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 nding proceeds unabated through extrahelical triplet repeats.

8 Several of these are non-polyglutamine triplet repeats.

9 replication in the recombination process of triplet repeats.

10 ative mutability of dispersed expanded human triplet repeats.

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

12 dentity with previously published cDNAs with triplet repeats.

13 p process, resulting in a median loss of ~60 triplet repeats.

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

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

16 elocalization to the NPC of expanded CAG/CTG triplet repeats.

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

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

19 The CTG triplet repeat allele length was positively correlated w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Trinucleotide, or triplet, repeats consist of 3 nucleotides consecutively

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

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

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

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

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

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

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

52 Triplet repeat diseases (TRDs) are caused by pathogenic

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 ic interventions in HD and potentially other triplet repeat disorders.

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

67 lying pathophysiological mechanisms of other triplet repeat disorders.

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

69 Similar to other triplet-repeat disorders, it is unknown why FRDA affects

70 a is a unique endonuclease that can initiate triplet repeat DNA expansions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 inhibition as an attractive therapy in some triplet repeat expansion diseases.

93 An unstable CAG triplet repeat expansion encoding a polyglutamine stretc

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

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

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

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

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

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

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

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

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

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

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

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

106 In addition to MutLgamma, triplet repeat expansion involves the mismatch recogniti

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

108 In humans, triplet repeat expansion is the molecular basis for ~40

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

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

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

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

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

114 of MutL proteins that has been implicated in triplet repeat expansion, but its action in this deleter

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 HDAC3 function in the same pathway to drive triplet repeat expansions.

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

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

147 into an innovative regulatory mechanism for triplet repeat expansions.

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

149 Triplet-repeat expansions cause several inherited human

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

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

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

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

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

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

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

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

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

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

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

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

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

163 1 at unwinding several substrates containing triplet repeat hairpins or another structured loop.

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

165 Expanded triplet repeats have been identified as the genetic basi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Drosophila melanogaster displays triplet repeat instability with features that recapitula

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 the stability and versatility of the d(CGA) triplet repeat motif and provides constraints for using

214 The d(CGA) triplet repeat motif is structurally dynamic and can tra

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

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

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

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

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

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

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

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

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

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

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

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

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

228 The triplet repeat polymorphism CTG18.1 was genotyped using

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 Triplet repeat sequence instability is associated with h

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 Triplet repeat tracts occur throughout the human genome.

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

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

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

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

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

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

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