ライフサイエンスコーパス: repeat length

1 e at onset are not entirely accounted for by repeat length.

2 etwork, as judged by a yeast-like nucleosome repeat length.

3 any genes differ in size due to variation in repeat length.

4 d <40 repeats and 1 (2%) had an intermediate repeat length.

5 d <40 repeats and 1 (2%) had an intermediate repeat length.

6 cing of 162 bp, consistent with the reported repeat length.

7 he repeat-containing RNA with increasing CGG-repeat length.

8 ion state of the other tails and nucleosomal repeat length.

9 at becomes more pronounced with increases in repeat length.

10 cordant for AO after correction for SCA2 CAG repeat length.

11 al variability remains after controlling for repeat length.

12 ssion analysis of the log of age of onset on repeat length.

13 IF4A helicase, and is strongly influenced by repeat length.

14 bstrates do not expand irrespective of their repeat length.

15 recommended population screening for AR CAG repeat length.

16 Joining efficiency decreased with repeat length.

17 ene (PABP2), in which (GCG)(6) is the normal repeat length.

18 nt of pH, type of divalent ion and chromatin repeat length.

19 FXN promoter silencing in FRDA is related to repeat length.

20 olding considering various cutoffs for ATXN2 repeat length.

21 n rates continue to increase with increasing repeat length.

22 rotein were not associated with expanded CAG repeat length.

23 fluences tlpB translation dependent on the G-repeat length.

24 relationship between brain function and G4C2 repeat length.

25 nts were screened for C9orf72 hexanucleotide repeat length.

26 ndogenous mouse HTT genes, with variable CAG-repeat lengths.

27 ibuting specific disease phenotypes to these repeat lengths.

28 This data revealed a bias in noncoding DNA repeat lengths.

29 d by the length of their constitutive HD CAG repeat lengths.

30 ubjects were age 18-50 years and had varying repeat lengths.

31 es from HD knock-in mice with increasing CAG repeat lengths.

32 sed sharply (up 720%) over a narrow range of repeat lengths.

33 rth, ISW1a tightens the spacing to canonical repeat lengths.

34 ng developmentally delayed males with normal repeat lengths.

35 all changes per added Gln at relatively long repeat lengths.

36 y landscapes for polyQ peptides of different repeat-lengths.

37 ntaining the FMR1 5'-UTR with various (CGG)n repeat lengths (0< or =n< or =99) and a downstream (luci

38 receptor (ar) gene containing different CAG repeat lengths (16-112 repeats).

39 p-HD subjects (age, 45.8 +/- 11.0 years; CAG repeat length, 41.6 +/- 1.8) and 11 age-matched control

40 etermine the polymorphic nature of the ATXN2 repeat length across a spectrum of neurodegenerative dis

41 m testosterone levels and inversely with CAG repeat length, age and duration of weakness.

42 of Huntington's disease, accounting for CAG repeat length, age, and the interaction of CAG repeat le

43 In wild-type progeny, only one unique repeat length allele was found in 576 alleles tested.

44 11 HD participants had known huntingtin CAG repeat length, allowing determination of a burden of pat

45 instability (MSI) phenotype characterized by repeat length alterations at microsatellite sequences.

46 lleles differing in length by three complete repeats, length alterations are observed at twice the fr

47 The repeat length, ancestry, and age of onset of all North A

48 Thus, short repeat length and acetylation can affect basic chromatin

49 can be improved beyond that obtained by CAG repeat length and age alone.

50 ation between cytosine-adenine-guanine (CAG) repeat length and age at onset of Huntington's disease i

51 how a strong inverse correlation between CAG repeat length and age of disease onset (AO).

52 There was a weak association between repeat length and age of disease onset.

53 No significant interactions between repeat length and age were detected.

54 those who did not, after controlling for CAG repeat length and age-related risk (p=0.006 and 0.0003,

55 ant predictors of motor diagnosis beyond CAG repeat length and age.

56 peat length, age, and the interaction of CAG repeat length and age.

57 e progression and the combined effect of CAG repeat length and age.

58 hod is extremely flexible with regard to the repeat length and base sequence of the initial oligoseed

59 varian cancer patients were genotyped for AR repeat length and BRCA mutation status.

60 o strong overall association between average repeat length and breast cancer risk (OR, 1.04 per CAG r

61 th of the targeted CAG repeat and on the CTG repeat length and concentration of the PMO.

62 roximity to clinical diagnosis (based on CAG repeat length and current age) and striatal volumes.

63 IGS subrepeat sequences for the influence of repeat length and estimated the statistical significance

64 and cellular toxicity that was dependent on repeat length and exacerbated during aging.

65 The correlation between repeat length and expansion rate identified the interval

66 gene proximity, androgen receptor exon1 CAG repeat length and expression of the PIWIL1 gene.

67 alysis revealed negative associations of CGG repeat length and FMR1 mRNA with connectivity strength o

68 untington's Disease models, differing in CAG repeat length and genetic background (115 and 250 CAG re

69 D age at death is determined by expanded CAG-repeat length and has no contribution from the normal CA

70 demonstrate that the effect is dependent on repeat length and is at least partially Dicer dependent.

71 read-through product is proportional to CAG repeat length and is present in all knock-in mouse model

72 We evaluated the association between AR-CAG repeat length and mammographic density, a strong breast

73 ck-ins by its method of construction, longer repeat length and more severe phenotype.

74 tion (SLiC), to identify linkage between CAG repeat length and nucleotide identity of heterozygous SN

75 Here we examine the role of GGGGCC repeat length and orientation on DNA replication using a

76 The effects of triplet repeat length and orientation were studied after multipl

77 Data on the association between the AR repeat length and ovarian cancer, both in general and am

78 epeat; 95% CI, 0.99-1.10) or between average repeat length and plasma hormone levels.

79 There was no association between AR repeat length and presence of a BRCA mutation.

80 females, only a significant association with repeat length and self-report attention (p < 0.01) was d

81 th for accurate STR genotyping, depending on repeat length and sequencing read length.

82 f 25,115 variations were observed, including repeat length and single nucleotide polymorphisms, corre

83 not accurately reproduce the effect of polyQ repeat length and solution conditions on Httex1 aggregat

84 on timing results from its impact on TG(1-3) repeat length and support a model in which Rif1 measures

85 in a manner dependent on both polyglutamine repeat length and temperature but independent of HTT pro

86 e H4 acetylation that is proportional to CGG repeat length and that correlates with responsiveness of

87 ple factors, including DNA sequence, triplet-repeat length and unknown cell-type-specific factors.

88 The CGG repeat lengths and FMR1 mRNA expression levels in periph

89 sed to evaluate the associations between CAG repeat lengths and race, stage, histologic grade, and PS

90 xhibiting large changes per added Gln at low repeat lengths and small changes per added Gln at relati

91 se diseases are exponential functions of the repeat lengths and that the probability of neural death

92 n of the histone octamer density (nucleosome repeat length) and find that a minimal change in this pr

93 In a model adjusted for age, CAG repeat length, and caloric intake, MeDi was not associat

94 ts interrupt contig assembly with increasing repeat length, and we estimate that the limit for their

95 ouse model, R6/2, carrying two different CAG repeat lengths, and a relatively high degree of overlap

96 Hexanucleotide expansions caused age-, repeat-length-, and expression-level-dependent accumulat

97 onfirm an unusually short average nucleosome repeat length, approximately 152 bp, in fission yeast an

98 nalyses of SSR variation by allele class and repeat length are complementary, and that some SSRs are

99 Above this threshold range, longer repeat lengths are associated with earlier ages-of-onset

100 ta show that gender-dependent changes in CAG repeat length arise in the embryo.

101 severity of the disease depends on the polyQ repeat length, arising only in patients with proteins ha

102 of one or two, compared to those with longer repeat lengths, as well as a nonrandom distribution of S

103 Among males, no repeat length associations were detected for any factor.

104 icing regulated by hnRNP L and depends on CA repeat length at a specific site in intron 1.

105 These results suggest a sensing strategy for repeat length based on the combination of the electrocat

106 The authors focus on CAG repeat length because recent research suggests that men

107 these tissues, we detected no difference in repeat length between disease subgroups (cerebellum p=0.

108 ted with frameshifts and with differences in repeat length between the neisserial genome sequences is

109 series of R6/2 mice carrying a range of CAG repeat lengths between 109 and 464.) This analysis revea

110 A significant reduction of CTG repeat length by 100-350 (CTG).(CAG) repeats often occur

111 CAG repeat length can be determined with high sensitivity an

112 These results imply that CAG repeat length can potentially serve as a useful marker t

113 some, and, when the gene harbors an expanded repeat length, can interfere with the degradation of a w

114 It is generally assumed that repeat length changes arise via replication slippage, ye

115 ccumulation of larger alleles as a result of repeat length changes in vitro, as confirmed by single c

116 o play a central role in the accumulation of repeat length changes.

117 a mechanism that could cause DNA damage and repeat-length changes in human cells.

118 lectrocatalytic strategy for determining the repeat length combined with existing methods for determi

119 One element is a threshold, or minimal repeat length, conferring frequent mutations.

120 iferase expression decreases with increasing repeat length, consistent with earlier observations of d

121 terminus (exons 2/3) and microtubule binding repeat length contribute to Tau release from the cell.

122 In the frontal cortex of patients with FTD, repeat length correlated with age at onset (r=0.63; p=0.

123 ying biophysical principles that mediate the repeat length dependence of aggregation, however, is far

124 egation process, qualitatively mirroring the repeat length dependence of disease risk.

125 lity is reinforced by studies showing strong repeat length dependence to the aggregation process, qua

126 imple and complex polyQ sequences, and their repeat-length dependence.

127 Here we show that CAG repeat length-dependent aberrant splicing of exon 1 HTT

128 oteins in body wall muscle displayed a polyQ repeat length-dependent decrease in body movement compar

129 The repeat length-dependent tendency of the polyglutamine se

130 We found repeat length-dependent transcriptional signatures to be

131 The structural polymorphism causes a repeat-length-dependent accumulation of transcripts abor

132 transgenic animals display dosage-dependent, repeat-length-dependent degeneration in neuronal tissues

133 The repeat-length-dependent differences in predicted aggrega

134 47) peptide in a concentration-dependent and repeat-length-dependent manner.

135 is well established and correlates with the repeat-length-dependent nucleation kinetics of polygluta

136 regulator Ssn6 (Cyc8) result in systematic, repeat-length-dependent variation in expression of targe

137 within one strain, we demonstrate that the G-repeat length determines posttranscriptional regulation

138 e nucleosomes, as set by the internucleosome repeat length, determines the preferred angle between th

139 haplotypes were associated with altered CAG-repeat length distribution or residual age at the onset

140 find no evidence for a threshold above which repeat length does not contribute toward age at onset, s

141 Alterations in trinucleotide repeat length during transmission are important in the p

142 ciparum is very diverse with respect to NANP repeat length even on a local level and that diversity a

143 ity to parameterize a mathematical model for repeat length evolution that we can use to infer biologi

144 is silent before disease-related (ATTCT)(n) repeat length expansion of its DUE sequence, despite the

145 tent with the hypothesis that somatic HD CAG repeat length expansions in target tissues contribute to

146 Age and CAG repeat length explained variance in longitudinal change

147 While Fmr1 message levels increased with repeat length, FMRP levels trended downward over the sam

148 Remarkably, the observed threshold repeat length for replication stalling in yeast (approxi

149 Mean androgen receptor gene CAG repeat length for white veterans was 21.9 (SD, 3.5) vers

150 prognostic value, independent of age and CAG repeat length, for predicting subsequent clinical diagno

151 nificant predictor of onset age, with larger repeat length gains associated with earlier disease onse

152 line and soma with a marked tendency towards repeat length gains.

153 x/x (29.6 nmol/liter), where x represents a repeat length greater than 6 (p = 0.001).

154 with healthy controls (OR = 5.57; P= 0.001; repeat length >30 units).

155 ive supranuclear palsy (OR = 5.83; P= 0.004; repeat length >30 units).

156 TCF4 is strongly associated with FECD, and a repeat length >50 is highly specific for the disease Thi

157 ompiling data for 3 arms of the study, a TGC repeat length >50 was present in 79% of FECD cases and i

158 ants aged 26 to 57 years had an expanded CAG repeat length (>/= 37).

159 Why the critical nucleus size changes with repeat-length has been unclear.

160 n ages of onset among patients with the same repeat length, however, suggests a role for modifying fa

161 leotide repeats may result in the changes of repeat length; however, such a mechanism seems less like

162 ese findings, we assessed the ataxin 2 polyQ repeat length in 1294 European ALS patients and 679 matc

163 otide repeat in TCF4 and FECD by determining repeat length in 66 affected participants with severe FE

164 r1 mRNA and FMRP levels as a function of CGG-repeat length in a congenic (CGG-repeat knock-in) mouse

165 Fibril stability also increases with repeat length in a nonlinear fashion.

166 some arrays as well as a shorter nucleosomal repeat length in bulk chromatin in embryos.

167 onships between inclusion patterns, age, and repeat length in CGG knock-in (KI) mice in comparison wi

168 isease risk and age-of-onset on expanded CAG repeat length in diseases like Huntington's disease (HD)

169 ive technique that allows the measurement of repeat length in individual FXN genes, was used to analy

170 ed by December 29, 2013, reporting ATXN2 CAG repeat length in patients with ALS and controls.

171 both aggregation and age of onset trend with repeat length in similar ways, exhibiting large changes

172 increases by nearly two-fold with increasing repeat length in the absence of any change in mRNA level

173 he relationship of CAG and GGN (polyglycine) repeat length in the AR gene.

174 These results suggest that the (TAAAA)(n) repeat length in the SHBG gene, but not the D327N varian

175 een the amplitude of late positivity and CGG repeat length in those with fragile X-associated tremor/

176 dge, our study is the first to report on CAG repeat lengths in a cohort of prostate cancer patients,

177 We describe here the use of very short polyQ repeat lengths in htt N-terminal fragments to slow this

178 Our data show that extreme CAG repeat lengths in R6/2 mice is paradoxically associated

179 At the same time, poly(Gln) peptides with repeat lengths in the 15-20 residue range, despite their

180 Repeat lengths in the cerebellum were smaller (median 12

181 6 behavioral traits with seven different CAG-repeat lengths in the huntingtin gene (Htt).

182 otifs and to detect subtle irregularities of repeat lengths in three solenoid protein families.

183 number and mRNA concentration (at fixed CGG-repeat length) in neuroblastoma-derived SK cells.

184 repeated copies of the PR promoter, with the repeat length increased in single base pair increments t

185 during mouse rod maturation, the nucleosomal repeat length increases from 190 bp at postnatal day 1 t

186 403 AD patients and 444 controls for CpG-CA repeat length indicated shifted allelic frequency distri

187 It is not clear if expansion repeat length is a reliable test in other populations.

188 Pathogenic repeat length is in the hundreds or thousands, but the m

189 Somatic mosaicism of repeat length is prominent in repeat expansion disorders

190 ansion bias observed in the distributions of repeat lengths is likely to be the cumulative effect of

191 HMOX1 gene is highly polymorphic, with long repeat lengths linked to decreased activity and inducibi

192 pression levels decrease with increasing CGG-repeat length, lowered protein may contribute to premuta

193 n wild-type and mutant genes on the basis of repeat length may offer new options for developing treat

194 differences in fibers formed with different repeat lengths may not be due to gross changes in the am

195 We used mixed models with repeated length measures to predict individual length ga

196 nsight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathoge

197 nucleus (n* approximately 3), while a longer repeat-length monomer (Q30) prefers a beta-hairpin confo

198 he high frequency and incremental effects of repeat length mutations provide molecular explanations f

199 At the long normal repeat length (n = 23), a family of H-DNAs of slightly d

200 At the premutation repeat length (n = 42) and higher negative supercoiling,

201 For the normal genomic repeat length (n = 9) our data are consistent with the f

202 Furthermore, we found that neither telomere repeat length nor telomeric silencing correlated with ch

203 h short DNA linkers L = 13-37 bp (nucleosome repeat length (NRL) = 160-184 bp).

204 ted nucleosomes where the shorter nucleosome repeat length (NRL) types are associated with transcript

205 ture of chromatin, we confirmed a nucleosome repeat length (NRL)-dependent folding.

206 es are characterized by different nucleosome repeat lengths (NRLs) of the linker DNA connecting the n

207 hanisms for fibers with different nucleosome repeat lengths (NRLs) with/without LH that are fixed to

208 A GGN repeat length of <16 was associated with an AUASI >7 (HR

209 A CAG repeat length of <21 was associated with an enlarged pro

210 peat so that it matches twice the apparent Z-repeat length of 12 nm.

211 cally different from the measured nucleosome repeat length of 165 bp.

212 This is close to the measured nucleosome repeat length of 190 bp.

213 One tumor sample had a CAG repeat length of 21, compared with germline length of 22

214 al, 1.14-2.39), compared with men with a CAG repeat length of 23 or longer.

215 More than 72% of the subjects had a GGN repeat length of 23, and those with a GGN repeat length

216 -terminal 586 aa of Htt with a polyglutamine repeat length of 82 (N586-82Q), under the control of the

217 idated the model by correctly predicting the repeat length of a blinded mouse line.

218 that maps out the nonlinear dependence with repeat length of a nucleation efficiency term that is li

219 th of approximately 30 bp of linker DNA or a repeat length of approximately 177 bp.

220 Repeat length of the CAG microsatellite polymorphism in

221 The CTG triplet repeat length of the largest allele was compared with th

222 d age of onset are strongly dependent on the repeat length of the polyglutamine (polyQ) sequence in t

223 all of the resulting expanded alleles having repeat lengths of <100 CTGs, a size that is not often as

224 CAG repeat lengths of 36 or greater were observed in six of

225 ing polyglutamine (poly(Gln)) sequences with repeat lengths of about 37 residues or more are associat

226 dichroism spectra of poly(Gln) peptides with repeat lengths of five, 15, 28 and 44 residues are all n

227 -like aggregates for poly(Gln) peptides with repeat lengths of greater than 37 residues.

228 why nucleus size increases to tetrameric at repeat lengths of Q23 or below.

229 ing the notion that the influence of poly(Q) repeat length on disease risk and age of onset is at the

230 ohort of men with prostate cancer, short CAG repeat length on the androgen receptor gene was associat

231 Predictors of survival were a shorter GAA repeat length on the smaller allele of the frataxin gene

232 dence that women with a higher number of CAG repeat lengths on the androgen receptor (AR) gene have i

233 CAG repeat lengths on the androgen receptor gene were evalua

234 ccessive nucleosomes (measured in nucleosome-repeat lengths or NRLs) that characterize different cell

235 We observed a repeat length-, PAM-, and strand-dependent reduction of

236 ities to bind telomeric DNA, affect telomere repeat length, participate in telomeric DNA replication,

237 disorders (BD) could be influenced both by a repeat length polymorphism (5HTTLPR) in the promoter reg

238 rsons with the SS genotype of the HO-1 (GT)n repeat length polymorphism compared with those with the

239 Repeat length polymorphism was confirmed for 68% of CFS

240 -specific helicase, results in increased CTD repeat length polymorphisms.

241 It also enabled a survey of repeat-length polymorphisms (RLPs) in human genomes and

242 studies show that the monomer of the shorter repeat-length (Q20) prefers an extended conformation and

243 e is not the predominant form in the polyGln repeat length range studied here.

244 The ATXN2 CAG repeat lengths ranged from 13 to 39 in patients with ALS

245 ace expression of alpha(1A) protein when CAG repeat lengths reached or exceeded the pathogenic range

246 ient of decreasing pathology with longer CAG repeat lengths, reflecting our previous findings with be

247 Variations in repeat length result in changes in expression and local

248 a fragment, and forward/reverse mutations of repeat length resulting in microsatellites of identical

249 ultimolecular G-quadruplexes are enhanced by repeat length, RNA-RNA interactions facilitated by G-qua

250 ividually matched with incident cases on CAG repeat length, sex, and age, who were not diagnosed with

251 evealed 23 (2.3%) unique and 51 (5.1%) total repeat length shifts ([+2], [-2], [+4], or [-4] bp).

252 Men with a CAG repeat length shorter than 23 (median length) had a 65%

253 GN repeat length of 23, and those with a GGN repeat length shorter than 23 had a 12% increased risk o

254 Both repeat lengths showed lower levels of NADPH oxidase and

255 y between different populations, with longer repeat lengths showing a clear association.

256 huntingtin gene with a greatly increased CAG repeat length, shows multiple effects of the altered pol

257 After accounting for constitutive repeat length, somatic instability was found to be a sig

258 Given that CAG repeat length strongly correlates with clinical severity

259 Patients with longer repeat lengths, such as (GCG)(13), developed severe limb

260 correlation between fibril length and polyQ repeat length, suggesting possible polyQ length-dependen

261 larger with advanced age and increasing CGG repeat length, supporting hypotheses that these patholog

262 Repeat lengths TA(11) and TA(16) differed significantly

263 ability is a threshold, defined as a minimal repeat length that confers frequent mutations.

264 matin in mouse liver nuclei has a nucleosome repeat length that is 15 bp, or more, shorter than the b

265 lected behavioral signatures for age and CAG-repeat length that most robustly distinguished between m

266 bias toward expansion events and changes in repeat length that occur in jumps, rather than by accumu

267 an iterative strategy yielded predicted CAG repeat lengths that were significantly positively correl

268 ecause an ethnic variation exists in the CAG repeat length, this polymorphism has been suggested to e

269 olyQ segments near or above the pathological repeat length threshold of about 37, aggregation of htt

270 lyGln) tracts expanded beyond a pathological repeat length threshold of approximately 38.

271 Modelling the progression of repeat length throughout the lifetime of individuals has

272 1 fibroblasts, all showing different CTG.CAG repeat lengths, thus demonstrating somatic instability w

273 ce for the detailed analysis of the roles of repeat length, tissue specificity and level of expressio

274 port a model in which Rif1 measures telomere repeat length to ensure that telomere replication timing

275 las have been developed based on age and CAG repeat length, to predict when HD motor onset will occur

276 stability and transcription are sensitive to repeat length, tract purity, and CpG methylation.

277 ha-satellite arrays, based on the 16-monomer repeat length typical of natural D17Z1 arrays, in which

278 t express huntingtin exon 1 with varying CAG repeat lengths under doxycycline (dox) control.

279 ce and WT controls, despite modest levels of repeat length variability demonstrated by single cell PC

280 Nine new repeat length variants were found in these lines allowin

281 echanisms leading to transcription-dependent repeat length variation are unclear.

282 We identified similar repeat length variation in the coding repeats of Runx-2,

283 life stress on depression is moderated by a repeat length variation in the transcriptional control r

284 We assayed microsatellite repeat-length variation among 13 populations of D. anana

285 variations, making them less likely to call repeat length variations as only a small percent of thes

286 detection did not report 94.2% of the exonic repeat length variations in part because the alignment t

287 as RepG sRNA is highly conserved, the tlpB G-repeat length varies among diverse H. pylori strains, re

288 an 1467 repeat units (the 25th percentile of repeat lengths) versus 7.4 years (6.3-10.9) in the group

289 Repeat length was determined by direct sequencing, short

290 The repeat length was greater than 1000 in 4 FECD cases.

291 The AR CAG repeat length was recorded.

292 residual variance after correction for SCA2 repeat length, we applied variance component analysis an

293 By varying repeat length, we generated expression libraries that in

294 digestion fragments over several nucleosome repeat lengths were analysed quantitatively and compared

295 The helical repeat lengths were consistent within a single filament

296 PolyA repeat lengths were relatively stable but already shorte

297 ich can be explained by a cyclic trend in TA repeat length with a period of approximately 5, which in

298 frequencies of seizures and correlations of repeat length with age at onset.

299 ion analysis to determine the association of repeat length with the risk of disease.

300 Based on modification of the G-repeat length within one strain, we demonstrate that the