-2 strain, and found that it enhances viral replication in human lung epithelial cells and primary h
158 we demonstrate Vpr-dependent rescue of HIV-1 replication in human macrophages from inhibition by cGAM
159  and apilimod were found to antagonize viral replication in human pneumocyte-like cells derived from
160 e immune responses play in early mucosal HIV replication in humans.
161 CE Host cells mount a response to curb virus replication in infected cells and prevent spread of viru
162 iched viral RNA binders, restrict SARS-CoV-2 replication in infected cells and provide a global map o
163 r degradation, leading to restriction of HIV replication in macrophages.
164 L2 expression, leading to restriction of HIV replication in macrophages.IMPORTANCE HIV continues to b
165 ifferences are unable to explain the lack of replication in Markel, 2020.
166 h the mutant virus showed slightly decreased replication in mice, it was not observed in cell culture
167 nteractions and adaptability of the virus to replication in mosquitoes and mammalian hosts is still e
168 e inactivated C16L/B22R gene of MVA enhances replication in numerous human cell lines.
169 tivity long after the period of active viral replication in peripheral blood.
170 knockdown and Tim-3 blockade increased HIV-1 replication in primary CD4(+) T cells, thereby suggestin
171 r activity of diverse HIV-subtypes and HIV-1 replication in primary T cells.
172                   RT-qPCR demonstrated viral replication in salmon brains up to 15 days postinjection
173          To assess the contribution of CHIKV replication in skeletal muscle cells to pathogenesis, we
174                       They can promote viral replication in the absence of FXR-HVD interactions albei
175 ation attenuates TMUV through reducing viral replication in the blood, brain, heart (ducklings), and
176 ae and some with persistent, low-level viral replication in the CNS.
177  transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells.
178  RSV-infected mice, without increasing viral replication in the lung.
179                    A subsequent burst of DNA replication in the next mitosis generates extensive DNA
180 ponsible for the viral RNA transcription and replication in the nucleus, and its functions rely on ho
181 IV-1 LTR promoter and facilitate HIV-1 viral replication in the nucleus.
182 ineered a CHIKV strain exhibiting restricted replication in these cells via incorporation of target s
183 us (CMV) promoter confirms autonomous genome replication in transfected cells, with initiation of rep
184 vage site in SARS-CoV-2 did not affect virus replication in Vero or Vero-E6 cells.
185  confirmed to effectively inhibit SARS-CoV-2 replication in vitro with EC50 values of 0.008muM and 9.
186 uently dissociate from replisomes during DNA replication in vivo.
187 ing the generalizability of results requires replications in independent samples.
188                                          DNA replication initiates from multiple genomic locations ca
189 biting expression or function of the plasmid replication initiation protein, RepE.
190  essential for replisome assembly during DNA replication initiation that is vulnerable to inhibition
191 unit origin recognition complex (ORC), a DNA replication initiator, defines the localization of the o
192 ominant anammox bacterium showed an index of replication (iRep) of 1.32, suggesting that 32% of this
193 al approaches are relatively common, spatial replication is generally low and unlikely to provide suf
194                                       Genome replication is initiated from specific origin sites esta
195                             In addition, DNA replication is required to maintain full Pol II occupanc
196 ted sample numbers in this study, additional replication is suggested for a clinical setting.
197 ve-sense viral RNA, a marker of active viral replication, is found predominantly in intestinal epithe
198 ar plaque morphology, viral RNA profile, and replication kinetics.
199      However, SP-2509 does inhibit viral DNA replication, late gene expression, and virus production.
200             RPS6KB1 negatively regulates MuV replication, likely through its interaction with the P p
201 rimed/prolytic state, turn expression of the replication/lytic/reactivation switch protein on to ente
202 ker scaffolds coupled to the polymerase/dNTP replication machinery leads, in the presence of a primer
203 l cycle organization to chromosome ploidy to replication mode and nature of the replicative polymeras
204 ty, we also found that T3D/T1L L3S2 launches replication more efficiently and produces higher yields
205 ive for Integrative Psychiatric Research for replication (N=37,076).
206            Both cohorts (discovery: n = 182; replication: n = 326) included treatment-seeking youth w
207  kinases and cholesterol homeostasis reduced replication of all three coronaviruses.
208                                              Replication of both strains is sensitive to exogenous ad
209 umulates, beginning with aberrant interphase replication of bridge DNA.
210 ition to the inhibition of the intracellular replication of HIV by autophagy, trehalose decreased vir
211 ic host defense mechanism that restricts the replication of intravacuolar pathogens such as Salmonell
212 ets are cellular organelles critical for the replication of many viral and bacterial pathogens, and t
213  using different kernels with shared inputs, replication of multiple identical kernels in memristor a
214  barrier by Pif1 could lead to the futile re-replication of newly synthetized DNA.
215                                 However, the replication of oligonucleotides long enough to encode ca
216 d chambers allowed for perfusion and enabled replication of pressure/volume relationships fundamental
217 bitory effect of 4-OI and DMF extends to the replication of several other pathogenic viruses includin
218                                Intracellular replication of the deadly pathogen Mycobacterium tubercu
219 DNA polymerases (Pols) provide roles in both replication of the genome and the repair of a wide range
220 are synthesized, processed and joined during replication of the human genome.
221                            The non-enzymatic replication of the primordial genetic material is though
222 the presence of a primer, P(1), to the gated replication of the scaffolds and to the displacement of
223 otein shell (or capsid) is a key step in the replication of viruses and in the production of artifici
224 ting that it may play a direct role in viral replication or coupled processes.
225 ting a possible defect at the level of viral replication or later in the lytic cascade.
226 mains harboring viral replication complexes, replication organelles.
227 ng a role for 2C in recruiting STING to RV-A replication organelles.
228 on, which allows DnaA oligomerization at the replication origin but the association state remains unc
229                                   Eukaryotic replication origins are licensed by the loading of the r
230              The selection and firing of DNA replication origins play key roles in ensuring that euka
231 iates from multiple genomic locations called replication origins.
232 embrane fusion, has been associated with the replication, pathogenicity, transmissibility, and inters
233 lows a wildtype response to various forms of replication perturbation and DNA damage in S phase, sugg
234                                   Conceptual replications play an important but separate role in vali
235 mulate the rules that govern the coupling of replication processes to alternative recognition-mediate
236                                              Replication protein A (RPA), a major eukaryotic ssDNA-bi
237 case complexes (VRCs) with the help of viral replication proteins and co-opted host proteins within l
238 h rolling circle and rolling circle-like DNA replication proteins.
239 ects is the major factor that determines the replication rate of scientific results.
240  has important roles including aiding normal replication rates and stabilizing stalled forks.
241 trast, in an HLTF-HIRAN mutant, unrestrained replication relies on the TLS protein REV1.
242  domain of NP (NP-Ct), but its role in virus replication remained unclear.
243                            We find that post-replication remethylation rate constants span approximat
244           Strand slipped hairpins during DNA replication, repair and/or recombination may contribute
245  processes that involve ssDNA, including DNA replication, repair, and damage signaling.
246            Our results demonstrate that ZIKV replication requires the activation of both mTORC1 and m
247 nd kasugamycin and CGS 15943 blocked plasmid replication, respectively, by inhibiting expression or f
248 ion-coupled homologous recombination and DNA replication restart.
249                                          DNA replication results in an increase in DNA copy number th
250  protein systems to investigate viral genome replication, RNA-binding affinity, ATP hydrolysis activi
251                 Evidence from an independent replication sample (N = 50; 10 females) further substant
252 f depression (discovery sample, N=30; active replication sample, N=81; sham replication sample, N=87)
253  N=30; active replication sample, N=81; sham replication sample, N=87).
254  profiles for all three CT signatures in the replication sample.
255 g or weak IRs based on the strength of their replication signals.
256                                     MERS-CoV replication significantly upregulated C-type lectin rece
257 es to exploit the IFN-alpha response for its replication, spread, and pathogenic function.
258 th respect to viral origin, transmission and replication strategies of the virus, and interactions be
259  sublethal ethanol concentrations causes DNA replication stress and an increased mutation rate.
260               Importantly, H. pylori-induced replication stress and DNA damage depend on the presence
261 nstrated that absence of SMC5/6 leads to DNA replication stress at late-replicating regions such as p
262                                         Mild replication stress enhances appearance of dozens of robu
263 e and DNA replication timing (RT) under mild replication stress in the context of the 3D genome organ
264 luding elevated microtubule dynamics and DNA replication stress that can be partially rescued to redu
265                                              Replication stress was enriched in the squamous subtype
266                               In response to replication stress, certain loci, such as common fragile
267 yperactive or expedited S phase entry causes replication stress, DNA damage and oncogenesis, highligh
268   In addition to chromosomal instability and replication stress, Gcna mutants accumulate DNA-protein
269 rise from the aberrant repair of spontaneous replication stress, however successful fragile site repa
270              Parallel populations adapted to replication stress, over 1000 generations, by acquiring
271 stalled forks and promote survival following replication stress, uncovering an unexpected link betwee
272 e strand break (DSB) repair and in resolving replication stress.
273 adation, collapse, and cell sensitivity upon replication stress.
274 omal segregation under certain conditions of replication stress.
275 demonstrated that FACT is needed to overcome replication stress.
276                                              Replication studies were performed in 188 patients diagn
277 with low-dose IFNs show a reduction in viral replication, suggesting the prophylactic effectiveness o
278 the role of Wisp1 as an inducer of beta cell replication, supporting the idea that the use of young b
279                                Transcription-replication (T-R) conflicts are profound threats to geno
280  interferon signaling pathway, we found that replication termination factor 2 (RTF2) restricts influe
281                                   During DNA replication, the genetic information of a cell is copied
282   The data provide direct evidence that self-replication through secondary nucleation occurs along th
283 ) plays a key role in the resolution of, and replication through, telomeric G-quadruplexes.
284  explore the transcriptional profile and DNA replication timing (RT) under mild replication stress in
285 hat while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much more sens
286  genome as revealed by microfluidic-assisted replication track analysis.
287 thways controlled by (pp)pGpp, including DNA replication, transcription, nucleotide synthesis, riboso
288 HV-infected LECs predominantly entered lytic replication, underwent cell lysis, and released new viru
289 nstrated by an essential role in forming the replication vacuole of Legionella pneumophila bacteria,
290  considerably; four studies used traditional replication/validation cohorts.
291                       Despite widely varying replication vesicle diameters, the resulting two rings o
292                                     No viral replication was detectable in the nose of any of the eig
293 anding of the regulatory mechanisms of HIV-1 replication, we adapted a recently described system to v
294 determine how CpG dinucleotides affect HIV-1 replication, we increased their abundance in multiple re
295                                         As a replication, we performed follow-up targeted sequencing
296 , pH of fusion, thermal stability, and virus replication were investigated.
297 aired eG contexts, which can form during DNA replication, were similarly poor substrates for AAG.
298 riers may be beneficial during break-induced replication where barriers are expected to pose a proble
299 V-1 replication, allowing for more efficient replication while potentially contributing to HIV-1 path
300 duction of Myc expression enhances beta-cell replication without induction of cell death or loss of i

 
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