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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
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
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
57 into a murine coronavirus and evaluated the replication and pathogenesis of the DUB mutant virus (DU
59 3p miRNA as a strong inhibitor of Salmonella replication and performing in-depth analysis of its mech
62 ctions in both nuclear and mitochondrial DNA replication and repair processes, preferentially unwindi
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
72 population by interfering with normal virus replication and/or by stimulating the innate immune resp
75 oplasmic proteins involved in DNA packaging, replication, and protein synthesis were detected at lowe
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
89 Here, we show that cells survive retroviral replication, both in vitro and in vivo in SIVmac-infecte
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
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
99 nd co-opted host proteins within large viral replication compartments in the cytosol of infected cell
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
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
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
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
125 s CtBP interacting protein (CtIP) to promote replication fork restart while suppressing new origin fi
127 ia pathway of ICL repair is activated when a replication fork stalls at an ICL(2); this triggers mono
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
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,
145 smic sites of nucleocapsid formation and RNA replication, housing key steps in the virus life cycle t
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
153 in the RV-A16 2C protein allowed for robust replication in cells expressing mSTING, suggesting a rol
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
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
164 L2 expression, leading to restriction of HIV replication in macrophages.IMPORTANCE HIV continues to b
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
170 knockdown and Tim-3 blockade increased HIV-1 replication in primary CD4(+) T cells, thereby suggestin
175 ation attenuates TMUV through reducing viral replication in the blood, brain, heart (ducklings), and
180 ponsible for the viral RNA transcription and replication in the nucleus, and its functions rely on ho
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
185 confirmed to effectively inhibit SARS-CoV-2 replication in vitro with EC50 values of 0.008muM and 9.
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
197 ve-sense viral RNA, a marker of active viral replication, is found predominantly in intestinal epithe
199 However, SP-2509 does inhibit viral DNA replication, late gene expression, and virus production.
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
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
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
219 DNA polymerases (Pols) provide roles in both replication of the genome and the repair of a wide range
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
228 on, which allows DnaA oligomerization at the replication origin but the association state remains unc
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
235 mulate the rules that govern the coupling of replication processes to alternative recognition-mediate
237 case complexes (VRCs) with the help of viral replication proteins and co-opted host proteins within l
247 nd kasugamycin and CGS 15943 blocked plasmid replication, respectively, by inhibiting expression or f
250 protein systems to investigate viral genome replication, RNA-binding affinity, ATP hydrolysis activi
252 f depression (discovery sample, N=30; active replication sample, N=81; sham replication sample, N=87)
258 th respect to viral origin, transmission and replication strategies of the virus, and interactions be
261 nstrated that absence of SMC5/6 leads to DNA replication stress at late-replicating regions such as p
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
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
271 stalled forks and promote survival following replication stress, uncovering an unexpected link betwee
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
280 interferon signaling pathway, we found that replication termination factor 2 (RTF2) restricts influe
282 The data provide direct evidence that self-replication through secondary nucleation occurs along th
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
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,
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
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