ライフサイエンスコーパス: repeat length

1 and the AO predicted on the basis of the CAG repeat length.

2 nts were screened for C9orf72 hexanucleotide 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 e at onset are not entirely accounted for by repeat length.

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

15 bstrates do not expand irrespective of their repeat length.

16 recommended population screening for AR CAG repeat length.

17 Joining efficiency decreased with repeat length.

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

19 rotein were not associated with expanded CAG repeat length.

20 relationship between brain function and G4C2 repeat length.

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

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

23 olding considering various cutoffs for ATXN2 repeat length.

24 n rates continue to increase with increasing repeat length.

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

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

27 e DNA, though it becomes crucial at long CAG repeat lengths.

28 ibuting specific disease phenotypes to these repeat lengths.

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

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

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

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

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

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

35 ng developmentally delayed males with normal repeat lengths.

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

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

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

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

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

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

42 tinct toxic processes triggered by different repeat lengths across cell types and diseases.

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

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

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

46 11 HD participants had known huntingtin CAG repeat length, allowing determination of a burden of pat

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

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

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

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

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

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

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

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

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

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

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

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

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

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 he extent of MBNL sequestration dependent on repeat length and expression level may account for some

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

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

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

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

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

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

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

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

92 ing atrophy to the genetic marker of HD (CAG-repeat length) and motor and cognitive symptoms.

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

94 Detailed analysis of CTG repeat length, and incorporation of confounding factors,

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

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

97 le, which reveals the identities, positions, repeat lengths, and interactions of 38 associated protei

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

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

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

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

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

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

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

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

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

107 Previously, CTG repeat length at birth has been correlated to patient ag

108 ibited a strong correlation with average CAG repeat length at the genomic DNA level determined by PCR

109 Repeat length (at ATXN1, ATXN2, ATXN3, ATXN7, TBP, ATN1,

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

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

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

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

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

115 Most cells maintain telomere repeat lengths by using the enzyme telomerase, although

116 CAG repeat length can be determined with high sensitivity an

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

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

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

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

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

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

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

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

125 Furthermore, the nucleosome repeat length defined the spatial unit of methylation sp

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

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

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

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

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

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

132 The repeat length-dependent tendency of the polyglutamine se

133 We found repeat length-dependent transcriptional signatures to be

134 izing effects are FAN1 concentration and CAG repeat length-dependent.

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

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

137 The repeat-length-dependent differences in predicted aggrega

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

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

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

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

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

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

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

145 ects can hasten or delay onset and other CAG repeat length-driven phenotypes.

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

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

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

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

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

151 Age and CAG repeat length explained variance in longitudinal change

152 CAG repeat length explains around half of the variation in a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 rtices, which correlated negatively with CGG repeat length in the PM carriers.

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

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

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

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

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

185 Repeat lengths in the cerebellum were smaller (median 12

186 6 behavioral traits with seven different CAG-repeat lengths in the huntingtin gene (Htt).

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

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

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

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

191 403 AD patients and 444 controls for CpG-CA repeat length indicated shifted allelic frequency distri

192 h Mrc1 functions are important in preventing repeat length instability.

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

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

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

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

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

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

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

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

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

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

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

204 n the strain sensitivity of Gamma versus the repeat-length ( n) sensitivity can be used to distinguis

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

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

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

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

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

210 is procedure predicts a quantized nucleosome repeat length (NRL) and that only fibres with longer NRL

211 ned by the regions with decreased Nucleosome Repeat Length (NRL) for ~20 nucleosomes near CTCF sites,

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

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

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

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

216 range of physiologically relevant nucleosome repeat lengths (NRLs).

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

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

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

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

221 ue impact chromatin fibers with a nucleosome repeat length of 167 and 197.

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

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

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

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

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

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

228 Repeat length of the CAG microsatellite polymorphism in

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

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

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

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

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

234 investigated the effect of increasing polyQ repeat length on HTT inclusion formation, location, neur

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

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

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

238 CAG repeat lengths on the androgen receptor gene were evalua

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

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

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

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

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

244 Repeat length polymorphism was confirmed for 68% of CFS

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

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

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

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

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

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

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

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

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

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

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

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

257 Both repeat lengths showed lower levels of NADPH oxidase and

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

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

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

261 Given that CAG repeat length strongly correlates with clinical severity

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

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

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

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

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

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

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

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

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

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

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

273 1 fibroblasts, all showing different CTG.CAG repeat lengths, thus demonstrating somatic instability w

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

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

276 owever, the contribution of the expanded CAG repeat length to the rate of disease progression after o

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

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

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

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

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

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

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

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

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

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

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

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

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

290 Repeat length was determined by direct sequencing, short

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

292 The AR CAG repeat length was recorded.

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

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

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 Attempts to correlate CTG repeat length with progressive DM1 phenotypes, such as m

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

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