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 echanisms can cause both primer and template slippage.

4 tially increase the level of transcriptional slippage.

5 confirms elevated levels of transcriptional slippage.

6 ing of such variation due to DNA replicative slippage.

7 eletions were possibly caused by replication slippage.

8 dergo geared rotation preferentially to gear slippage.

9 g limited DNA damage and p53 induction after slippage.

10 damage late in mitotic arrest and also after slippage.

11 losely linked with susceptibility to mitotic slippage.

12 nctional mitotic checkpoint (MC) and mitotic slippage.

13 required for a functional MC or for mitotic slippage.

14 ascent transcript due to upstream transcript slippage.

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

16 hrough molecular rearrangement and fibrillar slippage.

17 tating ligation of hairpins formed by strand slippage.

18 are equilibrium model system for beta-strand slippage.

19 attached kinetochores, MTs do not accelerate slippage.

20 utations) resulting from DNA template-strand slippage.

21 depress the cyclin B destruction rate during slippage.

22 tion of CTG repeat concatemers due to strand slippage.

23 be satisfied, cells exit mitosis via mitotic slippage.

24 spindle checkpoint and couples with mitotic slippage.

25 othesized to have occurred by DNA polymerase slippage.

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

27 23-nt RNA to attain resistance to transcript slippage.

28 he sequence requirements for transcriptional slippage.

29 hinder DNA polymerases and provoke template slippage.

30 he ribosome anticodon-codon interactions for slippage.

31 n oil tamponade with no incidence of retinal slippage.

32 inherently prone to further mis-pairing and slippage.

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

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

35 cilitating balance recovery after unexpected slippages.

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

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

38 f the 8- to 9-bp mature RNA-DNA hybrid, when slippage abruptly dropped by 10-fold.

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

45 related structure, which promotes DNA strand slippage and its consequent expansion of nucleotide repe

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

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

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

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

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

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

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

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

54 oci by reducing the substrate for polymerase slippage and recombination.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 n the present study, we have used transcript slippage as an assay to identify possible structural tra

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

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

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

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

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

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

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

79 The other involves slippage between adhesions and the substratum, which inc

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

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

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

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

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

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

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

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

88 However, easily detectable slippage continued until 14 more bonds were made.

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

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

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

92 Retinal slippage did not occur in any case.

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

94 Slippage directionality, base insertion and omission, is

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

96 by several mechanisms, including replication slippage, DNA repair and recombination.

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

98 on the chromosome to examine transcriptional slippage during elongation.

99 Polymerase slippage during initiation of intermediate and late RNA

100 RNA lead to increased transcription complex slippage during initiation.

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

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

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

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

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

106 he template can undergo efficient transcript slippage, during which the 3' end of the RNA slides upst

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

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

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

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

111 A(Lys) promotes a highly unusual single-tRNA slippage event in both prokaryotic and eukaryotic riboso

112 lesion precedes and facilitates the selected slippage event.

113 The remaining four loci had no slippage events detected.

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

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

116 Insertions increasing the frequency of slippage events within mononucleotide repeat tracts were

117 (29%) apparently originating from polymerase slippage events, in addition to frameshifts and point mu

118 A polymerase and models of the energetics of slippage events, respectively.

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

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

121 s/deletions originating from DNA replication slippage events.

122 Paradoxically, these replication 'slippage' events both create and destroy repetitive sequ

123 an polymerase (pol) mu catalyzes Streisinger slippage exclusively in repetitive DNA, requiring as lit

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

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

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

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

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

129 -FEN1 to suppress expansion implies that DNA slippage generates a 5'-flap in the nascent strand indep

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

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

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

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

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

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

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

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

147 li RNAP mutants with altered transcriptional slippage in vivo.

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

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

150 n, and doxorubicin, inhibit the formation of slippage-induced DNA products, but this block can be ove

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

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

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

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

155 Although replication slippage is a plausible explanation for tandem duplicati

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

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

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

159 This mitotic slippage is correlated with diminished expression of cdc

160 Replication slippage is induced at repetitive sequences that can be

161 teropolymeric 62-mer templates, where strand slippage is much less likely to occur, suggests that sti

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

163 Where slippage is stimulated, the resulting products have one

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 iated the duplication event by a replication slippage mechanism.

181 wth conditions presumably through a ribosome slippage mechanism.

182 nts in the selection of single- or dual-tRNA slippage mechanisms.

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

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

185 f the lesion providing evidence for a primer slippage mode if N was complementary to the 5' base.

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

187 Slippage mutations reveal rather similar patterns of mut

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

189 Transcript slippage occurs when an RNA transcript contains a repeti

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

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

192 Slippage of elongating RNA polymerase (RNAP) on homopoly

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

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

195 Slippage of muscles can be prevented by effective suturi

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

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

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

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

200 s a "desensitization to voltage," perhaps by slippage of the coupling between the voltage sensors and

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

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

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

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

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

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

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

208 Ribosomal frameshifting entails slippage of the translational machinery during elongatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 eshift mutations are "classical" Streisinger slippage, proposed for repetitive DNA, and "misincorpora

236 % vs11.3%; P = 0.013), partly because of the slippage rate (10.3% vs 3.6%; P = 0.005).

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

238 reporter gene that allowed us to measure the slippage rate at a mononucleotide repeat.

239 The slippage rate is determined by the electrodynamic coupli

240 d to a 7-fold increase in the microsatellite slippage rate.

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

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

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

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

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

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

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

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

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

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

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

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

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

254 somatic expansion results not by replication slippage, single stranded annealing or simple MutS-media

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

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

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

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

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

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

261 3-only protein Puma is induced after mitotic slippage, suppression of de novo protein synthesis that

262 tures may be intermediates in the DNA strand slippage synthesis associated with the expansion of nucl

263 ikely to occur, suggests that stimulation of slippage synthesis by DDI is not due to a direct effect

264 which has been found to modulate DNA strand slippage synthesis by DNA polymerase I, is a wedge-shape

265 DDI-induced slippage synthesis is more pronounced as the incubation

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 qual recombination as opposed to replication slippage, the most likely mechanism in other triplet rep

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

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

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

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

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

280 oducts, whose synthesis would require strand slippage to occur.

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

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

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

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

285 Slippage was markedly increased for the H247A-PCFT mutan

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

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

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

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

290 GTC repeats are achieved through replicative slippage, whereas large deletion events are found when G

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

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

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

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

300 We reasoned that transcript slippage would not occur in fully processive complexes.