ライフサイエンスコーパス: repeat tract

1 pansion of an intronic ATTCT pentanucleotide repeat tract.

2 ational increases in the length of a CTG.CAG repeat tract.

3 5'-flaps to stable internal loops inside the repeat tract.

4 s caused by expansion mutations in a d(GAA)n repeat tract.

5 eat markers that we developed that flank the repeat tract.

6 the IR is less than 3.6 kb from the CAG/CTG repeat tract.

7 to converge into a single haplotype near the repeat tract.

8 both expansions and contractions of the CAG repeat tract.

9 ith effectively decreasing the length of the repeat tract.

10 ation conferred by two interruptions of a 25-repeat tract.

11 plication from a primer complementary to the repeat tract.

12 duced by transcriptional slippage within the repeat tract.

13 ed with the position of a base lesion in the repeat tract.

14 ript at the HD repeat locus that contain the repeat tract.

15 n second motif lies either 3' or 5' of an AC repeat tract.

16 f a sequence interruption within the triplet repeat tract.

17 occurring approximately 125 bp apart in the repeat tract.

18 all mod alleles exhibited variability in the repeat tract.

19 lomeric repeat regions to terminal (TTAGGG)n repeat tracts.

20 ng destabilizes H.influenzae tetranucleotide repeat tracts.

21 nces but not those joined to double-stranded repeat tracts.

22 were greater for the longer tetranucleotide repeat tracts.

23 ght occur in much longer d[GCC](n).d[GCC](n) repeat tracts.

24 nd subtelomeric sequences and short terminal repeat tracts.

25 more abundant on telomeres with long TTAGGG repeat tracts.

26 lead to expansion and to contraction of CAG repeat tracts.

27 by means of end-to-end fusions of the mutant repeat tracts.

28 may be mediated by hairpins formed by these repeat tracts.

29 hs leading to expansions and contractions of repeat tracts.

30 hat both pms1 and msh2 mutations destabilize repeat tracts.

31 lor phenotype and reduction in length of the repeat tracts.

32 ons leads to alleles with longer perfect CGG-repeat tracts.

33 iation due to alterations in simple sequence repeat tracts.

34 TCF sites and extending towards the telomere repeat tracts.

35 hybrids enhances the instability of CTG.CAG repeat tracts.

36 ntribute to the genetic instability of these repeat tracts.

37 by expansion of CTG.CAG, GAA.TTC, or CGG.CCG repeat tracts.

38 incise DNA adjacent to damage, stabilize CAG repeat tracts.

39 distinguished by the extended length of the repeat tract (5-13 kb in postmortem tissue) and its loca

40 Excision of the Pu-Py mirror repeat tract abrogates the DNA damage response.

41 thway accumulate at convergently transcribed repeat tracts, accompanied by phosphorylation of ATR, CH

42 Mismatches partially stabilized the repeat tracts against expansion.

43 on are triggered by the accumulation of CCUG repeat tract alone.

44 Contractions of the repeat tract also occur, albeit at lower frequency.

45 thed DNA, slipped structures) at appropriate repeat tracts; also, numerous prior genetic instability

46 te within approximately 1-2 kb of the TTAGGG repeat tract and adjacent to a CpG-islands implicated in

47 sequence preference for the human telomeric repeat tract and predict that POT1 can bind both the 3'

48 All three alleles destabilize a long CAG repeat tract and yield more tract contractions than expa

49 a strong asymmetry between 3' and 5' ends of repeat tracts and is dependent upon the repeat motif, le

50 in replication stalling in duplex telomeric repeat tracts and the subsequent formation of telomeric

51 tive levels, it requires the presence of the repeat tract, and it occurs in both proliferating and no

52 g activity has not been reported for any HAT repeat tract, and recent literature has emphasized a pro

53 ted in deletion of approximately half of the repeat tract, and repair at an off-center location produ

54 xpanded with the length of the telomeric DNA repeat tract, and the number of telomeric nucleosomes in

55 The mechanism and timing of expansion of the repeat tract are poorly understood.

56 Longer CAG repeat tracts are associated with earlier ages at onset,

57 Dinucleotide repeat tracts are destabilized by mismatch repair (MMR)

58 tergenerational repeat expansion is unclear, repeat tracts are especially unstable during germline de

59 Inferences about longer repeat tracts are hampered by uncertainties about the pr

60 aki fragments and/or double-strand breaks in repeat tracts are intermediates in CTG amplification.

61 These repeat tracts are involved in the etiologies of Friedrei

62 Small DNA repeat tracts are located throughout the human genome.

63 wever, do not form stable hairpins until the repeat tracts are quite long.

64 We also find that the 45 CAG repeat tracts are significantly more unstable with mater

65 Expanded CAG repeat tracts are the cause of at least a dozen neurodeg

66 Unusual physical properties of CAG repeat tracts are thought to contribute to their instabi

67 These repeat tracts are unstable and mediate high frequency, r

68 CAG repeat tracts are unstable in yeast, leading to frequent

69 The FMR1 mRNA contains the transcribed CGG-repeat tract as part of the 5' untranslated region, whic

70 chain reaction amplification across the SCA7 repeat tract assessed expansion levels in tissues of the

71 The repeat tract associated with 20 of these 51 genes was se

72 The complex variant repeat tract at the 3'-end of the array is relatively st

73 t common FMR1 mutation is expansion of a CGG repeat tract at the 5' end of FMR1, which leads to cytos

74 asic site analog, synthesized in the triplet-repeat tract at the 5' end of the template strand, induc

75 type 1 (SCA1), which carries an expanded CAG repeat tract at the endogenous mouse Sca1 locus.

76 king sequence varies and is smaller than the repeat tract at ~10.0-10.5 bp per turn.

77 critical to avoid slippage of hybrids along repeat tracts at allele-specific test sites in the array

78 Five mononucleotide repeat tracts at four different chromosomal locations we

79 in bind within 3 kb of the start of terminal repeat tracts at many, but not all, subtelomeres.

80 disorder caused by expansion of a pentameric repeat tract (ATTCT.AGAAT)(n) in intron 9 of the gene th

81 Repeat tracts bearing two G-to-A interruptions (polymorp

82 e propose that shortened, terminal telomeric repeat tracts become uncapped, promoting recombinational

83 tures in the single strands of d(CGG).d(CCG) repeat tracts but with conflicting conclusions.

84 ion, a mononucleotide expansion from a polyA repeat tract (c.132dupA) that causes protein truncation,

85 Long CAG repeat tracts cause human hereditary neurodegenerative d

86 -5',8-cyclo-2'-deoxyadenosine (cdA) in a CAG repeat tract caused CTG repeat deletion exclusively duri

87 hat DNA polymerases stall within the CTG.CAG repeat tracts causing nicks or double-strand breaks that

88 To understand the causes of CAG repeat tract changes that occur in the passage of human

89 ual properties alter the organization of CAG repeat tract chromatin.

90 e abasic site was moved to the middle of the repeat tract, consistent with effectively decreasing the

91 The DM2 repeat tract contains the complex repeat motif (TG)(n)(T

92 contributes to the orientation dependence of repeat tract contraction and limits repeat tract expansi

93 s with the orientation dependence of CAG.CTG repeat tract contraction.

94 onally-induced RNA:DNA hybrids, occurring at repeat tracts (CTG)n, (CAG)n, (CGG)n, (CCG)n and (GAA)n,

95 hree PMOs to selectively target expanded CAG repeat tracts (CTG22, CTG25 and CTG28), and two PMOs to

96 coli MMR pathway and active on dinucleotide repeat tracts, defects in H. influenzae MMR do not affec

97 viously shown that transcription through CAG repeat tracts destabilizes them in a way that depends on

98 rcular templates, but DSB repair outside the repeat tract did not affect instability.

99 In human patients and mouse models, CAG repeat tracts display an ongoing instability in neurons,

100 ope-tagged Hmo1 selectively precipitates CAG repeat tracts DNAs that range from 26 to 126 repeat unit

101 encoded protein nonfunctional, whereas short repeat tracts do not affect the phenotype.

102 Expansions of a (GAA)(n)/(TTC)(n) repeat tract during its transmission from parent to chil

103 DNA secondary structures that map within the repeat tracts during reannealing of complementary strand

104 al site in the HeLa genome, the Pu-Py mirror repeat tract elicits a polar replication fork barrier.

105 We have investigated meiotic changes in CAG repeat tracts embedded in a yeast chromosome.

106 t of replication and repair mutations on CAG repeat tracts embedded in a yeast chromosome.

107 erformed a yeast one-hybrid screen using CAG repeat tracts embedded in front of two reporter genes.

108 We report that CAG repeat tracts, embedded in yeast chromosomes, have a non

109 Phase variants with a 10G repeat tract exhibited a 2-fold reduction in surface exp

110 dence of repeat tract contraction and limits repeat tract expansion in both orientations.

111 The frequency of repeat tract expansion is controlled by both the 5'-3' e

112 rstanding the molecular mechanism of CAG.CTG repeat tract expansion is therefore important if we are

113 s, DNA base sequence is a possible factor in repeat tract expansion.

114 single-strand ends in the pathway of CAG.CTG repeat tract expansion.

115 ce of our results to two competing models of repeat tract expansion.

116 ding DNA ligase I, increase the incidence of repeat tract expansions to the greatest extent.

117 er weakening their interactions leads to CAG repeat tract expansions, we have employed alleles named

118 is ordered entry is necessary to prevent CAG repeat tract expansions.

119 ctly ligated products generating a dimerized repeat tract formed substrates for rolling circle amplif

120 ity was associated with a switch in the PorA repeat tract from 11G to 10G.

121 ric polypurine-polypyrimidine (Pu-Py) mirror repeat tract from the human polycystic kidney disease (P

122 were instead able to incrementally generate repeat tracts from 100 to 200 CAGs in a yeast integratin

123 lecular triplex formation by 15 Pu.Py mirror repeat tracts from PKD1 intron 21 by 2D gel electrophore

124 The telomeric d(GGGGTT).d(AACCCC) repeat tracts (G4T2 repeats) in Tetrahymena thermophila

125 Replication initiated within the repeat tract generated significant expansion that was su

126 size, while saltatory expansions increase in repeat tracts > or = Okazaki fragment size.

127 me meiotic instability, and expansion of the repeat tract has been suggested to occur in the germ-lin

128 Single-stranded d(GAA)n repeat tracts, however, do not form stable hairpins unti

129 Only one of the DM2 repeat tracts, however, is found to expand.

130 The triplet repeat tract in a non-B conformation is the mutagen, not

131 e disease caused by expansion of a glutamine repeat tract in ataxin-1 (ATXN1).

132 the length of the simple sequence telomeric repeat tract in different cell types to the presence or

133 ithin the CpG island that abuts the expanded repeat tract in Dnmt1-deficient mice.

134 be important in modulating expansion of the repeat tract in germline and somatic cells.

135 on's disease (HD), caused by an expanded CAG repeat tract in HTT, genetic variation has been uncovere

136 ve stresses induce mutagenesis of a long CAG repeat tract in human cells.

137 RDA mutations involve expansion of a GAA*TTC-repeat tract in intron 1, which leads to an FXN mRNA def

138 Surprisingly the SCA8 repeat tract in sperm underwent contractions, with nearl

139 repeat mediated-gene silencing when the CGG-repeat tract in the 5' UTR exceeds 200 repeat units.

140 FRAXA coincides with a >200 CGG*CCG repeat tract in the 5' UTR of the FMR1 gene, and alleles

141 ion disease caused by expansion of a CGG.CCG-repeat tract in the 5' UTR of the FMR1 gene.

142 Expansion of a CGG-repeat tract in the 5'-untranslated region of the FMR1 g

143 d mutations that destabilize a minisatellite repeat tract in the ADE2 gene of Saccharomyces cerevisia

144 progressive expansion of a CAG trinucleotide repeat tract in the HD gene.

145 some formation causes kinking in a secondary repeat tract in the htt gene, comprised of CCG/CGG repea

146 rved; therefore, we chose to expand a 59 CAG repeat tract in vivo in Escherichia coli.

147 here that meiotic instability of the CAG/CTG repeat tract in yeast is associated with double-strand b

148 epeat stability, we constructed strains with repeat tracts in both orientations, either with or witho

149 cks or 1-base gaps within short (14 triplet) repeat tracts in DNA duplexes under physiological condit

150 uced function might destabilize expanded CAG repeat tracts in Drosophila, we crossed the SCA7 CAG90 r

151 thway in modulating the pathogenicity of the repeat tracts in HD, and possibly, in other trinucleotid

152 selection assay based on contraction of CAG repeat tracts in human cells, we screened the Prestwick

153 The abundance of long GAA trinucleotide repeat tracts in mammalian genomes represents a signific

154 o form in (CCTG)(58) x (CAGG)(58) and larger repeat tracts in plasmids at physiological superhelical

155 The capacity of (CTG.CAG)n and (GAA.TTC)n repeat tracts in plasmids to induce mutations in DNA fla

156 in plasmids harboring a pair of long GAA.TTC repeat tracts in the direct repeat orientation.

157 eatment with 5-aza-CdR strongly destabilized repeat tracts in the DMPK gene, with a clear bias toward

158 Expansions of CAG repeat tracts in the germ line underlie several neurolog

159 promote repeat expansion, using (CTG)*(CAG) repeat tracts in the size range that is typical for myot

160 These results show that Hmo1 binds to CAG repeat tracts in vivo and establish the basis of their n

161 but added only short stretches of telomeric repeat tracts in vivo and in vitro.

162 polymerase beta, of several tetranucleotide repeat tracts in which the repeat units varied by one or

163 rruption are biased toward the 3' end of the repeat tract (in reference to the direction of lagging-s

164 fic transient pausing pattern within the CNG repeat tracts; individual incorporation rates were slowe

165 G67S strains displayed a higher frequency of repeat tract instabilities relative to CAN1 duplication

166 olymerase slippage plays a major role in the repeat tract instability and meiotic instability is seve

167 ified in a screen for mutants that displayed repeat tract instability and mutator phenotypes.

168 rad27Delta mutants display both a repeat tract instability phenotype and a high rate of fo

169 In repeat-tract instability assays, however, the rfc1::Tn3

170 elta) mutations in both forward mutation and repeat-tract instability assays.

171 cated that they displayed both a mutator and repeat-tract instability phenotype.

172 The CCTG portion of the repeat tract is interrupted on normal alleles, but, as i

173 n of the overall length of the telomeric DNA repeat tract is likely to be a key requirement for its v

174 The lic2A 5' CAAT repeat tract is preceded by four 5' ATG codons (x, y, z1

175 ing strand of strains harboring the ARS, the repeat tract is relatively stable regardless of the orie

176 ing strand of strains harboring the ARS, the repeat tract is relatively unstable regardless of the or

177 Expansion of a tandem repeat tract is responsible for the Repeat Expansion dis

178 ions of (CAG)(95) are more frequent when the repeat tract is transcribed.

179 main unknown, the stability of trinucleotide repeat tracts is affected by their position relative to

180 hat a narrow length distribution of telomere repeat tracts is observed.

181 The expansion of CAG.CTG repeat tracts is responsible for several neurodegenerati

182 ation of the DNA structure, localized to the repeat tracts, is responsible for these behaviors.

183 TNR instability is modulated both by the repeat tract itself and by cellular proteins.

184 y demonstrated that the r(GGGGCC)n RNA forms repeat tract length-dependent G-quadruplex structures th

185 nt contractions and infrequent expansions in repeat tract length.

186 amatic changes in chromatin structure and in repeat tract length.

187 ls using SCA7 cDNA clones with different CAG repeat tract lengths.

188 er, is associated with an expansion of a CTG repeat tract located in the 3'-untranslated region of a

189 interruptions within the CCTG portion of the repeat tract may predispose alleles to further expansion

190 Stabilization of telomeric repeat tracts may also be achieved through a telomerase-

191 onal association with RNA suggested that HAT repeat tracts might bind RNA.

192 g replication mutations that destabilize CAG repeat tracts, mutations of RAD27, encoding the flap end

193 Triplet repeat tracts occur throughout the human genome.

194 G)(25) x (CCG)(25) and (CAG)(25) x (CTG)(25) repeat tracts occurred with similar low rates.

195 This widespread instability affects repeat tracts of all lengths and is usually attributed t

196 f polI destabilized tetranucleotide (5'AGTC) repeat tracts of chromosomally located reporter construc

197 d the expansions compared with uninterrupted repeat tracts of similar lengths.

198 frequency of frameshift mutations in the CA repeat tracts of the out-of-frame shuttle vector pZCA29

199 or instance, it was seen that mononucleotide repeat-tracts of Gs (or Cs) are highly unstable, a patte

200 The rate of recombination between directly repeated tracts of telomeric C1-3A/TG1-3 DNA was reduced

201 somes and linkers and the demonstration that repeating tracts of adenines can cause a curvature in DN

202 The expansions of long repeating tracts of CTG.CAG, CCTG.CAGG, and GAA.TTC are

203 strains harboring repeat tracts showed that repeat tracts often change in length.

204 possibility that indirect influences of the repeat tract on adjacent protein domains are contributor

205 effect of both the length and purity of the repeat tract on the propensity of slipped structure form

206 e that reveal the confounding effects of CGG-repeat tracts on both cloning and PCR.

207 also discuss how the effect of long CTG/CAG repeat tracts on splicing may contribute to the progress

208 nzyme cleavage in or near CGG*CCG or CTG*CAG repeat tracts on their genetic instabilities, both withi

209 ibition, whereas RNA duplexes containing CAG repeat tracts only induced gene-specific inhibition when

210 of the trinucleotide CAG, we have cloned CAG repeat tracts onto the 3' end of the Saccharomyces cerev

211 als can have either a pure uninterrupted CTG repeat tract or an allele with one or more CCG, CTA, CTC

212 ests that cooperative interactions in longer repeat tracts overwhelm perturbations to reassert the na

213 se variation of PorA is mediated by a poly-G repeat tract present within the promoter, leading to alt

214 most Haemophilus influenzae tetranucleotide repeat tracts, raising the possibility of multiple activ

215 Escape variants with alterations in the lgtG repeat tract rapidly accumulated in bacterial population

216 ted when the primer was complementary to the repeat tract rather than the flanking sequence.

217 hat interrupt the homogeneity of the CTG.CAG repeat tracts reduce the apparent recombination frequenc

218 this library suggests a preponderance of CA repeat tracts relative to their abundance in humans.

219 Notably, the periodicity of the repeat tract remained unchanged as a function of length

220 s with extremely long heterogeneous terminal repeat tracts, reminiscent of the long telomeres observe

221 e lengths and distribution of mononucleotide repeat-tracts revealed some interesting features.

222 proximately 100 bp upstream of the telomeric repeat tract sequence.

223 The repeat tract showed modest instability when it was not t

224 g from clonal expansion of strains harboring repeat tracts showed that repeat tracts often change in

225 features such as the start of each terminal repeat tract, SRE identity and organization, and subtelo

226 e rationalize the opposing effects of MMR on repeat tract stability with a model that accounts for CT

227 lta) do not have a significant effect on CAG repeat tract stability.

228 of the origin of replication relative to the repeat tract, supporting the 'fork-shift' model of repea

229 ble gene (NMB1994 or nadA) associated with a repeat tract (TAAA) not previously reported to be associ

230 tent predictors of SNP density, long (AT)(n) repeat tracts tending to be found in regions of signific

231 Mammalian telomeres contain a duplex TTAGGG-repeat tract terminating in a 3' single-stranded overhan

232 nsions (to give lengths longer than a single repeating tract) than deletions as observed for the CTG*

233 mouse lines containing a large expanded CTG repeat tract that replicated a number of the features of

234 ys, which included the CAG repeats and a CCG repeat tract that was thought to be invariant.

235 implicated in the expansion of trinucleotide repeat tracts that has been found to be responsible for

236 We previously showed that with d(CAG).d(CTG) repeat tracts there was a markedly greater tendency to f

237 quences on the ability of the nascent-strand repeat tract to expand during DNA replication.

238 y stable triplex structures which caused two repeat tracts to adhere to each other (sticky DNA).

239 0 repeats), orientation, or proximity of the repeat tracts to the origin (SV40) of replication.

240 that endometrial cancer cell lines with A10 repeat tract truncating mutations have a failure in the

241 rated that the outer halves of the telomeric repeat tracts turn over within a few hundred cell divisi

242 Repeat tracts undergo either conversion events between h

243 re the mechanisms by which CAG trinucleotide repeat tracts undergo length changes in yeast cells, we

244 Although we set out to expand this repeat tract using a recombination paradigm involving tw

245 In addition, a GT repeat tract was found adjacent to the 5'-splice donor s

246 sis of the nadA transcript revealed that the repeat tract was located upstream of the putative -35 el

247 The nucleotide following the CAG repeat tract was usually G in all species studied.

248 ndividuals, and the normal (CGG)54 fragile X repeat tract, was analyzed using a synchronized in vitro

249 o gain insight into possible function of the repeat tract, we looked for evolutionary conservation.

250 se of our experiments that yielded these CAG repeat tracts, we evaluated the role of repeat orientati

251 Variant CAA or AAG triplets in the CAG repeat tracts were found in all 268 human, 28 monkey and

252 ncy of slippage events within mononucleotide repeat tracts were identified in three known phase varia

253 shaped structure) in plasmids with a pair of repeat tracts where n> or =60 in the direct repeat orien

254 Shorter repeat tracts (where n = 0 or 17) were essentially inert

255 ion of hypersensitivity in the middle of the repeat tract, whereas V1 digestion is consistent with a

256 ult in increased rates of fragility of a CAG repeat tract while single or double deletions of RAD17 o

257 t expansions are biased to the 5' end of the repeat tract, while the tract contractions that do not r

258 leotide repeat expansion site, more than one repeat tract with similar sequences lie side by side.

259 ng a minimal in vitro system composed of the repeat tract, with and without unique flanking sequences

260 in packaging of healthy and diseased length repeat tracts within the genome.