ライフサイエンスコーパス: linkage disequilibrium

1 (while accounting for shared variance due to linkage disequilibrium).

2 not stable when some of the SNPs are in high linkage disequilibrium.

3 mating their effect sizes in the presence of linkage disequilibrium.

4 otential confounding associations as well as linkage disequilibrium.

5 100) and the thousands of surrogate SNPs in linkage disequilibrium.

6 minor allele frequencies and a fast decay of linkage disequilibrium.

7 epistatic loci do not systematically exploit linkage disequilibrium.

8 itro IgE synthesis, with six displaying high linkage disequilibrium.

9 Quantitative trait loci mapping confirmed linkage disequilibrium.

10 ain HLA allele combinations co-occur in high linkage disequilibrium.

11 e same problem if two causal variants are in linkage disequilibrium.

12 0, A/C at -214, and A/G at -119, that are in linkage disequilibrium.

13 eir genotype values across samples, known as linkage disequilibrium.

14 the centromeric KIR region and are in tight linkage disequilibrium.

15 equency and were independent with respect to linkage disequilibrium.

16 igh multiplicity of infection (2.7), and low linkage disequilibrium (500-bp) were observed in Chikhwa

17 e locus also displays consistent patterns of linkage disequilibrium across African populations and ha

18 dissection is often prevented by the strong linkage disequilibrium across the entire MHC complex.

19 turing into distinct strains and substantial linkage disequilibrium across the genome(1,2).

20 tion, as it leads to strong correlations and linkage disequilibrium across very distant sites in the

21 iate from the Hardy-Weinberg equilibrium and linkage disequilibriums after applying Bonferroni correc

22 hallenge with methods based on the admixture linkage disequilibrium (ALD) is to remove the effect of

23 ulations is dependent on many factors (e.g., linkage disequilibrium, allele frequencies, genetic arch

24 Complex structure of linkage disequilibrium also makes it challenging to sepa

25 udy (GWAS) summary data while accounting for linkage disequilibrium among variants.

26 ssible and inherently takes into account the linkage disequilibrium among variants.

27 parametric, nonparametric, joint linkage and linkage disequilibrium analyses using a microsatellite m

28 Local linkage disequilibrium analysis and allele mining identi

29 ware package that performs joint linkage and linkage disequilibrium analysis between a marker and a p

30 This is, in part related to differences in linkage disequilibrium and allele frequencies between et

31 In particular, the differences in linkage disequilibrium and allele frequency patterns acr

32 ecular genetic estimates of Ne computed from linkage disequilibrium and approximate Bayesian computat

33 The six novel SNPs in PRPF6 were in high linkage disequilibrium and associated with PRPF6 mRNA ex

34 le nucleotide polymorphisms (SNPs) in strong linkage disequilibrium and comprising a novel G3 haploty

35 Linkage disequilibrium and conditional analyses indicate

36 variation, Manhattan plot visualization for linkage disequilibrium and eQTL data, and an ontology se

37 lead to false identification due to complex linkage disequilibrium and interaction patterns.

38 Nucleotide Polymorphisms (SNPs) according to linkage disequilibrium and P-value or use all SNPs, hand

39 By taking into account linkage disequilibrium and sparseness of the data, the p

40 enging because of the uncertainty induced by linkage disequilibrium and the fact that some loci harbo

41 nic area near SLC2A9 that were not driven by linkage disequilibrium and were replicated in FHS.

42 is reversal could be explained by breakup of linkage disequilibrium, and direct selection on wing sha

43 d elevated polymorphism, unusual patterns of linkage disequilibrium, and lower levels of population d

44 type effects, single variants tagged through linkage disequilibrium, and population stratification.

45 patients, hence confirming previous data of linkage disequilibrium as a cause for disease associatio

46 th their mating type; IA(s) values show high linkage disequilibrium as is expected in clonal reproduc

47 3763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs.

48 s (Gly84-Gly85-Pro86-Met87) in near-complete linkage disequilibrium at the edge of the peptide-bindin

49 le variation, we also detected long-distance linkage disequilibrium at two underlying loci, GS-OH and

50 Using a linkage disequilibrium-based analysis, individual sampli

51 mapping methods, commonly referred to as the linkage disequilibrium-based mapping (LD mapping), have

52 is a considerable reduction in power for all linkage disequilibrium-based statistics.

53 he HapMap analysis further identified strong linkage disequilibrium between 5 single nucleotide polym

54 We leveraged differences in the pattern of linkage disequilibrium between diverse populations to fi

55 y leveraging differences in the structure of linkage disequilibrium between diverse populations, and

56 ic effects and variation in the structure of linkage disequilibrium between ethnicities.

57 , but its role in generating and maintaining linkage disequilibrium between HLA loci is unclear.

58 atasets that have no shared markers based on linkage disequilibrium between loci appearing in differe

59 nation in influenza, our method accounts for linkage disequilibrium between nucleotides at different

60 to reduce computational burden and to limit linkage disequilibrium between single-nucleotide polymor

61 ociated lincRNAs, we examined the pattern of linkage disequilibrium between SNPs in the lincRNAs and

62 alleles, and obtain initial estimates of the linkage disequilibrium between STRs and common SNPs.

63 Restricted recombination may promote linkage disequilibrium between the colour locus and inco

64 We also find linkage disequilibrium between the inverted region and t

65 to be strong enough to establish significant linkage disequilibrium between the mitochondrial and nuc

66 Differences in linkage disequilibrium between the two populations allow

67 we perform a high-resolution genome scan for linkage disequilibrium between unlinked genomic regions

68 ween racial/ethnic groups creates long-range linkage disequilibrium between variants with different a

69 overly conservative and fails to account for linkage disequilibrium between variants.

70 controls and detected an approximately 33-kb linkage disequilibrium block (containing the lead SNP rs

71 across all six environments and tagged to a linkage disequilibrium block comprising two promising ca

72 fined the chromosome 12E signal to a 1.95 Mb linkage disequilibrium block containing only one gene, s

73 Only 1 gene is found in the linkage disequilibrium block containing rs9828519: SLC9A

74 ypersensitive sites overlapping the rs874040 linkage disequilibrium block in human memory, but not in

75 A linkage disequilibrium block of polymorphisms located in

76 terest and that are also sole members of the linkage disequilibrium block surrounding a PGC-SCZ GWAS

77 us founder mutations, BRCA1, within the same linkage disequilibrium block, offered the unique opportu

78 or knowledge: one as a group structure (e.g. linkage disequilibrium blocks among SNPs) and the other

79 (plasticity) a priori candidate genes within linkage disequilibrium blocks for these loci.

80 differentially methylated regions within the linkage disequilibrium blocks of the single nucleotide p

81 ations have low genetic variability and high linkage disequilibrium, but relatively few autozygous se

82 ood ratio and uses a model that accounts for linkage disequilibrium by explicitly modeling haplotype

83 selective sweep, characteristic patterns of linkage disequilibrium can arise in the genomic region s

84 f single-nucleotide polymorphisms, and local linkage disequilibrium characteristics based on the huma

85 28 dogs from 3 breeds to compare the SNP and linkage disequilibrium characteristics together with the

86 ules mediate most of the risk, but extensive linkage disequilibrium complicates the localization of i

87 ons exhibit a clear gradient of short--range linkage disequilibrium consistent with a Central Asian d

88 S2377X and H1249R were in high linkage disequilibrium (D' = 0.95).

89 pe at 2 VDR SNPs (rs7968585 and rs731236) in linkage disequilibrium (D' = 0.98; r2 = 0.6).

90 ent duplication which, combined with a rapid linkage disequilibrium decay, makes it difficult to perf

91 We estimate, using linkage-disequilibrium decay patterns, that admixture oc

92 language in southern Chad and estimate from linkage-disequilibrium decay that this occurred 4,750-7,

93 Linkage disequilibrium decays within 10 kb (based on the

94 We found that linkage-disequilibrium decays at 100 Kb in this collect

95 Genome-wide linkage disequilibrium declined more slowly for the comm

96 that were selected based on the short-range linkage disequilibrium distance, which is inherent with

97 at inferring hard selective sweeps based on linkage disequilibrium distortions under different condi

98 various functional annotations and allow for linkage disequilibrium estimated from reference genotype

99 characteristics such as allele frequencies, linkage disequilibrium etc., is an integral component of

100 identified 3 common genetic variants in high linkage disequilibrium for severe pre-treatment pain, re

101 We used two methods (patterns of linkage disequilibrium from whole-genome SNPs and MSMC e

102 favored because it prevents the breakdown of linkage disequilibrium generated by migration; the selec

103 tibility and colouration, such as fine-scale linkage disequilibrium, genomic rearrangements and pleio

104 Patterns of linkage disequilibrium, homoplasy, and incompatibility a

105 ausal regulatory variants in regions of high linkage disequilibrium identified by expression quantita

106 nd g.69349694C>T) exhibited a high degree of linkage disequilibrium in all test populations.

107 Given the small blocks of linkage disequilibrium in Drosophila, we obtain near bas

108 otypes of un-genotyped variants based on the linkage disequilibrium in external reference panels such

109 l mechanisms of selection that maintain high linkage disequilibrium in MHC haplotype blocks.

110 identify approximately independent blocks of linkage disequilibrium in the human genome.

111 n this model, occasional clonality generates linkage disequilibrium in the short term.

112 We found two SNPs in strong linkage disequilibrium in the SLC19A3 locus associated w

113 Owing to complex patterns of linkage disequilibrium in this region, it is unclear whe

114 have been hampered by the presence of strong linkage disequilibrium in this region.

115 n (HLA) region are complicated by the strong linkage disequilibrium in this region.

116 We used genetic maps that capture detailed linkage disequilibrium information in European and Afric

117 riants [increasing to 87% (60%) when summary linkage disequilibrium information is available from tar

118 Linkage disequilibrium information was used to identify

119 In addition, by taking strong linkage disequilibrium into account, another 47 IBD-asso

120 ethod to select important SNPs by taking the linkage disequilibrium into account.

121 Linkage disequilibrium is positive (Dij'>0) among freque

122 rowed the number of significant SNPs in high linkage disequilibrium (LD) (r(2) > 0.8) with rs3865444

123 Assessing linkage disequilibrium (LD) across ancestral populations

124 ], are the true biological representation of linkage disequilibrium (LD) among multiple loci.

125 Linkage disequilibrium (LD) analysis indicated strong LD

126 Meiotic recombination breaks down linkage disequilibrium (LD) and forms new haplotypes, me

127 ty varies with minor allele frequency (MAF), linkage disequilibrium (LD) and genotype certainty.

128 al variant effect sizes while accounting for linkage disequilibrium (LD) and overlapping GWAS samples

129 s the exponential decay of admixture-induced linkage disequilibrium (LD) as a function of genetic dis

130 The linkage disequilibrium (LD) based quantitative trait loc

131 We demonstrate that heterogeneity in linkage disequilibrium (LD) between causal variants and

132 The existence of moderate to high levels of linkage disequilibrium (LD) between genetic markers and

133 emporary effective population size (Ne) from linkage disequilibrium (LD) between unlinked pairs of ge

134 ese approaches require information about the linkage disequilibrium (LD) between variants, there has

135 s were enriched in approximately independent linkage disequilibrium (LD) blocks (e.g. MHC).

136 The presence of conserved linkage disequilibrium (LD) blocks and haplotypes betwee

137 ate target genes and often extend beyond the linkage disequilibrium (LD) blocks containing risk SNPs

138 Length of individual linkage disequilibrium (LD) blocks varied along chromoso

139 notypes across multiple individuals based on linkage disequilibrium (LD) can facilitate the analysis

140 m genome-wide association studies (GWAS) and linkage disequilibrium (LD) data from a reference sample

141 While linkage disequilibrium (LD) decay (r(2) = 0.2) was lowes

142 ve enabled strategies that integrate linkage-linkage disequilibrium (LD) mapping in Populus.

143 ety of publicly available GWAS associations, linkage disequilibrium (LD) measures, functional genomic

144 population size (Ne) can be estimated using linkage disequilibrium (LD) observed across pairs of loc

145 we proposed an algorithm that considers both linkage disequilibrium (LD) patterns and familial transm

146 ently, gene statistics are constructed using linkage disequilibrium (LD) patterns from a relevant ref

147 Trans-ethnic comparison revealed different linkage disequilibrium (LD) patterns in HLA-DOA and HLA-

148 nt inference requires leveraging the complex linkage disequilibrium (LD) patterns in the cohort to co

149 ation of GWAS signals to gene-dense and high linkage disequilibrium (LD) regions, and correlations of

150 This study used the linkage disequilibrium (LD) score regression and genomic

151 ome annotations (e.g., exon or 5'UTR), total linkage disequilibrium (LD) scores and heterozygosity to

152 With differences in linkage disequilibrium (LD) structure and allele frequen

153 Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated a

154 limited mapping resolution due to extensive linkage disequilibrium (LD) that is characteristic of cr

155 In using multilocus linkage disequilibrium (LD) to infer recombination among

156 The analysis of linkage disequilibrium (LD) underpins the development of

157 A strong linkage disequilibrium (LD) was observed across the SLC2

158 ome-wide association studies, are usually in linkage disequilibrium (LD) with each other within a sma

159 A total of 2255 variants in linkage disequilibrium (LD) with GWAS identified SU/gout

160 mon variants that represent or are in strong linkage disequilibrium (LD) with previously-identified s

161 at one additional SNP, IL17RA rs41433045, in linkage disequilibrium (LD) with rs41396547, was associa

162 By exploiting linkage disequilibrium (LD), a real data application dem

163 tudies (GWAS) often contain multiple SNPs in linkage disequilibrium (LD), any of which may be causal.

164 itative genetic information sources, namely, linkage disequilibrium (LD), co-segregation (CS) and ped

165 pendent markers, often by pruning markers in Linkage Disequilibrium (LD), ignoring the information co

166 and cytoplasmic organelles, or cyto-nuclear linkage disequilibrium (LD), is both an important compon

167 sed to association studies that benefit from linkage disequilibrium (LD), the main challenge in ident

168 y models genome-wide variants to account for linkage disequilibrium (LD), thus prioritizing associati

169 association mapping are highly influenced by linkage disequilibrium (LD), we examined the extent of g

170 rmance of a single-sample estimator based on linkage disequilibrium (LD), which provides an estimate

171 using individual-based, population-based and linkage disequilibrium (LD)-aware methods with stringent

172 pproach for calculating risk scores involves linkage disequilibrium (LD)-based marker pruning and app

173 Recent work has hinted at the linkage disequilibrium (LD)-dependent architecture of hu

174 RES based on SNP prior information including linkage disequilibrium (LD)-weighted genic annotation sc

175 f Ohta's 1982 measures of between-population linkage disequilibrium (LD).

176 gions (haplotypes) due to the development of linkage disequilibrium (LD).

177 the relationship between test statistics and linkage disequilibrium (LD).

178 respectively) and showed string evidence of linkage disequilibrium (LD).

179 00 SNPs at these loci define BCa risk due to linkage disequilibrium (LD).

180 orrelated to the true causal variant through linkage disequilibrium (LD).

181 n traits can be further reduced based on the linkage disequilibrium (LD).

182 ormance of the single-sample method based on linkage disequilibrium (LD): (1) estimates based on sing

183 A methylation at CpGs was similar to that of linkage-disequilibrium (LD) correlation in genetic SNP v

184 w-coverage sequencing has been combined with linkage-disequilibrium (LD)-based genotype refinement to

185 tion based on hierarchical representation of linkage disequilibrium (LinDen).

186 Nevertheless, linkage disequilibrium makes it difficult to define, wit

187 Mapping by admixture linkage disequilibrium (MALD) is a whole genome gene map

188 This method is referred as multi-marker linkage disequilibrium mapping (mmLD).

189 Interestingly, with linkage disequilibrium mapping, 76.7% of the RTAs with a

190 another unidentified mutation within the bs linkage disequilibrium may be contributing to the bs phe

191 trate that rs744373 itself or a variation in linkage disequilibrium may provide a neurogenetic mechan

192 estry inference in adMixed Populations using Linkage Disequilibrium method (LAMP-LD) and evaluated th

193 Non-parametric-linkage analysis, linkage-disequilibrium-model analysis, single-SNP analys

194 and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previo

195 hin-population genetic variation, background linkage disequilibrium, number of ancestral populations,

196 d that 51 traits could be linked through the linkage disequilibrium of 115 associated loci and these

197 Because of the strong linkage disequilibrium of A*01 and B*08 alleles with the

198 multiple sclerosis (MS) risk, the ubiquitous linkage disequilibrium operating across the genome has s

199 ith the user's dataset, as well as visualize linkage disequilibrium pattern, infer haplotypes and des

200 Comparison of linkage disequilibrium patterns between the 13 lead SNPs

201 ii) to assess the extent to which the unique linkage disequilibrium patterns in African Americans can

202 enetic diversity, haplotype distribution and linkage disequilibrium patterns in the G. hirsutum and G

203 tion-specific loci may exist due to distinct linkage disequilibrium patterns.

204 r, we identified 44 of these Alu elements in linkage disequilibrium (r(2) > 0.7) with the trait-assoc

205 First, all known genes in strong linkage disequilibrium (r(2) > 0.8) with the reported si

206 We found that though these SNPs were in high linkage disequilibrium (r(2) > 0.8), the rare alleles of

207 We retrieved all SNPs in linkage disequilibrium (r(2) >/= 0.2) with the glioma-as

208 undred fourteen noncoding variants in strong linkage disequilibrium (r(2) >/= 0.8) with rs4888378 wer

209 e-nucleotide polymorphism (SNP) is in strong linkage disequilibrium (r(2) = 0.90, D' = 0.96) with the

210 SNP rs8041357, which is in complete linkage disequilibrium (r(2) = 1) with rs11543198, was a

211 nonymous SNPs, which are in moderate to high linkage disequilibrium (r(2)>0.5) with the GWAS SNPs.

212 observed for rs1333040 and for other SNPs in linkage disequilibrium (r(2)>0.8) with rs10757278.

213 56, a single-nucleotide polymorphism in high linkage disequilibrium (r(2)=0.7) with rs10995, which bo

214 nt effective population sizes estimated from linkage disequilibrium ranged from 88 to 825.

215 Linkage disequilibrium rapidly decayed around LanFTc1, s

216 We used linkage disequilibrium regression and polygenic profile

217 Using a new method, linkage disequilibrium regression, we derived genetic co

218 Two SNPs in high linkage disequilibrium, rs17026688 and rs17026651, that

219 Among them, two SNPs in strong linkage disequilibrium, rs7676822 and rs1911877, located

220 Linkage disequilibrium score regression and polygenic pr

221 Linkage disequilibrium score regression of 220 cell type

222 Linkage disequilibrium score regression was used to calc

223 Using linkage disequilibrium score regression, we estimate the

224 iation study statistics and to the method of linkage disequilibrium score regression.

225 d genetic correlations were calculated using linkage disequilibrium score regression.

226 osatellite set and conducted association and linkage disequilibrium (standardized index of associatio

227 tentially affected by selection, calculating linkage disequilibrium statistics, performing haplotype

228 , estimates of nucleotide diversity metrics, linkage disequilibrium statistics, recombination rates,

229 Differences in linkage disequilibrium structure and heterogeneity in al

230 Given considerable differences in linkage disequilibrium structure between populations of

231 effect allele frequency, effect size and the linkage disequilibrium structure of credible set variant

232 We further show that the strong linkage disequilibrium structure within the human MHC th

233 on variants, which was observed to depend on linkage disequilibrium structure.

234 Our approach properly takes into account the linkage-disequilibrium structure among variants, and its

235 By leveraging varying linkage disequilibrium structures across different popul

236 cularly evident for regions having extensive linkage disequilibrium such as the IBD5 locus.

237 subjects and was not exclusively a result of linkage disequilibrium, suggesting that multiple HLA epi

238 ter has 3 single-nucleotide polymorphisms in linkage disequilibrium: T/A at -663, T/C at -470, and C/

239 Linkage disequilibrium tagging polymorphisms and polymor

240 f classic HLA alleles identified two in high linkage disequilibrium that are associated with fIIP (DR

241 Frequent recombination limits linkage disequilibrium to about 100 bp in most of the ge

242 natural selection, haplotype frequencies and linkage disequilibrium to estimate the effects of both s

243 maps, RA GWAS risk loci, and adjustment for linkage disequilibrium to propose target genes of immune

244 outcrossing rapidly and drastically reduced linkage disequilibrium to very low levels even at short

245 ed by appropriately controlling for expected linkage disequilibrium using a genetic map.

246 otide polymorphisms (SNPs) with low pairwise linkage disequilibrium values and apolipoprotein E (APOE

247 Strong linkage disequilibrium was observed across a 200 kb regi

248 the allele frequency spectrum and long-range linkage disequilibrium, we detected strong signatures of

249 transcription factors, since all the SNPs in linkage disequilibrium were located in a regulatory DNA

250 for measuring mature mRNA levels and in high linkage disequilibrium with 65 lead type 2 diabetes GWAS

251 multaneously screen 2,756 variants in strong linkage disequilibrium with 75 sentinel variants associa

252 This variant is in high linkage disequilibrium with a known functional variant i

253 ylation associates with two polymorphisms in linkage disequilibrium with a known IBD susceptibility v

254 g expression of HLA-A RNA in vivo, in strong linkage disequilibrium with an HLA-A allele that confers

255 e lead variant, rs11556924, is not in strong linkage disequilibrium with any other variant and introd

256 Both SNPs were in strong linkage disequilibrium with asthma-associated 17q21 SNPs

257 ntitative trait locus of complex trait is in linkage disequilibrium with at least one marker.

258 y on candidate genes; four SNPs were in high linkage disequilibrium with candidate genes within 366 k

259 of single-nucleotide polymorphisms in strong linkage disequilibrium with causative polymorphisms that

260 These polymorphisms were in high linkage disequilibrium with each other (r(2) = 0.96) mea

261 me-wide analyses identified multiple SNPs in linkage disequilibrium with each other that were signifi

262 on 146 PrCa-risk SNPs, including all SNPs in linkage disequilibrium with each risk SNP, resulting in

263 hat IL13 polymorphism rs1295686 (in complete linkage disequilibrium with functional variant rs20541)

264 say to sequence a small number of regions in linkage disequilibrium with heading date QTL in thousand

265 9.10, p=2.35 x 10(-9)) which was in moderate linkage disequilibrium with HLA-B*27:05.

266 Inhibitory KIR2DL5A, carried in linkage disequilibrium with KIR2DS1, is expressed by per

267 nase 7 (PAK7, also called PAK5) which was in linkage disequilibrium with local haplotypes (P = 2.5 x

268 as other relevant candidate loci that are in linkage disequilibrium with MICA*008 i.e. HLA-B*08:01, r

269 n alleles identified, two thirds were not in linkage disequilibrium with nearby SNPs, implicating the

270 for IBD; IL23R, PTGER4, and SNX20 (in strong linkage disequilibrium with NOD2) for CD; and KCNQ2 (nea

271 motif, except the more than 100 GMAS SNVs in linkage disequilibrium with polymorphisms reported by ge

272 = 0.64; P = 1.4 x 10(-9)), and was in strong linkage disequilibrium with rs10498635.

273 th rs10846744 (P = 2x10(-4)), an SNP in high linkage disequilibrium with rs11057841 (r(2) = 0.93).

274 f association with CLU at rs1532278, in high linkage disequilibrium with rs11136000.

275 SA and WHI, but only rs12243326 is in strong linkage disequilibrium with rs12255372 in our Hispanic p

276 Rs3865444 is in linkage disequilibrium with rs12459419 which has been as

277 ss469415590 (TT or DeltaG), which is in high linkage disequilibrium with rs12979860, a genetic marker

278 lies in intron 8 of the gene, is in complete linkage disequilibrium with rs17026688 and is predicted

279 Marker rs2238448 in ADCY9, in linkage disequilibrium with rs1967309 (r(2)=0.8), was as

280 ymorphism in the ADCY9 gene, the majority in linkage disequilibrium with rs1967309, were associated w

281 with better residual cognition is in strong linkage disequilibrium with rs1990622A (r2 = 0.66), a pr

282 SNP rs2227473, in linkage disequilibrium with rs2227476, was also associat

283 of seven SNPs tested: rs1962, rs1042579 (in linkage disequilibrium with rs3176123), and rs1042580.

284 e rs12979860 polymorphism, which was in high linkage disequilibrium with rs368234815 (R(2) = 0.87).

285 luster of single-nucleotide polymorphisms in linkage disequilibrium with rs61183828 was located close

286 disease-variant-tagging SNP (rs117026326; in linkage disequilibrium with rs73366469), whose minor all

287 eotide polymorphism (SNP) rs2235749 (in high linkage disequilibrium with rs910080) modifies striatal

288 ctoside-binding lectin 9 (LGALS9) that is in linkage disequilibrium with rs944722.

289 olymorphism is observed in high species-wide linkage disequilibrium with sex.

290 known, trait-associated SNPs to be in strong linkage disequilibrium with SVs and demonstrate that our

291 ot affect RNA splicing, but it was in strong linkage disequilibrium with the G allele of the promoter

292 Both were in low linkage disequilibrium with the genome-wide association

293 0(-6); OR = 1.63), which is in near complete linkage disequilibrium with the HLA-DRB1*07:01 allele we

294 ntitative trait locus (cis-eQTL) variants in linkage disequilibrium with the index variant in 29 of t

295 her, the long-range meQTL was found to be in linkage disequilibrium with the most replicated locus of

296 nucleotide polymorphism rs6800541 is in high linkage disequilibrium with the nonsynonymous variant in

297 exonic deletion (P = 1.59 x 10(-8)) in full linkage disequilibrium with the reference HCP5 rs2395029

298 nd that a large fraction of L1s were in high linkage disequilibrium with their surrounding genomic re

299 kely to be causal relative to nearby SNPs in linkage disequilibrium with them.

300 that are causal and those that are merely in linkage-disequilibrium with causal mutations.