ライフサイエンスコーパス: microsatellite

1 s the major protein interacting with the MIF microsatellite.

2 th expanded body size restrain the number of microsatellite.

3 on the length and nucleotide context of the microsatellite.

4 EWS/FLI fusion in binding to sweet-spot GGAA-microsatellites.

5 lel, and provides the accurate genotyping of microsatellites.

6 nded survival, and reduced the occurrence of microsatellites.

7 to those of other sets of 13 tetranucleotide microsatellites.

8 re realistically accomplished with SNPs than microsatellites.

9 enzyme impedes transcription across expanded microsatellites.

10 st to existing methods that rely on observed microsatellites.

11 ewhere [2, 7-9]-together with 779 additional microsatellites [10], using direct population structure

12 Two functional MIF promoter polymorphisms, a microsatellite (-794 CATT5-8; rs5844572) and a single-nu

13 e (FST = 0.048, PhiST = 0.109, p < 0.01) and microsatellite allele frequencies (FST = 0.008, p < 0.01

14 eotide polymorphisms (SNPs), and polymorphic microsatellite alleles, we show that the genotypes of ne

15 tation rate in protein-coding mononucleotide microsatellites, allowing a full cataloging of the true

16 some nonhypermutated CRCs; and (4) elevated microsatellite alterations at selected tetranucleotide r

17 Elevated microsatellite alterations at selected tetranucleotide r

18 a novel mechanism to acquire MMR deficiency/microsatellite alterations.

19 Microsatellite analyses clearly showed that postrecovery

20 Additionally, we conducted mtDNA and microsatellite analyses to detect past and recent demogr

21 Our data revealed that, contrary to the microsatellite analyses, the eruption was associated wit

22 phic break, which was not significant in the microsatellite analyses.

23 f informative haplotypes compared with other microsatellite analysis approaches.

24 Microsatellite analysis showed a loss of about 2.36 Mb.

25 In this work, we use paralogue ratio tests, microsatellite analysis, read depth and fibre-FISH to de

26 Tumor LOH at 1p and 16q was determined by microsatellite analysis.

27 The same progeny was genotyped with 195 microsatellite and 8303 single nucleotide polymorphism (

28 We used 17 microsatellite and a mitochondrial markers to evaluate g

29 We analysed temporal stability at neutral microsatellite and adaptive MHC genetic variation over f

30 However, clustering analyses of microsatellite and Chd1 gene sequences support two diver

31 ations across a broad geographic range using microsatellite and mitochondrial DNA loci.

32 the roundscale spearfish, utilizing nuclear microsatellite and mitochondrial DNA sequence markers.

33 edary samples from arid regions with nuclear microsatellite and mitochondrial genotype information fr

34 s to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms.

35 for oil palm using co-dominant markers (i.e. microsatellite and SNPs) and two F1 breeding populations

36 Four hundreds and forty-four microsatellites and 36 SNPs were mapped onto 16 linkage

37 3 genetically diverse progeny by typing with microsatellites and 9230 single-nucleotide polymorphisms

38 oward intergenic regions in the nonconserved microsatellites and a genic bias in all detected tandem

39 oward intergenic regions in the nonconserved microsatellites and a genic bias in all detected tandem

40 ng of major histocompatibility complex-borne microsatellites and HLA-DPB1 alleles using DNA obtained

41 e to cells via loss-of-function mutations in microsatellites are called MSI target genes.

42 Microsatellites are commonly used to describe the genoty

43 Clinically, genomic GGAA-microsatellites are highly variable and polymorphic.

44 Microsatellites are multi-allelic and composed of short

45 Microsatellites are short tandem repeat sequences that a

46 Short tandem repeats (STRs), also known as microsatellites, are among the largest contributors of d

47 demonstrate the critical requirement of GGAA-microsatellites as EWS/FLI activating response elements

48 eq-based estimates approached those based on microsatellites as more loci with more missing data were

49 h mtDNA haplotypes and kinship inferred from microsatellite-based estimators of relatedness.

50 ontinuous forest to those in pasture through microsatellite-based paternity analysis of progeny.

51 This microsatellite-based platform confirms the potential to

52 gh-depth sequencing enables a high-precision microsatellite-based risk classifier analysis approach.

53 ocess for identifying and further evaluating microsatellite-based risk markers for lung cancer using

54 fusion) showed low affinity for smaller GGAA-microsatellites but instead significantly increased its

55 We found higher F ST using microsatellites, but that RAD-Seq-based estimates approa

56 program for automatically detecting somatic microsatellite changes.

57 Here we compare microsatellite data (8 loci) and RAD-Seq data (six datas

58 Also some of the available microsatellite data exhibited diploid allelic band patte

59 We examined microsatellite data from a quarter of the total populati

60 We also apply ABC to microsatellite data from three invasions of bumblebee in

61 ations belong to the same phylogroup, though microsatellite data indicate significant genetic diverge

62 We use a microsatellite data set to test hypotheses of population

63 We simulate microsatellite data to evaluate the power of ABC to dist

64 present study, fungal metabarcoding and tree microsatellite data were compared for the first time.

65 of ribosomal genes and Hox paralogs and with microsatellite data, brings a closer look at results of

66 Based on microsatellite data, STRUCTURE analyses identified two (

67 PCR-capillary electrophoresis using nine microsatellites demonstrates the accuracy of the fingerp

68 versely, our nuclear DNA results based on 12 microsatellites detected very little introgression from

69 xpression to correlate with venous invasion, microsatellites, direct liver invasion, and absence of t

70 Here we use microsatellite DNA and mitochondrial DNA markers to inve

71 also provide a simple approach to screen any microsatellite DNA database for parthenogens, which will

72 bility of cold-pressed hazelnut oil based on microsatellite DNA markers.

73 Microsatellite DNAs that form non-B structures are impli

74 ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element.

75 Myotonic dystrophy type 1 (DM1) is a CTG microsatellite expansion (CTG(exp)) disorder caused by e

76 Microsatellite expansion diseases are caused by unstable

77 al defects associated with C9orf72 and other microsatellite expansion diseases.

78 suggesting convergence of pathomechanisms in microsatellite expansion disorders and RBP proteinopathi

79 Microsatellite expansion disorders are pathologically ch

80 the combined number of patients in all other microsatellite expansion disorders.

81 like (MBNL) activity due to sequestration by microsatellite expansion RNAs is a major pathogenic even

82 Several microsatellite-expansion diseases are characterized by t

83 Microsatellite expansions are the leading cause of numer

84 nnectivity in biparentally inherited nuclear microsatellites explained the historical limits of invas

85 plication, and applied transcriptome-derived microsatellite (expressed-sequence tag simple-sequence r

86 The top 105 microsatellites from 71 genes were further analyzed in 9

87 ution modeling and paleobiolinguistics, with microsatellite genetic data and archaeobotanical data.

88 Based on microsatellites, genetic variation was similar in S and

89 t FA pathway, and is consistent with DSBs at microsatellites genome-wide in FANCJ depleted cells foll

90 tochondrial DNA (mtDNA) haplotypes (500 bp), microsatellite genotypes (17 loci) and sex from 128 indi

91 ametophyte plants (ramets) and in multilocus microsatellite genotypes (genets).

92 feed as well as Bayesian assignment tests of microsatellite genotypes, we document in situ brook trou

93 hat were concordant with the distribution of microsatellite genotypes.

94 Microsatellite genotyping demonstrated a common founder

95 Microsatellite genotyping revealed a decrease in clonal

96 We used microsatellite genotyping to assess genetic relatedness.

97 rs, and we compared results with traditional microsatellite genotyping.

98 r a single clone as determined by multilocus microsatellite genotyping.

99 The previous genetic linkage approach by microsatellite haplotyping was continued in new families

100 , understudied repetitive DNA regions called microsatellites have been identified as genetic risk mar

101 Here, we study the occurrence of microsatellite in mammal genomes and observe that animal

102 e the critical role of an EWS/FLI-bound GGAA-microsatellite in regulation of the NR0B1 gene as well a

103 We identified two variable polyglutamine microsatellites in chimpanzees and orangutans and found

104 ated from naturally occurring DSBs at (GAA)n microsatellites in Saccharomyces cerevisiae These data g

105 BB2/HER2 point mutations (8.2% [26 of 317]), microsatellite instability (7.6% [13 of 170]), and high

106 r depletion of MutSalpha from cells leads to microsatellite instability (MSI) and resistance to DNA d

107 Mismatch repair (MMR) deficiency (MMRD) and microsatellite instability (MSI) are prognostic for surv

108 Microsatellite instability (MSI) caused by mismatch repa

109 umulation of DNA replication errors known as microsatellite instability (MSI) is the hallmark lesion

110 median [range] age, 60.0 [19.0-75.0] years), microsatellite instability (MSI) phenotype, KRAS, and BR

111 Microsatellite instability (MSI) refers to the hypermuta

112 Colorectal cancers with microsatellite instability (MSI) represent 15% of all co

113 We sought to determine whether tumor microsatellite instability (MSI) typing along with immun

114 ed UVRAG(FS) in colorectal cancer (CRC) with microsatellite instability (MSI), and promotes tumorigen

115 s are resistant to genotoxic agents and have microsatellite instability (MSI), due to accumulation of

116 omarkers, including major mutational events, microsatellite instability (MSI), epigenetic features, p

117 from NRG/GOG0210 patients were assessed for microsatellite instability (MSI), MLH1 methylation, and

118 Microsatellite instability (MSI), the spontaneous loss o

119 smatch repair plays a key role in preventing microsatellite instability (MSI), which is a hallmark of

120 roximately 15% of colorectal cancers exhibit microsatellite instability (MSI), which leads to accumul

121 of recurrent indels that may serve to detect microsatellite instability (MSI).

122 ectal cancer (CRC) cells with high levels of microsatellite instability (MSI-H) accumulate mutations

123 In recurrent disease, the absence of microsatellite instability (the standard marker for MMR

124 al/family history of cancer or polyps, tumor microsatellite instability [MSI], mismatch repair [MMR]

125 ed on combinations of tumor markers: type 1 (microsatellite instability [MSI]-high, CpG island methyl

126 consenting probands and families, including microsatellite instability and DNA mismatch repair immun

127 includes defective DNA mismatch repair with microsatellite instability and POLE mutations in approxi

128 ted DNA polymerases and a distinct impact of microsatellite instability and replication repair defici

129 SBA cases (91%), and the higher incidence of microsatellite instability and tumor mutational burden i

130 ch repair (MMR) deficiency was determined by microsatellite instability and/or immunohistochemistry.

131 ed human CRC tissues and cell lines that had microsatellite instability contained truncations in the

132 Neither PTEN loss nor microsatellite instability correlated with efficacy.

133 approximately 20% that overlap greatly with microsatellite instability CRCs and some nonhypermutated

134 data were combined, providing rationale for microsatellite instability for 8 of the 9 cell lines in

135 s (CMSs) with distinguishing features: CMS1 (microsatellite instability immune, 14%), hypermutated, m

136 ic SETD2 aberrations are not associated with microsatellite instability in ccRCC.

137 Microsatellite instability in colorectal cancer predicts

138 is revealed that Immunoscore was superior to microsatellite instability in predicting patients' disea

139 Some colorectal and endometrial tumors with microsatellite instability not attributable to MLH1 hype

140 individuals' tumor tissue demonstrated high microsatellite instability of di- and tetranucleotides (

141 (HR: 1.99; 95% CI: 1.10, 3.56) but not with microsatellite instability or CpG island methylator phen

142 ) CRIS-A: mucinous, glycolytic, enriched for microsatellite instability or KRAS mutations; (ii) CRIS-

143 nal effects of mutations at other regions of microsatellite instability should be evaluated.

144 MIRMMR predicts microsatellite instability status in cancer samples usin

145 Patterns of concurrent mutations, microsatellite instability status, CpG island methylatio

146 gene expression that correlated with patient microsatellite instability status.

147 In stage II disease, for example, microsatellite instability supports observation after su

148 py, including tumor mutational burden (e.g., microsatellite instability), copy-number alterations, an

149 BRAF- and KRAS-mutation status, microsatellite instability, and CpG island methylator ph

150 cteristics (CpG island methylator phenotype, microsatellite instability, and the B-Raf protooncogene,

151 n tumor molecular characteristics (including microsatellite instability, CpG island methylator phenot

152 between CGI methylation and hypermutability, microsatellite instability, IDH1 mutation, 19p gain and

153 al cancer biomarkers and are associated with microsatellite instability, namely MLH1, PMS2, MSH2, MSH

154 Archival tissues were analyzed for microsatellite instability, PTEN status, and 487-gene se

155 icrosatellite-stable tumors from tumors with microsatellite instability, thus potentially improving c

156 owever, the mechanistic relationship between microsatellite instability, tumor-infiltrating immune ce

157 astatic DNA mismatch repair-deficient (dMMR)/microsatellite instability-high (MSI-H) colorectal cance

158 ted in 18% (13 of 78) of CRC tissues without microsatellite instability.

159 rs for DNA mismatch repair deficiency and/or microsatellite instability.

160 ated with a loss of mismatch repair genes or microsatellite instability.

161 ts those genetic alterations contributing to microsatellite instability.

162 potent indicator of tumor recurrence beyond microsatellite-instability staging that could be an impo

163 in these double somatic tumors than in other microsatellite-instability subgroups.

164 icrosatellite stable (MSS) tumours and 16 in microsatellite instable (MSI) tumours.

165 inent immune gene expression was observed in microsatellite-instable (MSI) tumors, as well as in a su

166 eradicating infiltrating GBM cells and tumor microsatellites is of utmost importance for the treatmen

167 t that there is an optimal "sweet-spot" GGAA-microsatellite length (of 18-26 GGAA repeats) that confe

168 Determination of microsatellite lengths or other DNA fragment types is an

169 icantly increased its affinity at sweet-spot microsatellite lengths.

170 es from 18 cancer types at more than 200,000 microsatellite loci and constructed a genomic classifier

171 Nine nuclear microsatellite loci failed to distinguish parental and h

172 c variation at the mitochondrial and nuclear microsatellite loci for 148 individuals, we identified t

173 The analyses were based on genotypes at 11 microsatellite loci for 318 individuals, spanning three

174 roe deer, we investigated variability at 12 microsatellite loci for Siberian roe deer from ten local

175 re, we used newly-developed and existing DNA microsatellite loci for the brooding coral Porites astre

176 30 bp of mitochondrial control region and 12 microsatellite loci from 94 individuals stranded around

177 approach to identify inherited variation of microsatellite loci from short sequence reads without pa

178 ed fox population expansion, we genotyped 21 microsatellite loci in modern and historical (1835-1941)

179 Genotyping of eight microsatellite loci indicated that the high early mortal

180 r sites, strongly influenced by five outlier microsatellite loci located in conserved intergenic regi

181 ies were analyzed along with genotypes at 12 microsatellite loci of 40 individuals coexisting in 3 Me

182 We conducted a genetic survey at 10 microsatellite loci of 482 coyotes originating from 11 e

183 Analysis of six chloroplast microsatellite loci revealed no variation.

184 notyping of 95% of the trees at nine nuclear microsatellite loci revealed that levels of genetic dive

185 Multilocus genotypes from 7 microsatellite loci suggested that most populations (10

186 We used 33 microsatellite loci to (1) reconstruct a pedigree for th

187 yped 233 American badgers in Wisconsin at 12 microsatellite loci to identify alternative statistical

188 Five microsatellite loci were screened across adult and seed

189 Mitochondrial DNA sequences and microsatellite loci were used to measure genetic diversi

190 istant basins in Chile were genotyped for 13 microsatellite loci, and allocated, through probabilisti

191 in color mutants, were genotyped with twelve microsatellite loci, being eleven of them identified as

192 hern Portugal), using two panels of 13 and 8 microsatellite loci, respectively.

193 l approaches and genotyping a large panel of microsatellite loci, we show that colony membership, mot

194 somal loci (17 introns and 3 exon segments), microsatellite loci, X- and Y-linked zinc-finger protein

195 d to mtDNA cytochrome b, intron AM2B1 and 15 microsatellite loci.

196 cross the Mediterranean were genotyped at 14 microsatellite loci.

197 pulations using both chloroplast and nuclear microsatellite loci.

198 eny from these trees were genotyped at eight microsatellite loci.

199 t, we identified 119 potentially informative microsatellite loci.

200 Historical studies used only a few microsatellite loci; therefore, our temporal comparisons

201 mposition of African tea based on 23 nuclear microsatellites loci (nSSRs) and three cpDNA intergenic

202 ollected and analyzed at cytochrome b and 11 microsatellites loci for investigating genetic variation

203 , Avpr1a and Oxtr each contain a polymorphic microsatellite locus located in their 5' regulatory regi

204 Microsatellite mapping found a bias toward intergenic re

205 Our results show that microsatellite mapping found a bias toward intergenic re

206 and linkage disequilibrium analyses using a microsatellite marker panel, genotyped in families to se

207 Microsatellite marker polymorphism was conserved across

208 We found that one microsatellite marker was very strongly associated with

209 Study-5 that were informative for 1p and 16q microsatellite markers (previously determined) and infor

210 p of Criollo pig breeds based on a set of 24 microsatellite markers and using different criteria.

211 f ancestry estimations using 678 genome-wide microsatellite markers in 249 individuals from 13 admixe

212 We characterized 28 microsatellite markers in Grevy's zebra and assessed cro

213 We have studied mitochondrial DNA and microsatellite markers in nine populations from Asia, No

214 y (Vaccinium macrocarpon) genotypes based on microsatellite markers is used to highlight the capabili

215 This is the first study to demonstrate that microsatellite markers provide valuable information for

216 We used nuclear microsatellite markers to examine the genetic diversity

217 ochondrial genes (COI, ND1 and ND5) and nine microsatellite markers to investigate the population gen

218 ion genetic structure of this pest in China, microsatellite markers were obtained by AFLP of sequence

219 These microsatellite markers will be the powerful tools for ge

220 inct populations were found in England using microsatellite markers, and mitochondrial diversity was

221 131 cM), using 618 captive-bred birds and 34 microsatellite markers, to investigate the extent of int

222 Using microsatellite markers, we assessed historical gene flow

223 d confirming previous findings using neutral microsatellite markers.

224 to 2.1 clones detected by a combination of 3 microsatellite markers.

225 waii, USA, were genotyped (n = 600) using 12 microsatellite markers.

226 west Ecuador using a suite of 10 polymorphic microsatellite markers.

227 studied less, and none of these studies use microsatellite markers.

228 te-replicating AT-rich regions with abundant microsatellites, mirror repeats, and repressive histone

229 fe survey genome produced valuable data from microsatellites, mobile genetic elements, and accurate d

230 Microsatellites (MSs) are tracts of variable-length repe

231 ing previously unknown repeat regions called microsatellites (MST).

232 Microsatellite multilocus genotypes of the pre-logging p

233 Microsatellite mutation rate, however, depends on the le

234 We combined information from nuclear microsatellites (nSSRs), nuclear and plastid DNA sequenc

235 ompare the genetic variation in nine nuclear microsatellites of six Balearic populations (three in ea

236 revealed indels at 54 million mononucleotide microsatellites of three or more nucleotides in length.

237 zygous for the long and short repeats of the microsatellite on their X-chromosomes and transfected th

238 We used microsatellite paternity analysis and hand pollinations

239 ea or aphidicolin treatment leads to loss of microsatellite polymerase chain reaction signals and to

240 The MIF promoter contains a 4-nucleotide microsatellite polymorphism (-794 CATT) that repeats 5 t

241 ventories from 2,082 worldwide languages and microsatellite polymorphisms from 246 worldwide populati

242 DNA was isolated, and microsatellite polymorphisms were exploited to quantify

243 in the PfK13 propeller domain, with flanking microsatellite profiles different from those observed in

244 utationally pooling Saccharomyces cerevisiae microsatellite profiles, and on samples obtained by pool

245 Here we developed a population-level microsatellite profiling approach, SID (Saccharomyces ce

246 into account of higher mutation rate in the microsatellite region compared to that of genome, limiti

247 nt of the nuclear rhodopsin gene (RH1) and 9 microsatellite regions (SSRs) were amplified and analyse

248 hisms located in the MIF gene, a -794CATT5-8 microsatellite repeat and a -173 G/C SNP.

249 cific targeting and efficient elimination of microsatellite repeat expansion RNAs both when exogenous

250 Microsatellite repeat expansions in DNA produce pathogen

251 pports a relationship between dNTP pools and microsatellite repeat instability.

252 Here we demonstrate that GGGGCC and CAG microsatellite repeat RNAs associated with C9orf72 in am

253 e observations suggest that transcription of microsatellite repeat-containing RNAs is more sensitive

254 Transcription of expanded microsatellite repeats is associated with multiple human

255 The dynamic mutability of microsatellite repeats is implicated in the modification

256 Previous analyses using microsatellites revealed no post-eruption changes in gen

257 ory region (the regulatory region-associated microsatellite, RRAM) that likely regulates gene express

258 a ~360 bp deletion (DupB), which includes a microsatellite (RS3) in the 5' promoter region of Avpr1a

259 nstability (MSI-H) accumulate mutations at a microsatellite sequence in the gene encoding transformin

260 We sequenced the 10-adenines microsatellite sequence in the TGFBR2 gene of 32 MSI-H c

261 f TGFBR2 with a 1-nucleotide deletion at its microsatellite sequence still produced a full-length TGF

262 specific DNA molecules covering the complete microsatellite sequence.

263 pression required preservation of the TGFBR2 microsatellite sequence; cells in which this sequence wa

264 EWS/FLI binds GGAA-microsatellite sequences in vivo and in vitro.

265 very two consecutive GGAA-repeats on shorter microsatellite sequences.

266 We developed and generated an 11-marker microsatellite set and conducted association and linkage

267 The phenotype of microsatellite signal instability is specific for FANCJ

268 Moreover, diverse endogenous microsatellite signals were also lost upon replication s

269 ly, the affinity for Delta22 binding to GGAA-microsatellites significantly decreased, and ultimately

270 rmethylation, and 12 of 78 (15%) tumors with microsatellite stability (P < .0001 for patients with do

271 ts were available for 303 patients (283 with microsatellite stability or low MSI [median age, 62 year

272 r a low CpG island methylator phenotype, and microsatellite stability), although formal tests for het

273 mitant MMR deficiency and compromised global microsatellite stability.

274 s temozolomide sensitivity while maintaining microsatellite stability.

275 r a low CpG island methylator phenotype, and microsatellite stability.

276 ts reveals 24 significantly mutated genes in microsatellite stable (MSS) tumours and 16 in microsatel

277 tation, negative for KRAS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, p

278 The genomic anomaly frequencies observed in microsatellite stable PDX reproduce those detected in no

279 tely differentiated invasive adenocarcinoma, microsatellite stable.

280 le (MSI) tumors, as well as in a subgroup of microsatellite-stable (MSS) tumors.

281 In the majority of microsatellite-stable colorectal cancers (CRCs), an init

282 SI (541 [146-8063]; P < .001), and lowest in microsatellite-stable tumors (70.5 [7-1877]; P < .001).

283 ted with shorter DFS and OS in patients with microsatellite-stable tumors but not in patients with MS

284 tern of MS indels can accurately distinguish microsatellite-stable tumors from tumors with microsatel

285 he subgroup analysis showed in patients with microsatellite-stable tumors that both KRAS (HR for DFS:

286 ith Lynch syndrome, MLH1-hypermethylated, or microsatellite-stable tumors.

287 (32.8 vs 13.5; P < .001) TILs compared with microsatellite-stable tumors.

288 factors in stage III disease is greater when microsatellite status and tumor location are taken into

289 weak HFC for parasite infection based on 27 microsatellites strengthened considerably with 14,585 SN

290 ferent alleles to both its hosts and DFT1 at microsatellite, structural variant, and major histocompa

291 outcomes and the overall burden of unstable microsatellites, suggesting that MSI may be a continuous

292 he somatic background indel mutation rate of microsatellites to assess mutation significance.

293 Here, we use genome-wide gene-associated microsatellites to investigate genetic signatures of nat

294 that are known (UGT1A1*28) or likely (HMOX-1 microsatellites) to impact bilirubinemia.

295 C580Y from 2 major clusters as identified by microsatellite typing.

296 lite instability immune, 14%), hypermutated, microsatellite unstable and strong immune activation; CM

297 immunoresponsive melanomas, lung cancers, or microsatellite-unstable GI cancers (P < .001).

298 Microsatellite-unstable tumors are hyper-mutated intesti

299 y became unmeasureable, when the size of the microsatellite was increased to the sweet-spot length.

300 ion events and subsequent mutation of poly-A microsatellites within L1.