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 y pyrimidine residues interspaced by AC-rich trinucleotides.

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

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

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

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

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

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

12 Dinucleotide, trinucleotide, and RGYW analyses showed that mutational

13 the electronic structure of mono-, di-, and trinucleotide anions in the gas phase.

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

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

16 a position was used to measure hydrolysis of trinucleotide at 37 degrees C.

17 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

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

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

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

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

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

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

24 The AR gene contains a trinucleotide CAG repeat, the length of which has been i

25 odegenerative diseases caused by an expanded trinucleotide (CAG) repeat coding for an extended polygl

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

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

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

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

30 P mutations are the cytosine residues of TCG trinucleotide combinations.

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

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

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

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

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

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

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

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

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

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

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

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

43 s have been associated with the expansion of trinucleotide DNA repeats, which may involve the formati

44 ucleotide binding domains bind and hydrolyze trinucleotide, even in the absence of metalloid.

45 Trinucleotide exchange (TriNEx) is a method for generati

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

47 Mutant DMPK mRNAs containing the trinucleotide expansion are retained in the nucleus of D

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

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

50 Trinucleotide expansions cause disease by both protein-

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

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

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

54 ' and 5'-GGC-3'/3'-CC[(15)N(3),2-(13)C-G]-5' trinucleotides gave rise to comparable numbers of 1,2-in

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

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

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

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

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

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

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

62 volved a technique that appears to achieve a trinucleotide insertion into tissue culture cells bearin

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

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

65 G(3).m(5)C(8) base pair of the junction core trinucleotide (italicized) has been removed.

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

67 loop from Escherichia coli tRNA(Phe) forms a trinucleotide loop in solution, but Mg(2+) and dimethyla

68 loop from Escherichia coli tRNA(Phe) forms a trinucleotide loop in solution, but Mg2+ and dimethylall

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

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

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

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

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

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

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

76 Using TP53 trinucleotide mutation signatures for lung cancer in smo

77 s to unique RNA segments containing multiple trinucleotide (NAG) repeats.

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

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

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

81 Rho guanine trinucleotide phosphatases are ubiquitious regulators of

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

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

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

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

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

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

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

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

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

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

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

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

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

95 Trinucleotide repeat (TNR) expansion is responsible for

96 DNA trinucleotide repeat (TNR) expansion underlies several n

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

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

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

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

101 Trinucleotide repeat (TNR) expansions and deletions are

102 Trinucleotide repeat (TNR) expansions and deletions are

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

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

105 1 gene due to an unstable expansion of a CGG trinucleotide repeat and its subsequent hypermethylation

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

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

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

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

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

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

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

113 Trinucleotide repeat diseases, such as Huntington's dise

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

115 Trinucleotide repeat disorders are severe, usually life-

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

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

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

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

120 promising molecule for antisense therapy of trinucleotide repeat disorders.

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

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

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

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

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

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

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

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

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

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

131 The TGC trinucleotide repeat expansion in TCF4 is strongly assoc

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Trinucleotide repeat expansion underlies at least 17 neu

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

147 A trinucleotide repeat expansion, inactivating the X-linke

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

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

150 essive neurodegenerative disorder cause by a trinucleotide repeat expansion.

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

152 Trinucleotide repeat expansions are the mutational cause

153 Trinucleotide repeat expansions in FMR1 abolish FMRP exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Trinucleotide repeat instability underlies >20 human her

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

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

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

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

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

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

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

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

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

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

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

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

187 iption stimulates the genetic instability of trinucleotide repeat sequences.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Trinucleotide repeats (TNRs) are unique DNA microsatelli

219 Trinucleotide repeats (TNRs) consist of tandem repeats o

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

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

222 Trinucleotide repeats (TNRs) occur throughout the genome

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

224 Trinucleotide repeats (TNRs) undergo frequent mutations

225 Trinucleotide repeats (TNRs) undergo high frequency muta

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

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

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

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

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

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

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

233 Trinucleotide repeats are a source of genome instability

234 Expanded trinucleotide repeats are associated with several neurop

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

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

237 Expanded trinucleotide repeats are responsible for a number of ne

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

239 Trinucleotide repeats can form secondary structures, who

240 Trinucleotide repeats can form stable secondary structur

241 Expansions of trinucleotide repeats cause at least 15 heritable human

242 Expanded trinucleotide repeats cause many neurological diseases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 ic instability and transcription of expanded trinucleotide repeats.

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

268 ponsible for HTLV-I RNA dimerization forms a trinucleotide RNA loop, unlike any previously characteri

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

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

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

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

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

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

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

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

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

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

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

280 Single trinucleotide sequences were deleted at random positions

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

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

283 o cleave exclusively host mRNAs at UA(A/C/U) trinucleotide sites to eliminate plasmid-free cells.

284 itive genomic targets is favored by specific trinucleotide spacers.

285 Use of trinucleotide-specific templates demonstrated that the p

286 dently genotype several disease-related long trinucleotide STRs.

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

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

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

290 int" in all the spectra of dinucleotides and trinucleotides that contain the guanine base.

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

292 100 kb the frequency distributions of their trinucleotides (triplet profiles) are the same in both s

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

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

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

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

297 The stiffness indices for the trinucleotides were the ones realized by M. M. Gromiha u

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

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

300 of CG dinucleotides and an excess of C(A/T)G trinucleotides within transcribed regions.