ライフサイエンスコーパス: trinucleotide repeat

1 are caused by expansion of a coding CAG DNA trinucleotide repeat.

2 iseases attributed to the amplification of a trinucleotide repeat.

3 to result from the expansion of an unstable trinucleotide repeat.

4 d for an exploration into the stability of a trinucleotide repeat.

5 at CTG.CAG tracts promote instability of DNA trinucleotide repeats.

6 bbed "Z," "HJ," "G4," and "H" DNA-as well as trinucleotide repeats.

7 ) with dinucleotide repeats and 6 (11%) with trinucleotide repeats.

8 ic instability and transcription of expanded trinucleotide repeats.

9 thesis accompanying gene conversion of these trinucleotide repeats.

10 sorders are associated with the expansion of trinucleotide repeats.

11 espiratory tract specimens and had longer p1 trinucleotide repeats.

12 presence of RecA, ADP-AlF4 and 64 different trinucleotide-repeating 15mer oligonucleotides was deter

13 We investigated the ability of trinucleotide repeats AAT and CAG to expand in size duri

14 on's disease, are caused by the expansion of trinucleotide repeats above a threshold of about 35 repe

15 Although expansion of trinucleotide repeats accounts for over 30 human disease

16 ing number of disorders known to result from trinucleotide repeat amplification, the molecular mechan

17 rders are associated with the expansion of a trinucleotide repeat and array length is positively corr

18 1 gene due to an unstable expansion of a CGG trinucleotide repeat and its subsequent hypermethylation

19 The disease is caused by expansion of a CAG trinucleotide repeat and manifests with progressive moto

20 of male CGG KI mice carrying an expanded CGG trinucleotide repeat and used to model FXTAS, but no stu

21 FraX, ageing, increases in the number of CGG trinucleotide repeats and decreases in %FMRP(+) lymphocy

22 ing an association of nucleosome assembly of trinucleotide repeats and genetic instability.

23 e results contribute to our understanding of trinucleotide repeats and the factors that regulate pers

24 te-like elements composed of dinucleotide or trinucleotide repeats, and a direct repeat sequence.

25 ng duplex RNAs complementary to the expanded trinucleotide repeat are potent and allele-selective inh

26 Trinucleotide repeats are a source of genome instability

27 Expanded trinucleotide repeats are associated with several neurop

28 Genetically unstable expanded CAG.CTG trinucleotide repeats are causal in a number of human di

29 CAG trinucleotide repeats are known to cause 10 late-onset p

30 s indicate that expansion and instability of trinucleotide repeats are not exclusively disease-associ

31 Expanded trinucleotide repeats are responsible for a number of ne

32 synthesis when DNA loops comprising the CAG trinucleotide repeats are sealed into the DNA strand.

33 CAG/CTG trinucleotide repeats are unstable, fragile sequences th

34 Inheritance of an expanded p(CCG)n trinucleotide repeat at the folate-sensitive fragile sit

35 A 27-bp trinucleotide repeat (CAG)(9) encoding polyserine was fo

36 Trinucleotide repeats can form secondary structures, who

37 Trinucleotide repeats can form stable secondary structur

38 ed with short RNAs that are enriched for the trinucleotide repeat (CAN)4.

39 one group of simple tandem repeats, the DNA trinucleotide repeats, can dramaticallyexpand in size du

40 Expansions of trinucleotide repeats cause at least 15 heritable human

41 Expanded trinucleotide repeats cause many neurological diseases.

42 ding the mechanism by which expanded CTG/CAG trinucleotide repeats cause neurodegenerative diseases,

43 Expansion of CAG/CTG trinucleotide repeats causes certain familial neurologic

44 th of the ORFs contain long stretches of the trinucleotide repeat CAX, encoding polyglutamine (with a

45 A region containing a stretch of (G/A)AG trinucleotide repeats, characteristic of a TRAP binding

46 ngton's disease is caused by an expanded CAG trinucleotide repeat coding for a polyglutamine stretch

47 The TNRC6 (trinucleotide repeat containing 6) family of proteins ha

48 s that TRIM65 interacts and colocalizes with trinucleotide repeat containing six (TNRC6) proteins in

49 een shown that lncRNA AK017368 competes with trinucleotide repeat containing-6A (Tnrc6a) for miR-30c.

50 pinach2, we detailed the dynamics of the CGG trinucleotide repeat-containing 'toxic RNA' associated w

51 The gene trinucleotide repeat-containing 4 (TNRC4) is predicted t

52 The breast cancer gene trinucleotide-repeat-containing 9 (TNRC9; TOX3) has been

53 netic disease caused by the expansion of CTG trinucleotide repeats ((CTG)exp) in the 3' untranslated

54 The pathological expansion of unstable trinucleotide repeats currently is known to cause 14 neu

55 Trinucleotide repeat disease alleles can undergo 'dynami

56 decades prior to the diagnosis of late-onset trinucleotide repeat disease.

57 isms (SNPs) is a promising therapy for human trinucleotide repeat diseases such as Huntington's disea

58 Trinucleotide repeat diseases, such as Huntington's dise

59 rstanding the molecular etiology of expanded trinucleotide repeat diseases.

60 nderstand the common genetic architecture of trinucleotide repeat disorders and any further genetic s

61 Trinucleotide repeat disorders are severe, usually life-

62 ich's ataxia were among the first pathogenic trinucleotide repeat disorders to be described in which

63 ion of repeated sequences in mouse models of trinucleotide repeat disorders, and somatic expansion of

64 e at onset of Huntington's disease and other trinucleotide repeat disorders.

65 targets (and hence therapeutics) in multiple trinucleotide repeat disorders.

66 as been reported to occur in a number of the trinucleotide repeat disorders.

67 repeat tracts in HD, and possibly, in other trinucleotide repeat disorders.

68 promising molecule for antisense therapy of trinucleotide repeat disorders.

69 capacity to incorporate ribonucleotides into trinucleotide repeated DNA sequences and the efficiency

70 n 1 (FMR1) gene contains a polymorphic (CGG) trinucleotide repeat element in its 5' untranslated regi

71 pairment, is caused by expansion of a (CGG)n trinucleotide repeat element located in the 5' untransla

72 e expansions in two of three large imperfect trinucleotide repeats encoded by the first exon of HOXA1

73 ive diseases caused by an expansion of a CAG trinucleotide repeat encoding a glutamine tract in the r

74 ve diseases caused by the expansion of a CAG trinucleotide repeat encoding a polyglutamine tract.

75 from S. douglasii and S. paradoxus contain a trinucleotide repeat encoding polyAsn that is lacking in

76 It is caused by an expansion of a CAG trinucleotide repeat encoding polyglutamine in the atrop

77 oteins is affected by their sequestration to trinucleotide repeat expanded mRNAs in several disorders

78 erative disorder caused by a premutation CGG-trinucleotide repeat expansion (55-200 CGG repeats) with

79 n autosomal dominant fashion and caused by a trinucleotide repeat expansion (CAG) in the gene encodin

80 of the general class of human diseases with trinucleotide repeat expansion but also provide an avenu

81 ponents in RNA-based and polyQ-protein-based trinucleotide repeat expansion diseases.

82 the continued expansions seen in humans with trinucleotide repeat expansion diseases.

83 e reference genome, confirming that BSS is a trinucleotide repeat expansion disorder.

84 orders, 12 case subjects with imprinting and trinucleotide repeat expansion disorders, as well as 106

85 FECD patient population with this (CTG.CAG)n trinucleotide repeat expansion exceeds that of the combi

86 ion has been identified recently as a stable trinucleotide repeat expansion in exon 1 of the poly(A)

87 nant neurodegenerative disease caused by CAG trinucleotide repeat expansion in HTT, resulting in a mu

88 This may have relevance to trinucleotide repeat expansion in human genetic disease.

89 The TGC trinucleotide repeat expansion in TCF4 is strongly assoc

90 is one such condition, resulting from a CGG trinucleotide repeat expansion in the 5' leader sequence

91 a neurodegenerative disorder caused by a CGG trinucleotide repeat expansion in the 5' UTR of the Frag

92 tardation is caused, in most cases, by a CGG trinucleotide repeat expansion in the 5'-untranslated re

93 n almost all cases by homozygosity for a GAA trinucleotide repeat expansion in the frataxin gene.

94 etic, neurological disorder resulting from a trinucleotide repeat expansion in the gene that encodes

95 t neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the HD gene.

96 e neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin (HTT) g

97 a neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin (HTT) g

98 rative disorder caused by a pathological CAG trinucleotide repeat expansion in the large multi-exon g

99 OPMD is caused by a trinucleotide repeat expansion in the PABPN1 gene that r

100 This muscle disease is due to a trinucleotide repeat expansion in the polyA-binding prot

101 erative disorder that is the result of a CGG trinucleotide repeat expansion in the range of 55-200 in

102 t association is with an intronic (CTG.CAG)n trinucleotide repeat expansion in the TCF4 gene, which i

103 the parent-of-origin effect associated with trinucleotide repeat expansion is not known.

104 The loss of FMR1 expression due to trinucleotide repeat expansion leads to fragile X syndro

105 two Huntington disease patients showed that trinucleotide repeat expansion mutations were present be

106 duals, and no tested unaffecteds, have a CAG trinucleotide repeat expansion of 50 to 60 triplets, as

107 Fragile X syndrome is caused by a CGG trinucleotide repeat expansion of the FMR1 gene.

108 re few studies on the effect of pre-mutation trinucleotide repeat expansion on the male human brain u

109 Huntington's disease is caused by a CAG trinucleotide repeat expansion that is translated into a

110 ne of 10 known diseases caused by a (CAG)(n) trinucleotide repeat expansion that is translated into a

111 Trinucleotide repeat expansion underlies at least 17 neu

112 trophy or Kennedy disease is caused by a CAG trinucleotide repeat expansion within the androgen recep

113 eases caused by a polyglutamine-encoding CAG trinucleotide repeat expansion, and is caused by an expa

114 A trinucleotide repeat expansion, inactivating the X-linke

115 hile the etiology of HD is known to be a CAG trinucleotide repeat expansion, the pathways by which th

116 affecting DNA fragility from those affecting trinucleotide repeat expansion-contraction instability.

117 relationship between non-B conformations and trinucleotide repeat expansion.

118 ontribute to the OGG1-dependent mechanism of trinucleotide repeat expansion.

119 es of neurodegenerative diseases caused by a trinucleotide repeat expansion.

120 essive neurodegenerative disorder cause by a trinucleotide repeat expansion.

121 on genetic form of mental retardation, a CGG trinucleotide-repeat expansion adjacent to the fragile X

122 vailable parent-child pairs, suggesting that trinucleotide-repeat expansion may be the mutagenic mech

123 Thus, our data link trinucleotide-repeat expansion to a form of RNA-directed

124 r HD causative mutations, that is, IT15 gene trinucleotide-repeat expansion.

125 gically important repetitive DNAs, including trinucleotide repeat expansions and homologous gene fami

126 Trinucleotide repeat expansions are the mutational cause

127 X syndrome, and myotonic dystrophy-caused by trinucleotide repeat expansions have been identified.

128 The involvement of trinucleotide repeat expansions in a number of other dis

129 Trinucleotide repeat expansions in FMR1 abolish FMRP exp

130 Homozygous GAA trinucleotide repeat expansions in the first intron of F

131 set neurodegenerative disorder caused by CGG trinucleotide repeat expansions in the fragile X mental

132 set neurodegenerative disorder caused by CGG trinucleotide repeat expansions in the fragile X mental

133 Trinucleotide repeat expansions may prove to cause patho

134 ng the germ-line cell compartments where the trinucleotide repeat expansions occur could help to eluc

135 l dominant, progressive disease, arises from trinucleotide repeat expansions present in the coding re

136 bility by creating transgenic flies carrying trinucleotide repeat expansions, deriving flies with SCA

137 The mechanisms of trinucleotide repeat expansions, underlying more than a

138 Because several other SCA subtypes show trinucleotide repeat expansions, we examined microsatell

139 e of aggregate formation, oligomers with AGG trinucleotide repeats fail to exhibit Psi-CD formation.

140 As a consequence, the trinucleotide repeat field has grown dramatically since

141 Large expansions of the trinucleotide repeat GAA*TTC within the first intron of

142 It is caused by a large expansion of the CGG trinucleotide repeat (>200 repeats) in the 5'-untranslat

143 retardation, is caused by expansion of a CCG trinucleotide repeat (>200) in the 5'-UTR of the FMR2 ge

144 s reveal that, in contrast to Pot1pN, tandem trinucleotide repeats (GTT) within d(GGTTACGGTTAC) are s

145 These results demonstrate that the trinucleotide repeat hairpins can convert to duplex via

146 have a profound effect on the ability of the trinucleotide repeat hairpins to convert to duplex.

147 The expansion of CAG.CTG trinucleotide repeats has been associated with an increa

148 ylation of cytosine in extended (CCG).(CGG)n trinucleotide repeats has been shown to cause fragile-X

149 We have previously shown that GAA trinucleotide repeats have undergone significant expansi

150 ) ageing; (ii) expansion of pre-mutation CGG trinucleotide repeats; (iii) reduction in the percentage

151 ed, during transmission, the fate of the CAG trinucleotide repeat in a transgene containing the exon

152 al disorder caused by the expansion of a CAG trinucleotide repeat in exon 1 of the gene coding for a

153 etardation 1 (FMR1) gene contains a (CGG)(n) trinucleotide repeat in its 5' untranslated region (5'UT

154 y in spite of critical expansions of the CGG trinucleotide repeat in male or female premutation carri

155 d for an association between an intronic TGC trinucleotide repeat in TCF4 and FECD by determining rep

156 lar disease caused by the expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene.

157 Expansion of a CTG trinucleotide repeat in the 3' UTR of the gene DMPK at t

158 the result of an unstable expansion of a CGG trinucleotide repeat in the 5' UTR of the fragile X ment

159 rative disorder, attributable to an expanded trinucleotide repeat in the coding region of the human H

160 caused by the abnormal expansion of a (GCG)n trinucleotide repeat in the coding region of the poly-(A

161 generative disease caused by an expanded CAG trinucleotide repeat in the first exon of the HD gene, w

162 In humans, Fragile X results from a trinucleotide repeat in the Fmr1 gene that renders it fu

163 c disease caused by expansion of an intronic trinucleotide repeat in the frataxin (FXN) gene yielding

164 This disease is caused by an expanded CAG trinucleotide repeat in the gene encoding the protein hu

165 s primarily caused by the expansion of a CAG trinucleotide repeat in the huntingtin (Htt) gene, which

166 s, is linked to an expanded and unstable CAG trinucleotide repeat in the huntingtin gene (HTT).

167 ion of a polyalanine tract-encoding (GCG)(n) trinucleotide repeat in the poly-(A) binding protein nuc

168 The length of the polymorphic CAG trinucleotide repeat in the polyglutamine region of the

169 Expansion of CAG trinucleotide repeats in ATXN1 causes spinocerebellar at

170 d were characterized by uninterrupted di- or trinucleotide repeats in both species; seven of these lo

171 Small-molecule compounds targeting trinucleotide repeats in DNA have considerable potential

172 methylation status of CpG sites close to the trinucleotide repeats in exon 1 of the human androgen re

173 er is known to influence the transmission of trinucleotide repeats in human disease.

174 Expanded GAA.TTC trinucleotide repeats in intron 1 of the frataxin gene c

175 ivated by tryptophan, TRAP binds to multiple trinucleotide repeats in target transcripts.

176 This disease is caused by expanded CTG trinucleotide repeats in the 3' UTR of the dystrophia my

177 and EXO1 can eliminate structures formed by trinucleotide repeats in the course of replication, rely

178 ine-guanine (CAG, translated into glutamine) trinucleotide repeats in the first exon of the human hun

179 caused by an expansion in the number of CAG trinucleotide repeats in the huntingtin gene.

180 not dependent on the presence of 12-copy GAA trinucleotide repeats in the promoter region and did not

181 Our findings also suggest that trinucleotide repeat instability can occur by mechanisms

182 ch, unbiased screens for factors involved in trinucleotide repeat instability have been lacking.

183 Trinucleotide repeat instability underlies >20 human her

184 es in methylation status might contribute to trinucleotide repeat instability, we examined the effect

185 tain mutations, including disease-associated trinucleotide repeat instability.

186 nsion of polyglutamine tracts encoded by CAG trinucleotide repeats is a common mutational mechanism i

187 Expansion of trinucleotide repeats is associated with a growing numbe

188 scovery that the expansion of microsatellite trinucleotide repeats is responsible for a prominent cla

189 hat the abundance of large expansions of GAA trinucleotide repeats is specific to mammals.

190 Instability of CAG DNA trinucleotide repeats is the mutational mechanism for se

191 ntifying the mechanism by which the expanded trinucleotide repeat leads to abnormal cellular function

192 i within the human genome where expansion of trinucleotide repeats leads to disease.

193 Alterations in trinucleotide repeat length during transmission are impo

194 atellites and minisatellites, telomeres, and trinucleotide repeats (linked to fragile X syndrome, Hun

195 ults from expansion and methylation of a CCG trinucleotide repeat located in exon 1 of the X-linked F

196 on, results from the hyperexpansion of a CGG trinucleotide repeat located in the 5' untranslated regi

197 ype 2 (SCA2) is caused by expansion of a CAG trinucleotide repeat located in the coding region of the

198 level by expansion and methylation of a CGG trinucleotide repeat located within the FMR1 locus.

199 h the genetic instability of the (GAA).(TTC) trinucleotide repeats located within the frataxin gene.

200 rand nucleation of duplex DNA within GC-rich trinucleotide repeats may result in the changes of repea

201 sorder caused by pathological expansion of a trinucleotide repeat motif present within exon 4 of the

202 e length distribution of all 10 nonredundant trinucleotide repeat motifs in 20 complete eukaryotic ge

203 tween our FRDA YAC transgenic mice and other trinucleotide-repeat mouse models, which do not show pro

204 tington's disease (HD) patients with similar trinucleotide repeat mutations can have an age of onset

205 A-A noncanonical pairs in (CAG)n and (GAC)n trinucleotide repeats (n = 1, 4) and the consequent chan

206 attained into the molecular pathology of the trinucleotide repeat neurodegenerative diseases over the

207 h is caused by the expansion of an imperfect trinucleotide repeat, occurred in seven patients from si

208 ic mice model carrying an expanded CGG((98)) trinucleotide repeat of human origin but have not previo

209 The fact that (1) trinucleotide repeats often become increasingly unstable

210 ystrophy and is caused by expansion of a CTG trinucleotide repeat on human chromosome 19.

211 through promiscuous OTEs produced by tandem trinucleotide repeats present in many dsRNAs and genes.

212 of the Huntington's model of GFP containing trinucleotide repeats (Q103-GFP).

213 thylation in a number of genes which contain trinucleotide repeat regions, including the androgen rec

214 s have been associated with the expansion of trinucleotide repeat regions.

215 and a more heterogeneous group in which the trinucleotide repeat remains untranslated.

216 d oligonucleotides comprising all tetra- and trinucleotide repeats revealed an inverse correlation be

217 provides a high-resolution view of a toxic, trinucleotide repeat RNA.

218 ncing mediated by direct interactions of the trinucleotide-repeat RNA and DNA.

219 The trinucleotide repeat sequence CGG/CCG is known to expand

220 n unusual secondary structures formed by the trinucleotide repeat sequence d[CCG]n, and associated wi

221 either plasmid dimers of DNAs with a single trinucleotide repeat sequence tract or by monomeric DNAs

222 The expansion of a trinucleotide repeat sequence, such as CAG/CTG, has been

223 of asthmatic individuals, and variations of trinucleotide repeat sequences as identified in several

224 nary analysis identified 185 mono-, di-, and trinucleotide repeat sequences dispersed throughout the

225 etic instability, specifically expansion, of trinucleotide repeat sequences such as (CTG)(n).(CAG)(n)

226 nt role in preventing instability of CAG/CTG trinucleotide repeat sequences, as the expansion frequen

227 Famous in the medical world are the trinucleotide repeat sequences, such as (CTG)(n), and th

228 Trinucleotide repeat sequences, such as (GAA)n repeats i

229 iption stimulates the genetic instability of trinucleotide repeat sequences.

230 For selected trinucleotide-repeating sequences, the DNA-dependent ATP

231 In humans, trinucleotide repeats show extreme meiotic instability,

232 e involvement of other MMR proteins in short trinucleotide repeat slip-out repair is unknown.

233 ing mutation is the expansion of an unstable trinucleotide repeat, specifically a CAG repeat that enc

234 fects of DNA methyltransferase inhibitors on trinucleotide repeat stability in mammalian cells.

235 identified differed mostly in the numbers of trinucleotide repeats (TCA, TCG, or TCT) in the serine r

236 ve disorder caused by the expansion of a CTG trinucleotide repeat that is transcribed as part of an u

237 er in humans caused by an expansion of a CAG trinucleotide repeat that produces choreic movements, wh

238 functions by targeting T:T mismatches in CTG trinucleotide repeats that are responsible for causing n

239 nt for human disease etiology, we identified trinucleotide repeats that exist within exons of known g

240 isms such as uniparental disomy and unstable trinucleotide repeats that were not suspected from anima

241 The expansion of a polymorphic trinucleotide repeat (the sequence CAG that codes for gl

242 n gene into two regions: one consisting of a trinucleotide repeat (TNR) and the other consisting of t

243 tion initiation regions (IRs) at three human trinucleotide repeat (TNR) disease loci were examined in

244 contribute to disorders including cancer and trinucleotide repeat (TNR) disease.

245 In most trinucleotide repeat (TNR) diseases, the primary factor

246 Trinucleotide repeat (TNR) expansion and deletion are re

247 (CTG)(n) . (CAG)(n) trinucleotide repeat (TNR) expansion in the 3' untransla

248 Trinucleotide repeat (TNR) expansion is responsible for

249 DNA trinucleotide repeat (TNR) expansion underlies several n

250 that MSH2-MSH3 and the BER machinery promote trinucleotide repeat (TNR) expansion, yet how these two

251 are prone to the devastating consequences of trinucleotide repeat (TNR) expansion.

252 n yeast results in a significant increase in trinucleotide repeat (TNR) expansion.

253 lso reveals its important role in preventing trinucleotide repeat (TNR) expansion.

254 Trinucleotide repeat (TNR) expansions and deletions are

255 Trinucleotide repeat (TNR) expansions and deletions are

256 Trinucleotide repeat (TNR) expansions cause nearly 20 se

257 Trinucleotide repeat (TNR) instability in humans is gove

258 Trinucleotide repeat (TNR) instability is of interest be

259 n of affected progeny due to expansions of a trinucleotide repeat (TNR) region within the HTT gene.

260 re fragile sites (RFSs) characterized by CGG trinucleotide repeat (TNR) sequences.

261 on repair (BER) of an oxidized base within a trinucleotide repeat (TNR) tract can lead to TNR expansi

262 Expansion of trinucleotide repeats (TNR) has been implicated in the e

263 Of particular interest are flaps containing trinucleotide repeats (TNR), which have been proposed to

264 DNA trinucleotide repeats (TNRs) are found at a higher-than-

265 Genomic regions containing trinucleotide repeats (TNRs) are highly unstable, as the

266 Trinucleotide repeats (TNRs) are sequences whose expansi

267 Expansions of trinucleotide repeats (TNRs) are the genetic cause for a

268 Trinucleotide repeats (TNRs) are unique DNA microsatelli

269 Disease-causing expansions of trinucleotide repeats (TNRs) can occur very frequently.

270 Trinucleotide repeats (TNRs) consist of tandem repeats o

271 (CAG)(n) trinucleotide repeats (TNRs) in the 3' untranslated regi

272 Expansion of trinucleotide repeats (TNRs) is responsible for a number

273 Expansion of trinucleotide repeats (TNRs) is the causative mutation i

274 Trinucleotide repeats (TNRs) occur throughout the genome

275 Inverted repeats (IRs) and trinucleotide repeats (TNRs) that have the potential to

276 Trinucleotide repeats (TNRs) undergo frequent mutations

277 Trinucleotide repeats (TNRs) undergo frequent mutations

278 Trinucleotide repeats (TNRs) undergo high frequency muta

279 GC-rich trinucleotide repeats (TNRs) were most abundant in prote

280 pathways modulate the dynamic mutability of trinucleotide repeats (TNRs), which are implicated in ne

281 Studies of the enhanced instability of long trinucleotide repeats (TNRs)-the cause of multiple human

282 erations due to the tendency of the unstable trinucleotide repeat to lengthen when passed from one ge

283 The propensity of trinucleotide repeats to expand was evaluated in a paral

284 unstable and progressive expansion of a CAG trinucleotide repeat tract in the HD gene.

285 The abundance of long GAA trinucleotide repeat tracts in mammalian genomes represe

286 G expansion remain unknown, the stability of trinucleotide repeat tracts is affected by their positio

287 To explore the mechanisms by which CAG trinucleotide repeat tracts undergo length changes in ye

288 nd patterns of rNMPs, including sites within trinucleotide-repeat tracts.

289 DNA trinucleotide repeats (TRs) can exhibit dynamic expansio

290 e-mutation carriers of FraX (with 55-200 CGG trinucleotide repeats) were originally considered unaffe

291 conformation was discovered in (CCG)*(CGG)n trinucleotide repeats, which are associated with fragile

292 modynamic stability when compared to the DM1 trinucleotide repeats, which could make them better targ

293 DNA binding to a site consisting of multiple trinucleotide repeats, while the BESS domain directs a v

294 was developed by substituting the mouse CGG8 trinucleotide repeat with an expanded CGG98 repeat from

295 ought that FraX results from having >200 CGG trinucleotide repeats, with consequent methylation of th

296 CA6 is caused by abnormal expansion in a CAG trinucleotide repeat within exon 47 of CACNA1A, a bicist

297 rative disorder caused by expansion of a CAG trinucleotide repeat within one allele of the huntingtin

298 egenerative disease caused by expansion of a trinucleotide repeat within the first intron of the gene

299 ns, we have identified and characterised CCG-trinucleotide repeats within a 40 Mb YAC contig spanning

300 by expansion of repeat sequences - typically trinucleotide repeats - within the respective disease ge