ライフサイエンスコーパス: triplet repeat

1 tability is dependent on the sequence of the triplet repeat.

2 ot altered by the expression of the expanded triplet repeat.

3 C might play a role in DSB repair within the triplet repeat.

4 to SSCs from the C-rich strand of the FMR-1 triplet repeat.

5 have been shown previously to target the DM1 triplet repeat.

6 containing either two or three copies of the triplet repeat.

7 Several of these are non-polyglutamine triplet repeats.

8 replication in the recombination process of triplet repeats.

9 ative mutability of dispersed expanded human triplet repeats.

10 result from expansion of CTG/CAG or CGG/CCG triplet repeats.

11 dentity with previously published cDNAs with triplet repeats.

12 progression are related to the length of the triplet repeats.

13 pied the DMPK1 gene harboring longer CTG.CAG triplet repeats.

14 nding proceeds unabated through extrahelical triplet repeats.

15 ing on DNA slippage events that occur in DNA triplet-repeats.

16 robing strategies, we also show that the GAA triplet repeat adopts an unusual DNA structure, demonstr

17 The CTG triplet repeat allele length was positively correlated w

18 congenital disorder that is associated with triplet repeat allele size.

19 DA) patients are homozygous for expanded GAA triplet-repeat alleles in the FXN gene.

20 in collagen peptides composed of Pro-Hyp-Gly triplet repeats, allowing for truncation to the smallest

21 nt in the structure of telomere, centromere, triplet repeat and other DNAs, information about the det

22 Our catalog of human triplet repeats and their surrounding flanking regions c

23 own of Dnmt1 in human cells destabilized CAG triplet repeats, and Dnmt1 deficiency in mice promoted i

24 can load yPCNA onto 5'-ssDNA flaps, (CAG)13 triplet repeats, and homoduplex DNA.

25 tructures can form from palindromes and from triplet repeats, and they are also intermediates in V(D)

26 e triplet repeat sequence (CAG)n and related triplet repeats are associated with dynamic DNA mutation

27 AG codon in certain repeats, indicating that triplet repeats are at high risk for mutation in the abs

28 conclude that the expansion and deletion of triplet repeats are enhanced by mutations that reduce th

29 ts with fragile X syndrome, the expanded CGG triplet repeats are hypermethylated and the expression o

30 Most of the triplet repeats are PTG, and nearly all of the triplet r

31 Disease-causing triplet-repeats are transcribed, but how this influences

32 Expanded triplet-repeats are unstable in somatic cells, and tissu

33 The most common triplet repeats associated with such diseases are CAG, C

34 Notably, triplet-repeat-associated variegation was not restricted

35 formers (SSCs) from the C-rich strand of the triplet repeat at the FMR-1 locus are rapidly and select

36 CUG triplet repeat binding protein, CUGBP1, plays a critical

37 An RNA CUG triplet repeat binding protein, CUGBP1, regulates splici

38 CUG triplet repeat-binding protein-1 (CUGBP1) binds to C/EBP

39 DNA (S-DNA) structures when DNAs containing triplet repeat blocks of myotonic dystrophy or fragile X

40 ergy crosstalk between pairs of lesions in a triplet repeat bulge loop and an adjacent duplex domain.

41 We show here that replacement within a triplet repeat bulge loop domain of a guanosine residue

42 We have embedded the hexameric triplet repeats (CAG)(6) and (CTG)(6) between two (GC)(3

43 FMR1, is unique compared with the many other triplet repeat-causing diseases, making it ideal for ide

44 at transcription transiently dissociates the triplet repeat complementary strands enabling the non-tr

45 Trinucleotide, or triplet, repeats consist of 3 nucleotides consecutively

46 AA-66) of cells contained alleles with >/=66 triplet-repeats, constituting a plausible mechanism for

47 iplet repeats are PTG, and nearly all of the triplet repeats contain a threonine residue, providing m

48 xia patients are homozygous for expanded GAA triplet-repeats containing 66 to 1,700 triplets.

49 AP, while toeprint results suggest that nine triplet repeats contribute to TRAP binding.

50 romosome termini, and the disease-associated triplet repeat (CTG).(CAG)n.

51 A triplet repeat (CTG)n encodes a putative signal sequence

52 The rate of triplet repeat deletion decreased in an E. coli strain d

53 s one of the latest additions to the list of triplet repeat diseases and is distinct from the other S

54 The abnormal number of repeats found in triplet repeat diseases arises from 'repeat instability'

55 Members of this latter group, also known as triplet repeat diseases, are caused by the expansion of

56 In contrast to other triplet repeat diseases, expanded alleles found in affec

57 e development and onset of DNA expansion and triplet repeat diseases.

58 repeat expansion that may be common to other triplet repeat diseases.

59 er design and understanding the mechanism of triplet repeat diseases.

60 6, implicated in repeat instability in other triplet-repeat diseases, were highly expressed in plurip

61 ues is a common theme in the pathogenesis of triplet-repeat diseases.

62 gene silencing and hence severity in several triplet-repeat diseases.

63 has been learned about the pathogenesis of "triplet repeat" diseases through mouse models for spinoc

64 Myotonic dystrophy type 1 (DM1) is a triplet repeating disorder caused by expanded CTG repeat

65 ore common in Huntington's disease and other triplet repeat disorders.

66 lying pathophysiological mechanisms of other triplet repeat disorders.

67 of Huntington's disease (HD), one of several triplet-repeat disorders characterized by movement defic

68 In vitro, single-stranded triplet repeat DNA forms highly stable hairpins, dependi

69 sequences, provided that Srs2 encounters the triplet repeat DNA immediately on entering the duplex.

70 Single-stranded triplet repeat DNA in vitro forms stable hairpins in a s

71 seases have been linked to the properties of triplet repeat DNA sequences during replication.

72 yrrole-imidazole polyamide targeting GAA.TTC triplet-repeat DNA partially blocked repeat expansion by

73 n-dependent dynamics and order within (CAG)n triplet repeat DNAs, properties of relevance to the biol

74 Moreover, expansions of the triplet-repeat domain of the IT15 gene encoding htt was

75 Repair of oxidative lesions at or near triplet repeat domains can enhance DNA expansion events

76 These static and dynamic influences within triplet repeat domains expand the conformational space a

77 involves the transient formation within the triplet repeat domains of non-native slipped DNA structu

78 perties of regions proximal to and/or within triplet repeat domains, thereby potentially modulating l

79 he lengthening of tracts of CTG, CGG and GAA triplet repeats during progression of a pedigree has bee

80 dy one form of this instability, deletion of triplet repeats during replication of template (CAG)(n)s

81 f unusual DNA structures within the expanded triplet repeat element.

82 ice with a precise deletion of the short CAG triplet repeat encoding 7Q in the mouse HD gene (Hdh(Del

83 we show that M-Probes can detect genes with triplet repeats exceeding a programmed threshold.

84 During propagation of the iPSCs, GAA.TTC triplet repeats expanded at a rate of about two GAA.TTC

85 were found to have an identical polyalanine triplet repeat expansion ([GCG](9)) in the PABP2 gene.

86 Here, we identify the triplet repeat expansion (EXP) RNA-binding proteins as c

87 In contrast, there is no correlation of triplet repeat expansion and deletion instability with p

88 ived from individuals homozygous for the GAA triplet repeat expansion compared with normal controls.

89 Triplet repeat expansion diseases (TREDs) are characteri

90 repeat sequence d[CCG]n, and associated with triplet repeat expansion diseases, mechlorethamine may s

91 An unstable CAG triplet repeat expansion encoding a polyglutamine stretc

92 ative conditions that each derive from a CAG triplet repeat expansion in a specific gene.

93 The CTG18.1 triplet repeat expansion in TCF4 has recently been found

94 y was greater in FECD cases with the CTG18.1 triplet repeat expansion in TCF4 than in those without t

95 In myotonic dystrophy type 1 (DM1), triplet repeat expansion in the 3' untranslated region o

96 pe I myotonic dystrophy (DM1) is caused by a triplet repeat expansion in the 3'-untranslated region (

97 ystrophy (DM) is associated with a (CTG) (n) triplet repeat expansion in the 3'-untranslated region o

98 axia caused primarily by an intronic GAA.TTC triplet repeat expansion in the frataxin (FXN) gene.

99 MD) is a rare myopathy caused by polyalanine triplet repeat expansion in the gene for poly(A) binding

100 a neuromuscular disorder associated with CTG triplet repeat expansion in the myotonin protein kinase

101 Myotonic dystrophy (DM) is caused by a triplet repeat expansion in the non-coding region of eit

102 Reconstituting triplet repeat expansion in vitro, we previously found t

103 er of genotoxic agents can alter the rate of triplet repeat expansion in whole populations of mammali

104 of many neurodegenerative diseases in which triplet repeat expansion is implicated.

105 tes salient phenotypic features of the human triplet repeat expansion mutation.

106 These are among the shortest disease-causing triplet repeat expansion mutations described thus far, a

107 hybrid capture method to determine the exact triplet repeat expansion number in the Huntington's gene

108 hat results from low FXN levels due to a GAA triplet repeat expansion or, occasionally, from missense

109 The TCF4 triplet repeat expansion resulted in a more severe form

110 VGs and the mutation in the FRDA gene, a GAA triplet repeat expansion, was investigated.

111 wledge of DNA mismatch repair involvement in triplet repeat expansion, which encompasses in vitro bio

112 ebellar Ataxia 8 (SCA8) appears unique among triplet repeat expansion-induced neurodegenerative disea

113 ructure, confirming a proposed mechanism for triplet repeat expansion.

114 e index cases with FECD (69.7%) harbored the triplet repeat expansion.

115 ld be useful in diagnosing diseases based on triplet repeat expansion.

116 CUG RNAs and proportional to the size of the triplet repeat expansion.

117 The occurrence of triplet-repeat expansion (TRE) during transmission of ge

118 st and reporter construct models for GAA.TTC triplet-repeat expansion have been reported, studies on

119 ides new insight into a general mechanism of triplet-repeat expansion in iPSCs.

120 an X-linked motoneuron disease due to a CAG triplet-repeat expansion in the androgen receptor (AR) g

121 e results raise the possibility that the GAA triplet-repeat expansion may result in an unusual yet st

122 d by engineering a ribozyme that excises the triplet-repeat expansion region from a truncated myotoni

123 ion, shRNA silencing of MSH2 impeded CTG.CAG triplet-repeat expansion.

124 Moreover, longer repeats showed faster triplet-repeat expansion.

125 A silencing of MSH2 and MSH6 impeded GAA.TTC triplet-repeat expansion.

126 e in comparison with other large, non-coding triplet repeat expansions [(CGG)(n)and (CTG)(n)] which r

127 ismatch repair protein function in mediating triplet repeat expansions and discuss potential therapeu

128 Also, because triplet repeat expansions are important for human diseas

129 or) associated with these open reading frame triplet repeat expansions are substrates for the cystein

130 By measuring triplet repeat expansions as they evolve over time, indi

131 distribution of hairpin folding and generate triplet repeat expansions by polymerase-catalyzed extens

132 olymerase beta effectively catalyzes CAG/CTG triplet repeat expansions by slippage initiated at nicks

133 ataxia patients are homozygous for large GAA triplet repeat expansions in intron 1 of the X25 gene.

134 Small-pool PCR revealed typical large triplet repeat expansions in the DM1 cells.

135 Although dominant gain-of-function triplet repeat expansions in the Huntingtin (HTT) gene a

136 tch repair has been implicated as a cause of triplet repeat expansions that cause neurological diseas

137 tion-deletion heterologies but also triggers triplet repeat expansions that cause neurological diseas

138 We conclude that Srs2 selectively blocks triplet repeat expansions through its helicase activity

139 ection technique to determine whether (CAG)n triplet repeat expansions were present in DNA from malig

140 slippage, the most likely mechanism in other triplet repeat expansions.

141 esis mediates all of the disease-associated, triplet repeat expansions.

142 ry are effectively competed by RNAs with CGG triplet repeat expansions.

143 Triplet-repeat expansions cause several inherited human

144 Here we show that the relatively short triplet-repeat expansions found in myotonic dystrophy an

145 lippage in DNA replication or repair to give triplet-repeat expansions like those associated with neu

146 the trpP TRAP binding site consists of nine triplet repeats (five GAG, three UAG, and one AAG) that

147 s observation for DNA containing CTG and CGG triplet repeats flanked by mixed sequence DNA.

148 reich ataxia is caused by expansion of a GAA triplet repeat (GAA-TR) in the FRDA gene.

149 ia (FRDA) are homozygous for an expanded GAA triplet repeat (GAA-TR) mutation in intron 1 of the FXN

150 h ataxia (FRDA) is caused by an expanded GAA triplet-repeat (GAA-TR) mutation in the FXN gene.

151 commonly caused by large expansions of a GAA triplet-repeat (GAA-TR) sequence in the first intron of

152 Expansions of the triplet repeat, GAA/TTC, inside the first intron of the

153 or deletion of one codon within a very short triplet repeat, (GAC)5, which encodes five consecutive a

154 the selective unwinding activity of Srs2 on triplet repeat hairpin DNA helps explain the genetic evi

155 nwinding DNA substrates with an extrahelical triplet repeat hairpin embedded in a duplex context.

156 mary, Srs2 maintains its facile unwinding of triplet repeat hairpins embedded within duplex DNA, supp

157 1 at unwinding several substrates containing triplet repeat hairpins or another structured loop.

158 the idea that Srs2 might selectively unwind triplet repeat hairpins.

159 The expansion of DNA triplet repeats has been shown to be responsible for abo

160 Expanded triplet repeats have been identified as the genetic basi

161 n has a biological basis in expanded genetic triplet repeats; however, some have claimed that it occu

162 insertion-deletion polymorphism, and an ATT triplet repeat in 131 unrelated diabetic patients and 11

163 emonstration of replication attenuation by a triplet repeat in a eukaryotic system in vivo.

164 is the unstable hyperexpansion of a GAA.TTC triplet repeat in the first intron of the frataxin gene.

165 r an abnormal expansion of a polymorphic GAA triplet repeat in the first intron of the X25 gene, whic

166 determine the meiotic instability of the CGG-triplet repeat in the fragile-X gene, FMR1, we examined

167 c chromosomes have large expansions of a GAA triplet repeat in the FRDA gene (E alleles), and strong

168 expansion of a polymorphic and unstable GAA triplet repeat in the FRDA gene, but the mechanisms for

169 ington's disease (HD), caused by an expanded triplet repeat in the huntingtin (Htt) gene, results in

170 ive disease caused by the expansion of a CAG triplet repeat in the SCA1 gene.

171 systemic disorder caused by expansion of CTG triplet repeats in 3'-untranslated region of DMPK gene.

172 ference human genome, we have catalogued all triplet repeats in genic regions.

173 e strong expansion bias seen in expanded CTG triplet repeats in myotonic dystrophy.

174 d displacement limited to the two downstream triplet repeats in our constructs.

175 Expansion of CTG triplet repeats in the 3' untranslated region of the DMP

176 uscular dystrophy caused by expanded CTG.CAG triplet repeats in the 3' untranslated region of the DMP

177 The abundance of (A-R-N)(4) and (A-R-N)(5) triplet repeats in the E. coli genome suggests additiona

178 (HD) is caused by an expansion of exonic CAG triplet repeats in the gene encoding huntingtin protein

179 (HD) is caused by an expansion of exonic CAG triplet repeats in the gene encoding the huntingtin prot

180 ight into GAA-TR instability we analyzed all triplet repeats in the human genome.

181 the mechanism of instability of the GAA.TTC triplet repeats in the human genome.

182 nerative disorder caused by expansion of CAG triplet repeats in the huntingtin (HTT) gene (also calle

183 ated with length variation of trinucleotide (triplet) repeats including Huntington's disease, heredit

184 The derivatives contained various triplet repeat inserts ((CTG.CAG), (CGG.CCG), (GAA.TTC),

185 r leading strand synthesis, we conclude that triplet repeat instability can also occur on the leading

186 ese results suggest that UvrA is involved in triplet repeat instability in cells.

187 st the effects of antisense transcription on triplet repeat instability in human cells.

188 Drosophila melanogaster displays triplet repeat instability with features that recapitula

189 local chromatin structure may play a role in triplet repeat instability.

190 However, the mechanism(s) of CTG.CAG triplet-repeat instability is not fully understood.

191 These studies suggest that in FRDA, GAA.TTC triplet-repeat instability occurs in embryonic cells and

192 to further modulate the fork-shift model of triplet-repeat instability.

193 lay important roles in telomere, centromere, triplet repeat, integration sites and other DNAs, and th

194 is a robust mechanism for expanding CTG.CAG triplet repeats involved in the etiology of hereditary n

195 The GAA triplet repeat is known to adopt a triplex structure, an

196 The length of the triplet repeat is the most important factor in determini

197 In humans, expansion of intragenic triplet repeats is associated with various diseases, inc

198 Mutational expansion of certain triplet repeats is responsible for several hereditary ne

199 In mammalian cells instability of triplet-repeats is dependent on the location of the orig

200 ch is defined by the presence of the Gly-X-Y triplet repeats, is amongst the most versatile and wides

201 replication, repair or recombination of the triplet repeat, leading to expansion.

202 The effects of triplet repeat length and orientation were studied after

203 The CTG triplet repeat length of the largest allele was compared

204 th the observed negative correlation between triplet-repeat length and the age at onset of disease.

205 on multiple factors, including DNA sequence, triplet-repeat length and unknown cell-type-specific fac

206 is mainly caused by massive expansion of CGG triplet repeats located in the 5'-untranslated region of

207 a uniform, single stranded loop, the (CAG)6 triplet repeat looped domain exhibits order and dynamics

208 e 4C (CRS4C) peptides that have a unique CPX triplet repeat motif.

209 Our data demonstrate that the GAA triplet repeat mutation in Friedreich ataxia is destabil

210 age-dependent, further expansion of the GAA triplet-repeat mutation.

211 anding the genetic processes responsible for triplet repeat mutations in the COMP gene.

212 DMPK mRNAs) carrying variable numbers of CUG triplet repeats (n = 0 to 500).

213 n's disease (HD) is one of eight established triplet repeat neurodegenerative disorders, which are co

214 as the massive repeat expansions in type II triplet repeat neurological diseases.

215 a positive correlation of Krachmer grade to triplet repeat number (P = .002) and a nominal associati

216 ociation of the keratoplasty proportion with triplet repeat number (P = .04).

217 ner that provides the relative proportion of triplet repeat oligonucleotides in seconds per sample.

218 asmids without active transcription into the triplet repeat, or those maintained in exponential growt

219 CYC184 was used to investigate the effect of triplet repeat orientation on recombination and extent o

220 llized, and determined the structure of a 12-triplet repeating peptide containing the natural type II

221 sease that affects males, results from a CAG triplet repeat/polyglutamine expansions in the androgen

222 The triplet repeat polymorphism CTG18.1 was genotyped using

223 The binding sequence is composed of eleven triplet repeats, predominantly GAG, separated by two or

224 e disorders caused by the lengthening of CAG triplet repeats present in the coding sequences of seemi

225 combination of short tandem repeat analysis, triplet repeat-primed polymerase chain reaction assay, a

226 They may also have implications for triplet repeat processing at a replication fork.

227 ndings provide a mechanism for initiation of triplet repeat processing in nonreplicating DNA that is

228 rative disease, is caused by an expanded CAG triplet repeat producing a mutant huntingtin protein (mH

229 amination of length polymorphisms at 20 long triplet-repeats repeats in S. cerevisiae, and by compari

230 eats expanded at a rate of about two GAA.TTC triplet repeats/replication.

231 ions and also carried alleles with 44 and 66 triplet-repeats, respectively.

232 r work demonstrated that CTG*CAG and GAA*TTC triplet repeats (responsible for DM1 and Friedreich's at

233 We sought to determine how expression of triplet repeat RNA causes the varied phenotype typical o

234 The second complex was found to contain CUG triplet repeat RNA-binding protein 1 (CUGBP1) and the tr

235 The triplet repeat sequence (CAG)n and related triplet repea

236 Triplet repeat sequence (TRS) inserts containing (CTG.CA

237 The orientation of the triplet repeat sequence (TRS) relative to the unidirecti

238 rative disorder caused by expansion of a CAG triplet repeat sequence encoding a polyglutamine tract i

239 Triplet repeat sequence instability is associated with h

240 the viral mRNA 5' cap and a highly conserved triplet repeat sequence of the viral mRNA 5' UTR.

241 nces of double-strand breaks (DSBs) within a triplet repeat sequence on its genetic instabilities (ex

242 he 5' end, either two or three copies of the triplet repeat sequence, UAGUAG or UAGUAGUAG.

243 vo methylation of a greatly expanded CGG.CCG triplet repeat sequence.

244 n also mediated genetic instabilities of the triplet repeat sequence.

245 Large intronic expansions of the triplet-repeat sequence (GAA.TTC) cause transcriptional

246 ich ataxia (FRDA) is a hyperexpansion of the triplet-repeat sequence GAA.TTC within the first intron

247 herited ataxia, is caused by an expanded GAA triplet-repeat sequence in intron 1 of the FXN gene.

248 lyze somatic instability of the expanded GAA triplet-repeat sequence in multiple tissues obtained fro

249 are homozygous for expanded alleles of a GAA triplet-repeat sequence in the FXN gene.

250 hus, somatic instability of the expanded GAA triplet-repeat sequence may contribute directly to disea

251 sive chromatin spreads from the expanded GAA triplet-repeat sequence to cause epigenetic silencing of

252 jective was to test whether the expanded GAA triplet-repeat sequence undergoes further expansion in D

253 upstream and downstream of the expanded GAA triplet-repeat sequence, without any change in transcrip

254 accumulation of large expansions of the GAA triplet-repeat sequence.

255 differs from all previous results with three triplet repeat sequences (including CTG.CAG), which are

256 The expansion of triplet repeat sequences (TRS) associated with hereditar

257 Genetic expansion of DNA triplet repeat sequences (TRS) found in neurogenetic dis

258 Genetic instability investigations on three triplet repeat sequences (TRS) involved in human heredit

259 ith uvrA, uvrB and uvrAuvrB mutants with the triplet repeat sequences (TRS) involved in myotonic dyst

260 Since the triplet repeat sequences (TRS) were symmetrically positi

261 Genomic expansion of the triplet repeat sequences 5'-(CTG)n and 5'-(CGG)n leads t

262 This suggests that misaligned triplet repeat sequences are subject to proofreading, bu

263 res formed by the individual single-stranded triplet repeat sequences are thermally and thermodynamic

264 Although the triplet repeat sequences d(GAC)n and d(GTC)n also form h

265 xpansion of disease-associated (CAG)n/(CTG)n triplet repeat sequences have implicated both MutSbeta a

266 Expansions and deletions of triplet repeat sequences that cause human hereditary neu

267 , the newly discovered capacities of certain triplet repeat sequences to cause gross chromosomal rear

268 Also, the persistence lengths of the triplet repeat sequences were approximately 60% the valu

269 ked for gene expansion in genomes possessing triplet repeat sequences, CNG, where N = A, C, G, or T.

270 Triplet repeat sequences, such as CAG/CTG, expand in the

271 However, similar to the triplet repeat sequences, the ability of one of the two

272 for the Friedreich ataxia and the fragile X triplet repeat sequences.

273 aracteristics may be a common feature of all triplet repeat sequences.

274 s-specific differences in instability of GAA triplet-repeat sequences.

275 This portion of SM, comprised of RXP triplet repeats, shows homology to the carboxyl-terminal

276 We discuss this stable, triplet repeat, single-stranded structure and its interc

277 sed by expansion in different genes of a CAG triplet repeat stretch, which encodes an elongated polyg

278 orientation, and sequence composition of the triplet repeat suggested an important role of DNA second

279 subunit of AMP-activated protein kinase and triplet-repeat syndromes and in mitochondrial DNA, have

280 caused by an expansion of a polymorphic CGG triplet repeat that results in silencing of FMR1 express

281 sites containing a series of 9 or 11 (G/U)AG triplet repeats that are generally separated by two or t

282 However, the overall tendency of triplet repeats to expand ceased on differentiation into

283 The triplet repeat tract in a non-B conformation is the muta

284 esence of a sequence interruption within the triplet repeat tract.

285 ingle abasic site analog, synthesized in the triplet-repeat tract at the 5' end of the template stran

286 Triplet repeat tracts occur throughout the human genome.

287 ted at nicks or 1-base gaps within short (14 triplet) repeat tracts in DNA duplexes under physiologic

288 Its translation initiation region contains triplet repeats typical of TRAP-regulated mRNAs.

289 FEN1 cleavage of foldback flaps, bubbles, or triplet repeats was increased by an additional increment

290 disease-relevant lengths of (CTG)n x (CAG)n triplet repeats were examined.

291 rint studies revealed that the central seven triplet repeats were protected by bound TRAP, while toep

292 Most other triplet repeats were restricted to <20 triplets.

293 However, GAA.TTC triplet repeats were stable in FRDA fibroblasts and neur

294 on, molecules of 224-245 bp in length (64-71 triplet repeats) were able to form topological isomers u

295 oth situated immediately upstream of the GAA triplet repeat, were therefore examined for somatic muta

296 In DM1, the expansion is an rCUG triplet repeat, whereas the DM2 expansion is an rCCUG qu

297 icrom of each dNTP), polymerase beta expands triplet repeats with the help of weak strand displacemen

298 Conjugates targeting the CAG triplet repeat within huntingtin (HTT) mRNA selectively

299 disease is caused by the expansion of a CAG triplet repeat within the context of the 3144-amino acid

300 of the upstream pabB gene, while six of nine triplet repeats within the TRAP binding site are located