ライフサイエンスコーパス: slippage

1 e appreciably (a second regime of frictional slippage).

2 evel of folate-independent proton transport (slippage).

3 ating in the cell exiting mitosis by mitotic slippage.

4 he ribosome anticodon-codon interactions for slippage.

5 n oil tamponade with no incidence of retinal slippage.

6 inherently prone to further mis-pairing and slippage.

7 y because of high expansion rates due to DNA slippage.

8 ecrease up to two orders of magnitude due to slippage.

9 echanisms can cause both primer and template slippage.

10 tially increase the level of transcriptional slippage.

11 confirms elevated levels of transcriptional slippage.

12 ing of such variation due to DNA replicative slippage.

13 eletions were possibly caused by replication slippage.

14 dergo geared rotation preferentially to gear slippage.

15 g limited DNA damage and p53 induction after slippage.

16 damage late in mitotic arrest and also after slippage.

17 losely linked with susceptibility to mitotic slippage.

18 nctional mitotic checkpoint (MC) and mitotic slippage.

19 required for a functional MC or for mitotic slippage.

20 ascent transcript due to upstream transcript slippage.

21 BC and DE beta-turns results in beta-strand slippage.

22 hrough molecular rearrangement and fibrillar slippage.

23 tating ligation of hairpins formed by strand slippage.

24 are equilibrium model system for beta-strand slippage.

25 attached kinetochores, MTs do not accelerate slippage.

26 utations) resulting from DNA template-strand slippage.

27 depress the cyclin B destruction rate during slippage.

28 tion of CTG repeat concatemers due to strand slippage.

29 be satisfied, cells exit mitosis via mitotic slippage.

30 spindle checkpoint and couples with mitotic slippage.

31 othesized to have occurred by DNA polymerase slippage.

32 cation gaps as opposed to simple replication slippage.

33 (ZYG11) degrades cyclin B1, allowing mitotic slippage.

34 he sequence requirements for transcriptional slippage.

35 hinder DNA polymerases and provoke template slippage.

36 cilitating balance recovery after unexpected slippages.

37 ses), breakage (2.0%), early removal (1.4%), slippage (1.3%), or leakage (0.4%).

38 se-9 and -3 together accelerated the rate of slippage ~40% (to ~13-15 h).

39 Sequence slippage accounts for at least 52% of insertions and 38%

40 eutic efficacy of taxanes depends on whether slippage after SAC arrest culminates in continued cell s

41 us codons cannot be explained by replication slippage alone.

42 tal lattice whose motion results in material slippage along lattice planes.

43 n B, suggesting an increased rate of mitotic slippage and adaptation to the spindle checkpoint.

44 are associated with the combined effects of slippage and Ekman drift and/or surface drag; 59% are di

45 , CCNG1 depletion by RNA interference delays slippage and enhances paclitaxel-induced apoptosis.

46 and proposed an alternative mechanism of RNA slippage and extension requiring the sigma dissociation

47 , the regions in RNAP involved in elongation slippage and its molecular mechanism are unknown.

48 lid 'tribofilms', which together ensure easy slippage and long wear life.

49 GGS prevents band slippage and lower reintervention rate at 3 years.

50 For LAGB, band slippage and micronutrient deficiency were the most freq

51 nduces aberrant, multipolar mitoses, mitotic slippage and multinucleation, triggering an apoptotic ce

52 sequences, an apparent result of replication slippage and nonreciprocal recombination.

53 ood mutation biases, probably affecting both slippage and point mutations and often showing 3'-5' pol

54 translesion synthesis polymerases perform a slippage and realignment extension across from the damag

55 ing polymer chains may result in interfacial slippage and reduced performance.

56 ly, cells that are normally prone to mitotic slippage and resistant to spindle disruption-mediated mi

57 r repetitive sequences induce DNA polymerase slippage and stalling, leading to length and sequence va

58 rearrangement results from a combination of slippage and strand switching at sites of microhomology

59 , our findings implicate CCNG1 in regulating slippage and the outcome of taxane-induced mitotic arres

60 s to microsatellites in that DNA replication slippage and unequal crossover recombination are importa

61 Aurora-A promotes aberrant mitosis, mitotic slippage, and cell death.

62 ce that CAG . CTG expansions can occur by 3' slippage, and our results help define PRR as a key cellu

63 ein that directly influences transcriptional slippage, and provides a clue about the molecular mechan

64 erase eta: tandem base substitutions, strand slippage, and small insertions/deletions.

65 occur through base substitutions rather than slippage, and the relative probability of gaining versus

66 ar consequences of proofreading and membrane slippage are discussed as well as the impact on future d

67 ir dissociation, base unstacking, and strand slippage are discussed in the context of sequence depend

68 Such microfluidic devices with tunable slippage are essential for the amplified interfacial tra

69 extent of their functional utilization of RT slippage are merited.

70 ats that occur by replication misalignment ("slippage") are also DnaK dependent.

71 ch all influence the probability and rate of slippage, are the strongest predictors of mutability.

72 These results support DNA polymerase slippage as a common underlying mechanism, and they indi

73 from the aggregates into the film; and (ii) slippage as the film expands.

74 RNAP) undergoes promoter-proximal transcript slippage at 5' ends of transcription units, adding quasi

75 hown to depend on programmed transcriptional slippage at a conserved GAAAAAA sequence, resulting in t

76 l base-flipping can be sufficient for strand slippage at DNA duplex termini.

77 ne the effect of microbubble geometry on the slippage at high resolution.

78 ion error by polymerase zeta, and polymerase slippage at repeat junctions - on the generation of MNVs

79 balance between expansion due to polymerase slippage at repeated DNA sequences and point mutations c

80 transcriptases can be strong stimulators for slippage at slippage-prone template motif sequence 3' of

81 thin theoretical frameworks that incorporate slippage at the QCM surface electrode or alternatively a

82 icrosatellites as a surrogate measure of the slippage-based mutation rate to explore factors that inf

83 uggesting pairing of the inserted purine and slippage before further replication.

84 with weak van der Waals interaction, severe slippage between 2D material and substrate could dominat

85 One involves slippage between the cytoskeleton and adhesions, that de

86 observed anatomy consistent with replication slippage, but could only identify the germline microhomo

87 tations display the hallmarks of replication slippage, but lack suitable germline microhomology avail

88 is that G quadruplexes may cause replication slippage by blocking replication process.

89 i study complements an accompanying study of slippage by yeast RNAP II and provides the basis for fut

90 Transcriptional slippage can alter the coding capacity of mRNAs and is u

91 ation of simple repeat sequences, polymerase slippage can generate single-strand loops on either the

92 Such strand slippage can occur in either strand, i.e. near either th

93 am of the template is responsible for primer slippage, causing incorporation of strings of guanosines

94 cessful translocation attempts of the second slippage codon from the A- to the P- sites.

95 find that Dpo4 predominantly uses a template slippage deletion mechanism when replicating repetitive

96 itive mutants and were also isolated using a slippage-dependent reporter gene.

97 still not known for the decades-old template slippage description.

98 Retinal slippage did not occur in any case.

99 NAP translocation state as the main motor in slippage directionality and efficiency.

100 Slippage directionality, base insertion and omission, is

101 tors such as mobile elements, DNA polymerase slippage, DNA double-strand break, inefficient DNA repai

102 ly checkpoint (SAC), thus undergoing mitotic slippage due to defective AURKB and impaired SAC activit

103 st two different mechanisms, backward strand slippage during DNA replication and unequal crossing-ove

104 on the chromosome to examine transcriptional slippage during elongation.

105 Polymerase slippage during initiation of intermediate and late RNA

106 RNA lead to increased transcription complex slippage during initiation.

107 erse transcriptase (RT) result from template slippage during polymerization.

108 h we infer to result from a 'to-fro' form of slippage during positive-strand synthesis.

109 rapidly in cells and did not promote mitotic slippage during prolonged drug-induced mitotic arrest.

110 Thus, strand slippage during replication by wild type Pol delta may b

111 is still widely assumed that DNA polymerase slippage during replication plays an important role in t

112 sary for mitotic events and prevents mitotic slippage during spindle checkpoint activation.

113 The Knudsen diffusion and slippage effect play a dominant role in the later produc

114 In a purified in vitro system, the slippage efficiency ranges from 5% to 75% depending on t

115 This review catalogues several types of slippage errors, presents the cellular processes that ac

116 We provide evidence of a novel template slippage event during replication rescue.

117 lesion precedes and facilitates the selected slippage event.

118 The remaining four loci had no slippage events detected.

119 rally accepted to be a consequence of strand slippage events during DNA replication, which are uncorr

120 he nucleotide level, microsatellites undergo slippage events that alter allele length and base change

121 (29%) apparently originating from polymerase slippage events, in addition to frameshifts and point mu

122 winding was repeatedly interrupted by sudden slippage events, ultimately preventing unwinding over a

123 from the 3' terminus, presumably replication slippage events.

124 s/deletions originating from DNA replication slippage events.

125 g the scope for utilization of transcription slippage for gene expression, the stimulatory structure

126 Dme1_chrX_2630566, a candidate for utilizing slippage for its GagPol synthesis, exhibits strong slipp

127 s to cause premature securin degradation and slippage from an unsatisfied spindle assembly checkpoint

128 mbly defects and mitotic arrest, followed by slippage from mitotic arrest, multinucleation, and apopt

129 tments also inhibited induction of p53 after slippage from prolonged arrest.

130 Such slippage generates a front-back communication mechanism

131 be abandoned, as the associated risk of band slippage has not been prospectively assessed.

132 However, the sequence features that mediate slippage have not been characterized.

133 peat-mediated deletions involving polymerase slippage, homologous recombination, and nonhomologous en

134 er the first nucleotide is added by template slippage, however, hPolkappa can efficiently realign the

135 surface slippage in carbon nanotubes, and no slippage in boron nitride nanotubes that are crystallogr

136 xpectedly large and radius-dependent surface slippage in carbon nanotubes, and no slippage in boron n

137 the small molecule MLN4924, inhibits mitotic slippage in human cells, suggesting the potential for an

138 ted that the length threshold for polymerase slippage in mononucleotide runs is 4N.

139 ohomology (1-6 bp) anticipated to prime such slippage in one-third of FLT3-ITDs.

140 or the first time the phenomenon of a strand slippage in septins.

141 s numerous sequence variations, accommodates slippage in tertiary and secondary interactions, and exh

142 oxygen species (ROS) generation by electron slippage in the electron transfer chain.

143 -anchored motors is reduced because of their slippage in the lipid bilayer, an effect that we directl

144 in anaphase, tetraploidy, and faster mitotic slippage in the presence of a spindle inhibitor.

145 ransposon-derived enzyme TGIRT exhibits more slippage in vitro than the retroviral enzymes tested inc

146 ge for its GagPol synthesis, exhibits strong slippage in vitro.

147 dues in the beta subunit of RNAP that affect slippage in vivo and in vitro.

148 li RNAP mutants with altered transcriptional slippage in vivo.

149 g run-specific variation in the frequency of slippage, in the accumulation of +1 vs. -1 frameshifts a

150 ual mechanisms of mitotic arrest and mitotic slippage induced by antimitotics in tumors.

151 duction of in vitro noise through polymerase slippage inherent in DNA amplification, which we charact

152 , and actin filaments appear to constitute a slippage interface between the cytoskeleton and integrin

153 of double-strand breaks and represent strand-slippage intermediates consistent with Streisinger's cla

154 s in secondary DNA structure formed by their slippage intermediates.

155 Mitotic slippage involves cells exiting mitosis without proper c

156 We found that a major culprit for mitotic slippage involves reduction of MAD2 at the kinetochores,

157 Transcriptional slippage is a class of error in which ribonucleic acid (

158 Although replication slippage is a plausible explanation for tandem duplicati

159 Strand slippage is a structural mechanism by which insertion-de

160 tisfied on abnormal spindles and not because slippage is accelerated.

161 The observed eta(6)-eta(4) cage-slippage is analogous to the eta(5)-eta(3) ring-slippage

162 Whether mitotic slippage is caused by APC/C(CDC20) activity that is able

163 Replication slippage is induced at repetitive sequences that can be

164 element where the resulting transcriptional slippage is required for transposase synthesis.

165 Where slippage is stimulated, the resulting products have one

166 Because the probability of slippage is strongly correlated with run length, however

167 These analyses suggest that P-site tRNA slippage is the driving force for +1 ribosomal frameshif

168 er level of control of the timing of mitotic slippage is through p31(comet)-mediated suppression of M

169 t to the extent in which specific polymerase slippage is utilized in gene expression.

170 Loss of register, or transcriptional slippage, is particularly likely on homopolymeric runs i

171 itotic arrest is believed to trigger mitotic slippage, its upstream regulation remains obscure.

172 ng allowed the rate constant for P-site tRNA slippage (k(s)) to be estimated as k(s) approximately 1.

173 However, precocious mitotic exit by mitotic slippage limits the cytotoxicity of spindle poisons.

174 Structure-mediated slippage may be exhibited by other polymerases and enric

175 This slippage may be promoted by a loss of cohesive forces an

176 ther groups of organisms and that 'stem-ward slippage' may be a widespread but currently unrecognized

177 We have shown recently that a polymerase slippage mechanism at these sites could produce transcri

178 We have shown recently that a polymerase slippage mechanism can generate the transcript variants

179 eichenowi sequences implicates a replication slippage mechanism in the generation of TRs from an init

180 lian and archaeal orthologs, uses a template slippage mechanism to create single base deletions on ho

181 lkappa uses a classical Streisinger template-slippage mechanism to generate -1 deletions in repetitiv

182 wth conditions presumably through a ribosome slippage mechanism.

183 eading the template and by a primer-template slippage mechanism.

184 th template misreading and a primer-template slippage mechanism.

185 iated the duplication event by a replication slippage mechanism.

186 Such structures also inhibit slippage-mediated base omission which can be more freque

187 sults reveal a major influence of Glu(89) on slippage-mediated errors and dNTP incorporation fidelity

188 We propose a mechanical slippage model involving the RNAP translocation state as

189 APN2 also suppresses 2-base pair (bp) slippage mutagenesis in RNH201-deficient cells.

190 Slippage mutations reveal rather similar patterns of mut

191 d reverse complement sequences suggests that slippage occurs preferentially during synthesis of poly(

192 Transcript slippage occurs when an RNA transcript contains a repeti

193 eline was also an independent risk factor of slippage (odds ratio 2.769, 95% confidence interval 1.37

194 d) suggesting that Glu(89) can influence the slippage of both strands.

195 Slippage of elongating RNA polymerase (RNAP) on homopoly

196 dressing the problem about the target period slippage of ENSO.

197 Slippage of mRNA is suppressed by 3' truncation of the t

198 s, which is potentially important to prevent slippage of mRNA.

199 Slippage of muscles can be prevented by effective suturi

200 RPICIOLs occurred in three cases because of slippage of one of the iris-claw haptics and spontaneous

201 localized hypermutation, through polymerase slippage of simple sequence repeats (SSRs), to generate

202 chanism of this variable expression involves slippage of tetranucleotide repeats located within the r

203 This could be due to slippage of the brace during use, increased fatigue due

204 rocesses, probably acting in concert, due to slippage of the DNA complementary strands relative to ea

205 a role for these structures in promoting the slippage of the DNA complementary strands.

206 We observed frequent slippage of the helicase, which is fully suppressed by t

207 rves as a shield to guard against occasional slippage of the leading strand from the core channel.

208 anticodon pairing in the P site and promotes slippage of the mRNA in the 5' direction.

209 splacements of >50 nm, stalls, and backwards slippage of the MT even under low loads.

210 c site, but can readily bypass the lesion by slippage of the primer 3' di- or trinucleotide and reali

211 end of a nascent transcript due to upstream slippage of the transcript without movement of the DNA t

212 Ribosomal frameshifting entails slippage of the translational machinery during elongatio

213 srupted in the absence of EF-G, resulting in slippage of the translational reading frame.

214 e supporting crankshaft rotation rather than slippage of the trityl groups was obtained from molecula

215 s indicated that the PRF occurred through +1 slippage of the tRNA(phe) from UUU to UUC within a conse

216 y A site and EF-G action either leads to the slippage of the tRNAs into the -1 frame or maintains the

217 t adenosine repeats erroneously generated by slippage of the viral RNA polymerase confer a translatio

218 the poly(rA/dT) tract and leads to base-pair slippage of this sequence upon deformation into a cataly

219 a new insight into the mechanism of mitotic "slippage" of the arrested cells.

220 n be effectively transferred with negligible slippage or decoupling.

221 reading the template, as opposed to a primer slippage or dislocation mutagenesis mechanism.

222 t skips the templating base, without causing slippage or flipping out of the base, to incorporate a c

223 on of a UvrD monomer along ssDNA with little slippage or futile ATP hydrolysis during translocation.

224 uses, including those that contain ribosomal slippage or RNA editing without prior knowledge of the v

225 whether shorter runs were unable to support slippage or whether the resulting frameshifts were obscu

226 the trypanosome are reminiscent of "mitotic slippage" or endoreplication observed in some other euka

227 rmal cell division (endoreplication, mitotic slippage, or cytokinesis failure).

228 ence for dGTP insertion is explained by a 5'-slippage pattern in which the unmodified G rather than G

229 The 5'-slippage pattern may be generally facilitated in cases w

230 side of the adduct G 1*, using an unusual 5'-slippage pattern, in which the unadducted G 2, rather th

231 NA anticodon dissociates, and following mRNA slippage, peptidyl-tRNA re-pairs to mRNA at a matched tr

232 s, malpositioned bands, pouch dilation, band slippage, perforation, gastric volvulus, intraluminal ba

233 on for pouch-related problems including band slippage, pouch dilation, and hiatal hernia were studied

234 at replacement of the U tract in TPhi with a slippage-prone A tract still allows efficient terminatio

235 stant HT29 or by enforcing mitotic arrest in slippage-prone DLD-1 cells, evokes a switch in fate, ind

236 phosphorylation and die in mitosis, whereas slippage-prone DLD-1 colon carcinoma cells display weak

237 ratio of dNTPs specified by the RNA template slippage-prone sequence and its 5' adjacent base.

238 ratio of dNTPs specified by the RNA template slippage-prone sequence and its 5' adjacent base.

239 Transcriptional realignment at slippage-prone sequences also generates productively uti

240 This polymerase has a slippage-prone spacious active site region.

241 es can be strong stimulators for slippage at slippage-prone template motif sequence 3' of such 'slipp

242 % vs11.3%; P = 0.013), partly because of the slippage rate (10.3% vs 3.6%; P = 0.005).

243 llow chimps to have a larger per-repeat unit slippage rate and/or a shorter focal length compared to

244 The slippage rate is determined by the electrodynamic coupli

245 Alleles of RPB1 (RPO21) with elevated slippage rates were identified among 6-azauracil-sensiti

246 ly creates single-base deletions by template slippage rather than by dNTP-stabilized misalignment.

247 ith a dinucleotide repeat sequence, sequence slippage re-alignment followed by Top1-mediated religati

248 reporter in the DNA substrate, the template slippage reaction results in a prechemistry fluorescence

249 In microtubule (MT) poisons, slippage requires cyclin B proteolysis, and it appears t

250 cts, the RNA structure requirements for this slippage resemble those for hairpin-dependent transcript

251 We show that when treated with Taxol, slippage-resistant HT29 colon carcinoma cells display ro

252 naling axis, either by inhibition of Cdk1 in slippage-resistant HT29 or by enforcing mitotic arrest i

253 Primer-template DNA slippage resulting in single nucleotide deletions is a b

254 phosphoUb conformation in which beta5-strand slippage retracts the C-terminal tail by two residues in

255 nomic evidence underscores the importance of slippage retrotransposition in the alteration and expans

256 n ratios of the nucleotides specified by the slippage sequence and the 3' nt context.

257 ith and without an error-prone transcription slippage sequence), partial phenotypic suppression of a

258 page site, the length and composition of the slippage site motif, and the identity of its 3' adjacent

259 cture, the proximity of the stem loop to the slippage site, the length and composition of the slippag

260 he GGG sequence 3' adjacent to the U6A shift/slippage site, which is important for ribosomal frameshi

261 ge-prone template motif sequence 3' of such 'slippage-stimulatory' structures.

262 isadvantages such as an excessive polymerase slippage ("stutter") that causes difficulties in automat

263 gth, suggesting that processes additional to slippage, such as faulty repair, contribute to mutations

264 ion G2252U of the 50S P site stimulates mRNA slippage, suggesting that decreased affinity of tRNA for

265 3-only protein Puma is induced after mitotic slippage, suppression of de novo protein synthesis that

266 The results reveal that slippage synthesis occurs from the majority of TSS-regio

267 for TSS selection, reiterative initiation ("slippage synthesis"), and transcript yield; and we defin

268 xes that can readily carry out homopolymeric slippage synthesis, this study reveals that T7 RNA polym

269 ut not adjacent sequences in contrast to the slippage that characterizes the great majority of pure m

270 ppage is analogous to the eta(5)-eta(3) ring-slippage that has been proposed to take place in related

271 and probably intralamellar displacement and slippage that leads to thinning of the central cornea an

272 consistent with partial eta(5)-eta(3) ligand slippage that occurs in the transition state of the sele

273 n a dynamic fashion, causing configurational slippage that often leads to repeat expansion associated

274 second toxic molecule that is more prone to slippage, the overall substrate selectivity dramatically

275 eotidyl transferase (TdT) primes replication slippage through N-nucleotide addition, with longer synt

276 ubR1, presumably allowing APC/C activity and slippage through the checkpoint.

277 tripolar mitosis was transformed to mitotic slippage, thus eliminating a sub G1 peak.

278 but taxane-exposed cells eventually undergo slippage to exit mitosis.

279 other invokes a process akin to replication slippage to form a chimeric gene in a single event.

280 of MDB provides possible pathways for strand slippage to occur, which ultimately leads to repair esca

281 n that duplications can occur by replication slippage, unequal sister chromatid exchange, homologous

282 ognitive perception and for preventing their slippage using predictive control of grip force.

283 template backbone near the proposed site of slippage via the Glu(89) side chain.

284 t detected, and the propensity for sustained slippage was also found to be lower.

285 ), consistent condom use without breakage or slippage was associated with significantly reduced risk

286 Slippage was markedly increased for the H247A-PCFT mutan

287 irradiating the complex 1 subset2c, and ring slippage was revealed.

288 To determine if MTs accelerate slippage, we followed mitosis in human RPE-1 cells expos

289 that act independently of mitotic arrest or slippage, were assessed in the tumor biopsies.

290 y build force and fail (so-called frictional slippage), whereas at low substrate stiffness, clutches

291 Stem-ward slippage, whereby fundamental taphonomic biases cause fo

292 osed that these mutations result from strand slippage, which in repetitive sequences generates misali

293 Lack of back-bonding facilitates alkyne slippage, which is energetically less costly for gold th

294 only previous proposal of stem loop mediated slippage, which was in Ebola virus expression, was based

295 en exit mitosis in a process termed "mitotic slippage," which generates tetraploid cells and limits t

296 in functions as a gatekeeper, preventing DNA slippage, whilst allowing its passage into the capsid, a

297 edicts two distinct regimes: (i) "frictional slippage," with fast retrograde flow and low traction fo

298 nd IOL subluxation (3 [13%]) owing to haptic slippage within 3 months of the procedure.

299 age lambda N protein reduces transcriptional slippage within actively growing cells and in vitro.

300 ingle-base deletions through template-strand slippage within short repetitive DNA regions much more r