ライフサイエンスコーパス: trinucleotide

1 (CA)3-3', where XYZ represented the variable trinucleotide.

2 o any 20 bp DNA sequence followed by the NGG trinucleotide.

3 systems matching amino acids with anticodon trinucleotides.

4 ers were used to predict possible initiation trinucleotides.

5 amics simulations of model aminoacylated RNA trinucleotides.

6 xposure on sidechain interactions than other trinucleotides.

7 mors contained T>G base substitutions at GTG trinucleotides.

8 e containing cyclic dinucleotides and cyclic trinucleotides.

9 otides demonstrate that these cyclic di- and trinucleotides activate distinct host receptors and thus

10 the addition of the corresponding initiating trinucleotide also dramatically reduced the NTP levels n

11 m 40 BES-SSRs based on long motifs SSRs (>/= trinucleotides) analyzed in high-resolution genotyping,

12 uncation of full-length UvrB), a polythymine trinucleotide and ADP.

13 epeats have significant association with the trinucleotide and hexanucleotide coding repeats in most

14 e lesion by slippage of the primer 3' di- or trinucleotide and realignment to the template sequence d

15 e adenine dinucleotide (NAD>p) and ACA>p RNA trinucleotide, and multiple additions of GUCCA>p RNA pen

16 Dinucleotide, trinucleotide, and RGYW analyses showed that mutational

17 : amino acids, an invariant 3'-terminal CCA, trinucleotide anticodons and tRNA bodies.

18 In most cases, the trinucleotide anticodons of tRNA are important identity

19 conformational preferences of aminoacylated trinucleotides are determined by their nucleotide compos

20 d N = U/C/7-deaza-G) and/or C/AUU-3' (C > A) trinucleotide at the 5'- and 3'-ends of SIMRA compound a

21 modulates splicing of introns containing CAG trinucleotides at their 3' splice junctions.

22 l bases, but also contributions from di- and trinucleotides at various positions within or near the b

23 lso, we find that, in the Bacteroidetes, the trinucleotide AUG is underrepresented in the vicinity of

24 ive matrix factorization (NMF) into discrete trinucleotide-based mutational signatures indicative of

25 me negligible when taking into consideration trinucleotide-based mutational signatures, owing to lack

26 held in place by stacking of the 5'-terminal trinucleotide between aromatic side chains while a highl

27 yme can assemble long RNAs from a mixture of trinucleotide building blocks, including a two-fragment

28 that are linked by a functionally important trinucleotide bulge over timescales extending up to mill

29 ng the transport cycle, it required not only trinucleotide, but also MBP, suggesting it is part of a

30 HD is caused by a trinucleotide CAG repeat expansion that encodes a polygl

31 inant neurodegenerative disorder caused by a trinucleotide (CAG)(n) repeat expansion in the coding se

32 ponsible for FXS is a large expansion of the trinucleotide CGG repeat in the 5' untranslated region o

33 ponsible for FXS is a large expansion of the trinucleotide CGG repeats that leads to DNA methylation

34 CDR positions using tailored degenerate and trinucleotide codons that mimic natural human antibodies

35 s based on principal component, rarefaction, trinucleotide composition and contig spectrum analyses.

36 lasmids could be inferred by comparing their trinucleotide composition to that of all completely sequ

37 e physicochemical properties into the pseudo trinucleotide composition, quite similar to the PseAAC (

38 d also include an unexpected class of cyclic trinucleotide compounds.

39 emplated polymerization of 5'-phosphorylated trinucleotides containing a wide variety of appended fun

40 ntly, 25% of all mutations were G-->T in one trinucleotide context (CGC; the underlined G is the posi

41 ncer mutations, tabulated according to their trinucleotide context, into a linear combination of know

42 Thus, the ACC trinucleotide core is now shown to be important for the

43 ue set of intramolecular interactions at the trinucleotide core of the crossing strands, which are no

44 FECD) is an RNA-mediated disease caused by a trinucleotide CTG expansion in an intron within the TCF4

45 Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3'

46 e N(alpha)-Boc-protected amino acids and the trinucleotides d(T(1)B(2)T(3)) where B(2) is the target

47 The most common mutation is a trinucleotide deletion (DeltaGAG), which causes a deleti

48 n 20 in two affected HSAN IE siblings, and a trinucleotide deletion in exon 20 in the latter patient

49 Importantly, aminoacylated CCA trinucleotides display a systematically higher solvent e

50 minase activity was rescued by introducing a trinucleotide DNA patch spanning the target cytosine and

51 Trinucleotide exchange (TriNEx) is a method for generati

52 Our simulations suggest that 3'-modified trinucleotides exhibit higher solvent exposure of the am

53 Fragile X syndrome (FXS), caused by a trinucleotide expansion (>200 CGG repeats) in the fra

54 e known to stall replication forks and cause trinucleotide expansion diseases such as Huntington's di

55 The trinucleotide expansion encodes for an expanded polyQ tr

56 ic dystrophy type 1 (DM1) is caused by a CTG trinucleotide expansion in the 3' untranslated region (3

57 editary neuromuscular disorder caused by CAG trinucleotide expansion in the gene encoding the androge

58 d neurodegenerative disorder caused by a CAG trinucleotide expansion in the huntingtin gene (HTT), wh

59 ive degenerative disorder caused by aberrant trinucleotide expansion in the huntingtin gene.

60 r the disease This association suggests that trinucleotide expansion may play a pathogenic role in th

61 Trinucleotide expansions cause disease by both protein-

62 Initially, the enzyme removes di- or trinucleotides from viral DNA ends to expose 3'-hydroxyl

63 disorder caused by a mutant expansion of the trinucleotide GAA within an intronic FXN RNA.

64 n in catalytic rate in vitro and large-scale trinucleotide (GAA)n repeat expansions in vivo, implying

65 ence repeat loci, i.e., mononucleotide G and trinucleotide GGT, in isolates from liquid and solid cul

66 In the presence of initiating di- or trinucleotides, however, the amount of NTP needed to ach

67 /absence of specific combinations of di- and trinucleotides, (iii) nucleotide interactions by means o

68 lated region (UTR) of RNA that contain a UAG trinucleotide in their core.

69 with transcriptional repression, and at CAG trinucleotides in embryonic stem cells, where it positiv

70 We have investigated the effects of trinucleotides in the AUG-proximal region (APR) (i.e. po

71 In mammals, mCH is found at CAC trinucleotides in the nervous system, where it is associ

72 s were designed that comprised all potential trinucleotide initiation sequences.

73 ture of bacterial primases is conserved, the trinucleotide initiation specificity for A. aeolicus was

74 Within the macro domain of mH2A1.2, a trinucleotide insertion (-EIS-) sequence not found in mH

75 s and conserved gene starts, gene stops, and trinucleotide intergenic sequences similar to those in p

76 Trinucleotide interrupts in the repeating CAG pattern as

77 how that intrastrand folding in repeated CAG trinucleotides is also determined by the number of repea

78 estigated the ability of each of 64 possible trinucleotides located at the PAM position to induce CRI

79 r 10 dinucleotide loci and 6 x 10(-6) for 52 trinucleotide loci (which were longer).

80 ons and molecular dynamics simulations using trinucleotide model systems revealed that modified sugar

81 re we show that in mice DND1 binds a UU(A/U) trinucleotide motif predominantly in the 3' untranslated

82 ation origin element composed of a repeating trinucleotide motif that we term the DnaA-trio.

83 C-to-G mutations in intrinsically preferred trinucleotide motifs (TCA/TCG/TCT).

84 cleotide sequence descriptors identified two trinucleotide motifs (TCC and TGC) that were present onl

85 dditionally, regularly oscillating period-10 trinucleotide motifs non-T, A/T, G and their complements

86 Hfq bound repeated trinucleotide motifs of A-R-N (A-A/G-any nucleotide) oft

87 ifferent between patients and show biases in trinucleotide mutation context.

88 Using TP53 trinucleotide mutation signatures for lung cancer in smo

89 le structural patterns such as dinucleotide (trinucleotide or higher order) may exist.

90 ic mutation spectra of each compound through trinucleotide patterns of base substitution.

91 n cancers, in terms of extended (longer than trinucleotide) patterns as well as variability of the si

92 omers of the ribosomal P-site substrate, the trinucleotide peptide conjugate CCA-pcb, have been desig

93 T1, characterized their cutting preferences, trinucleotide periodicity patterns and coverage similari

94 Rho guanine trinucleotide phosphatases are ubiquitious regulators of

95 isoforms harbor conserved N-terminal guanine trinucleotide phosphate (GTP) binding domains and, accor

96 amidites and a single orthogonally protected trinucleotide phosphoramidite (Fmoc-TAG; Fmoc = 9-fluore

97 the expansion of a cysteine-adenine-guanine trinucleotide (polyglutamine) repeats in exon one of the

98 improvement of the latter, which enables the trinucleotide polymerase to react 10(2)-10(3)-fold faste

99 s, and, intriguingly, false positives show a trinucleotide profile very similar to one found in human

100 Our model consists of three dior-trinucleotide profiles identified through principle comp

101 CRISPR-Cas systems require the presence of a trinucleotide protospacer adjacent motif (PAM) for effic

102 A by Cas9-RNA require recognition of a short trinucleotide protospacer adjacent motif (PAM).

103 zinc-binding domain defined class-associated trinucleotide recognition and substitution of these amin

104 th ADP, the SRX is not seen, indicating that trinucleotide-relaxed myosins are responsible for the SR

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

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

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

108 Trinucleotide repeat (TNR) expansion and deletion are re

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

110 Trinucleotide repeat (TNR) expansion is responsible for

111 DNA trinucleotide repeat (TNR) expansion underlies several n

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

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

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

115 Trinucleotide repeat (TNR) expansions and deletions are

116 Trinucleotide repeat (TNR) expansions and deletions are

117 Trinucleotide repeat (TNR) expansions cause nearly 20 se

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

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

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

121 1 gene due to an unstable expansion of a CGG trinucleotide repeat and its subsequent hypermethylation

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

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

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

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

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

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

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

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

130 Trinucleotide repeat diseases, such as Huntington's dise

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

132 Trinucleotide repeat disorders are severe, usually life-

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

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

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

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

137 promising molecule for antisense therapy of trinucleotide repeat disorders.

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

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

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

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

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

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

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

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

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

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

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

149 The TGC trinucleotide repeat expansion in TCF4 is strongly assoc

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

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

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

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

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

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

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

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

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

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

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

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

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

163 Trinucleotide repeat expansion underlies at least 17 neu

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

165 A trinucleotide repeat expansion, inactivating the X-linke

166 essive neurodegenerative disorder cause by a trinucleotide repeat expansion.

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

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

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

170 Trinucleotide repeat expansions in FMR1 abolish FMRP exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 Trinucleotide repeat instability underlies >20 human her

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

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

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

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

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

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

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

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

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

199 iption stimulates the genetic instability of trinucleotide repeat sequences.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Trinucleotide repeats (TNRs) are unique DNA microsatelli

229 Trinucleotide repeats (TNRs) consist of tandem repeats o

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

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

232 Trinucleotide repeats (TNRs) occur throughout the genome

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

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

235 DNA trinucleotide repeats (TRs) can exhibit dynamic expansio

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

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

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

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

240 Trinucleotide repeats are a source of genome instability

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

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

243 Expanded trinucleotide repeats are responsible for a number of ne

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

245 Trinucleotide repeats can form secondary structures, who

246 Trinucleotide repeats can form stable secondary structur

247 Expansions of trinucleotide repeats cause at least 15 heritable human

248 Expanded trinucleotide repeats cause many neurological diseases.

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

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

251 Expansion of CAG trinucleotide repeats in ATXN1 causes spinocerebellar at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 espiratory tract specimens and had longer p1 trinucleotide repeats.

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

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

270 otides around a polymorphic site--the site's trinucleotide sequence context--to study polymorphism le

271 We also identified distinct editing site trinucleotide sequence contexts for each APOBEC3 protein

272 were subsequently replaced with a randomized trinucleotide sequence donated by the DNA cassette terme

273 s demonstrated that the preferred initiation trinucleotide sequence for A. aeolicus primase was 5'-d(

274 ion by random substitution of one contiguous trinucleotide sequence for another.

275 In the majority of organisms, this trinucleotide sequence is not encoded in the genome and

276 TRDs) are caused by pathogenic expansions of trinucleotide sequence repeats within coding and non-cod

277 ease (HD) is caused by an expansion of a CAG trinucleotide sequence that encodes a polyglutamine trac

278 The deleted trinucleotide sequence was then replaced by a DNA casset

279 The secondary structure of repeated trinucleotide sequences results in the development of se

280 on that matches protein amino acids with the trinucleotide sequences specified in mRNA.

281 ent spurious recombination events and unwind trinucleotide sequences that are prone to hairpin format

282 Single trinucleotide sequences were deleted at random positions

283 gineered transposon termed MuDel, contiguous trinucleotide sequences were removed at random positions

284 lementary DNA targets at sites adjacent to a trinucleotide signature sequence called the protospacer

285 itive genomic targets is favored by specific trinucleotide spacers.

286 Use of trinucleotide-specific templates demonstrated that the p

287 dently genotype several disease-related long trinucleotide STRs.

288 mbers, a unique subdomain holds a methylated trinucleotide substrate into the active site through con

289 -chiral polymerases that use either mono- or trinucleotide substrates that are activated as the 5'-tr

290 Stem I contains the specifier trinucleotide that base pairs with the anticodon of cogn

291 tructure (1.92A) of UP1 bound to a 5'-AGU-3' trinucleotide that resembles sequence elements of severa

292 bit dynamic expansions by integer numbers of trinucleotides that lead to neurodegenerative disorders.

293 ave been associated with length variation of trinucleotide (triplet) repeats including Huntington's d

294 100 kb the frequency distributions of their trinucleotides (triplet profiles) are the same in both s

295 riety of the frequency distribution of their trinucleotides ("triplet profiles").

296 ent article, focusing on the special case of trinucleotides (triplets), examined several gigabases of

297 A new method, called Trinucleotide Usage Profile (TUP), is proposed based onl

298 None of these trinucleotides were known to be recognition sequences us

299 T/TD-DFT calculations in solution), we study trinucleotides with key sequences (TCG/T5mCG) in the UV-

300 is caused by mutational expansion of the CAG trinucleotide within exon 1 of the huntingtin (Htt) gene