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1                                              eQTLs and eGenes provide great supporting evidence for G
2                           At 49 of these 140 eQTLs, gene expression was nominally associated (p < 0.0
3 ent cis-eQTLs at 109 GWAS loci, including 93 eQTLs not previously described.
4    We identified cis-acting and trans-acting eQTL for key immune and metabolic response genes and sep
5 portion of genetic variance explained by all eQTL (hCOJO(2)) was 31% (0.060/0.192), meaning that 69%
6 candidate gene identified by GWAS is also an eQTL or eGene, there is strong evidence to further study
7 fy loci where autoimmune-disease risk and an eQTL are driven by a single shared genetic effect.
8           This variant was reported to be an eQTL of the ZXDC gene, biologically linked to monocyte I
9                              We conducted an eQTL investigation of microarray-based gene and exon exp
10           These observations suggest that an eQTL analysis that includes disease-affected brain tissu
11 nctional analysis, gene fusion detection and eQTL mapping.
12 visualization for linkage disequilibrium and eQTL data, and an ontology search for phenotypes, traits
13 us (SLE) through the integration of GWAS and eQTL data from the TwinsUK microarray and RNA-Seq cohort
14 plex-disease susceptibility loci by GWAS and eQTL integration have predominantly employed microarrays
15 ilitating the understanding of both GWAS and eQTL results and functional genomics data.
16 p a framework for the integration of PPI and eQTL into a heterogenous network model, enabling efficie
17 tified novel associations between asthma and eQTLs for 4 genes related to nucleotide synthesis/signal
18 ve maps of cis-acting hippocampal meQTLs and eQTLs provide a link between disease-associated SNPs and
19    Cis-acting SNPs of hippocampal meQTLs and eQTLs significantly overlap schizophrenia-associated SNP
20 d meta-analysis of all published Arabidopsis eQTL datasets.
21 he number of GWAS catalog SNPs identified as eQTL in the conditional analyses increases with 24% as c
22 e-based information, ENCODE ChIP-seq assays, eQTL, population haplotype, functional prediction across
23 y than in standard unconditional whole blood eQTL databases.
24  and guidelines for estimating aFC from both eQTL and allelic expression data sets and apply it to Ge
25 functional annotation data, especially brain eQTL, methylation QTL, brain expression featured in deep
26 3, P=3.0 x 10(-6)) and the independent Brain eQTL Almanac (N=134, P=0.028).
27 s of the transcription factor CTCF and brain eQTLs.
28 ico functional analyses for these 11 SNPs by eQTL analysis, two of which, PTPN2 SNPs rs2847297 and rs
29 these, for 37, the association was driven by eQTLs located in established risk loci for allergic dise
30                                    Candidate eQTL analyses in in LCLs in the Hutterites suggest that
31 d the greatest frequency of candidate-causal eQTLs using exon-level RNA-Seq, and identified novel SLE
32 analysis showed that 35% of genes with a cis eQTL have at least two independent cis eQTLs; for severa
33         We provide an online conditional cis eQTL mapping catalog for whole blood, which can be used
34       Also, 12% (671) of the independent cis eQTLs identified in conditional analyses were not signif
35 ; for several genes up to 13 independent cis eQTLs were identified.
36 a cis eQTL have at least two independent cis eQTLs; for several genes up to 13 independent cis eQTLs
37                     Associations between cis-eQTL markers and host response phenotypes using 383 pigs
38           These analyses identified both cis-eQTL and trans-eQTL impacting individual genes, and CONF
39                 FIRE scores discriminate cis-eQTL SNVs from non-eQTL SNVs in the training set with a
40 c curve (AUC) of 0.807, and discriminate cis-eQTL SNVs shared across six populations of different anc
41 nts, which are highly enriched for islet cis-eQTL.
42 ting expression quantitative trait loci (cis-eQTL) for 869 expressed genes (qval < 0.05).
43 ting expression quantitative trait loci (cis-eQTL) has become a popular approach for characterizing p
44  cis-expression quantitative trait loci (cis-eQTL) maps.
45 cis expression quantitative trait locus (cis-eQTL) for SLC2A2 in 1,226 human liver samples, suggestin
46 cis-expression quantitative trait locus (cis-eQTL) variants in linkage disequilibrium with the index
47       FIRE scores are also predictive of cis-eQTL SNVs across a variety of tissue types.
48  We have performed the first genome-wide cis-eQTL analysis of human hippocampal tissue to include not
49                             A set of 145 cis-eQTLs depended on type I interferon signaling.
50 QTLs at 14,118 CpG methylation sites and cis-eQTLs for 302 3'-mRNA transcripts of 288 genes.
51  variants are difficult to identify, and cis-eQTLs occur frequently, it remains challenging to identi
52 lic traits, we identified 140 coincident cis-eQTLs at 109 GWAS loci, including 93 eQTLs not previousl
53 eQTLs) impact expression of local genes (cis-eQTLs).
54                            We identified cis-eQTLs for 12,400 genes at a 1% false-discovery rate.
55 We detected over 19,000 independent lead cis-eQTLs and over 6000 independent lead trans-eQTLs, target
56                Although detecting local, cis-eQTLs is now routine, trans-eQTLs, which are distant fro
57  cis-expression quantitative trait loci (cis-eQTLs) and/or splicing eQTLs.
58  cis-expression quantitative trait loci (cis-eQTLs) using a set of 92 genomic annotations as predicti
59                     We identify numerous cis-eQTLs that contribute to the marked differences in immun
60  unit for quantifying the effect size of cis-eQTLs and a mathematically convenient approach for syste
61 other diverse tissue types revealed that cis-eQTLs for islet-specific genes are specifically and sign
62 We also identified copy-number variant (CNV) eQTLs, including some that appear to affect gene express
63 r studies, and two loci exhibited coincident eQTLs (P < 1 x 10-5) in subcutaneous adipose tissue for
64                   After adjusting for common eQTLs and the major axes of gene expression covariance,
65 ene-by-environment interactions by comparing eQTLs under different conditions.
66                                  Conditional eQTL analysis allows a distinction between dependent and
67                     We performed conditional eQTL analysis in 4,896 peripheral blood microarray gene
68 ronger enrichment for response than constant eQTLs in GWAS signals of several autoimmune diseases.
69 mber of them were unexplored in conventional eQTL mapping.
70 ical power) to detect eQTLs over the current eQTL mapping approaches.
71  0.05), 2,743 (12%) showed context-dependent eQTL effects.
72  systematically identified context-dependent eQTLs using a hypothesis-free strategy that does not req
73   We show that our RA patient cohort derived eQTL network is more informative for studying RA than th
74 ease of approximately 50% in power to detect eQTL.
75 ce (in terms of statistical power) to detect eQTLs over the current eQTL mapping approaches.
76 sion remain unclear, particularly for distal eQTLs, which these studies are not well powered to detec
77                                      Distant eQTL formed 125 significant distant eQTL hotspots with t
78  Distant eQTL formed 125 significant distant eQTL hotspots with their targets significantly enriched
79               Hence, we utilize the epilepsy eQTL data for the functional interpretation of epilepsy
80                   We also show that epilepsy eQTLs are enriched within epilepsy-causing genes: an epi
81                   In conclusion, an epilepsy-eQTL analysis is superior to normal hippocampal tissue e
82 re significantly more enriched with epilepsy-eQTLs than with normal hippocampal eQTLs from two larger
83  normal hippocampal eQTLs than with epilepsy-eQTLs.
84 covered with a larger blood-based expression eQTL resource.
85 DNA methylation (meQTL) and gene expression (eQTL) in 110 human hippocampal biopsies.
86 ssue Expression (GTEx) data are used to find eQTLs and eGenes.
87 s many tissues to increase power for finding eQTLs and eGenes.
88                    There was no evidence for eQTL effects for WNT4.
89 icularly Negative-Binomial-based) models for eQTL mapping.
90 thods and fits within existing pipelines for eQTL discovery.
91  we introduce a new haplotype-based test for eQTL studies that looks for haplotypic effects on expres
92                                          For eQTLs, we observed a strong correlation between sample s
93 hat aFC estimates independently derived from eQTL and allelic expression data are highly consistent,
94 n genome-wide analyses impact a single gene, eQTL that impact many genes are particularly valuable fo
95 e of RNA-Seq and performing integrative GWAS-eQTL analysis against gene, exon, and splice-junction qu
96  epilepsy-eQTLs than with normal hippocampal eQTLs from two larger independent published studies.
97 a) are more enriched with normal hippocampal eQTLs than with epilepsy-eQTLs.
98 proportion can be attributed to identifiable eQTL of large effect, typically in cis.
99         As an example, our method identifies eQTLs by leveraging methylated CpG sites in a LIM homeob
100 al adult human brains, our method identifies eQTLs that were undetected using standard tissue-by-tiss
101  same confounding factor methods to identify eQTL that replicate between matched twin pair datasets i
102 ank), which provides an easy way to identify eQTLs that are associated with the conditional quantile
103                                        iFORM/eQTL can particularly discern the role of cis-QTLs, tran
104                   This platform, named iFORM/eQTL, was assembled by forward-selection-based procedure
105 d genetic and genomic data set through iFORM/eQTL gain new discoveries on the genetic origin of gene
106 to identify and replicate a few broad impact eQTL although the overall number was small even when app
107 or confounding factors to model broad impact eQTL as non-genetic variation.
108 ower of the analysis or produce broad impact eQTL false positives, and the tendency of methods that a
109 factor methods when considering broad impact eQTL recovery from synthetic data.
110 f these results, we discuss the broad impact eQTL that have been previously reported from the analysi
111 tify variation likely caused by broad impact eQTL when constructing the sample covariance matrix used
112 able the identification of such broad impact eQTL, we introduce CONFETI: Confounding Factor Estimatio
113 cting issues when searching for broad impact eQTL: the need to account for non-genetic confounding fa
114 s for association mapping is able to improve eQTL mapping accuracy, and inferring individual and grou
115                                           In eQTL catalogs, gene expression is often strongly associa
116 tecting significant genes (called eGenes) in eQTL studies and analyzing the effect sizes of cis-SNPs
117 th gene expression levels, are identified in eQTL mapping studies.
118  of all loci with identified AH is 4%-23% in eQTLs, 35% in GWASs of high-density lipoprotein (HDL), a
119 tic variant and were primarily identified in eQTLs derived from pathophysiologically relevant tissues
120  both cis- and trans-eQTLs; (3) incorporates eQTLs identified in different tissues; and (4) uses simu
121 istinction between dependent and independent eQTLs.
122                               By integrating eQTL, Hi-C and ChIP-seq data, we show that the pleiotrop
123 ative analysis combining CKD GWAS and kidney eQTL results can identify candidate genes for CKD.
124 issing, with the sentinel SNP of the largest eQTL explaining 87% (0.052/0.060) of the variance attrib
125 s) with WGS and RNA-seq, and found that lead eQTL variants called with WGS were more likely to be cau
126                          We found that local eQTL were more frequently mapped to adjacent genes, disp
127 apping studies routinely identify many local eQTLs, the molecular mechanisms by which genetic variant
128            The genetic architecture of local eQTLs linked to the expressed genes was particularly com
129  screen a physical region for specific local eQTLs that could harbour candidate genes for phenotypic
130                Expression quantitative loci (eQTL) analysis is a vital aid for the identification and
131 ts using expression quantitative trait loci (eQTL) analysis and clinical phenotypes.
132          Expression quantitative trait loci (eQTL) analysis is a method to identify genetic variation
133    Using expression quantitative trait loci (eQTL) analysis, we found that the C7 rs6876739 CC genoty
134 ,587 cis-expression quantitative trait loci (eQTL) and 6,695 trans-eQTL associated with the 433 signi
135 ncluding expression quantitative trait loci (eQTL) and disease-associated mutations.
136  to both expression quantitative trait loci (eQTL) and genome-wide association study (GWAS) signals.
137 using an expression quantitative trait loci (eQTL) approach.
138 ependent expression quantitative trait loci (eQTL) by using linear mixed models to perform genome-wid
139 ysis and expression quantitative trait loci (eQTL) data showed that this locus contributes to MICALL2
140 and four expression quantitative trait loci (eQTL) datasets.
141 h as for expression quantitative trait loci (eQTL) detection, require perfect matching between both d
142 d 25 660 expression quantitative trait loci (eQTL) for 17 311 genes, capturing an unprecedented range
143 udies of expression quantitative trait loci (eQTL) have shown that regulatory variants play a crucial
144 udies of expression quantitative trait loci (eQTL) indicate that genetic variation frequently alters
145  such as expression quantitative trait loci (eQTL) or Hi-C genome conformation data and reports the m
146 ify 5311 expression quantitative trait loci (eQTL) regulating the expression of 4105 genes, including
147 ome-wide expression Quantitative Trait Loci (eQTL) studies in humans have provided numerous insights
148 numerous expression Quantitative Trait Loci (eQTL) studies.
149 entioned expression quantitative trait loci (eQTL) using a statistically disciplined approach that jo
150 ation of expression quantitative trait loci (eQTL), the genetic determinants of variation in gene exp
151  Mapping expression quantitative trait loci (eQTL), we identify 417 response eQTLs (reQTLs) with vary
152 rlapping expression quantitative trait loci (eQTL)-associated single nucleotide polymorphisms of mess
153 i-tissue expression quantitative trait loci (eQTL).
154 AA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are locate
155          Expression quantitative trait loci (eQTLs) across all annotated transcripts were mapped and
156 d 21,183 expression quantitative trait loci (eQTLs) and 6,768 splicing quantitative trait loci (sQTLs
157 pping of expression quantitative trait loci (eQTLs) and allele-specific expression (ASE).
158 ncluding expression quantitative trait loci (eQTLs) and DNase I sensitivity quantitative trait loci (
159  tissue, expression quantitative trait loci (eQTLs) are genetic variants associated with gene express
160          Expression quantitative trait loci (eQTLs) are genetic variants that affect gene expression.
161 ponds to expression quantitative trait loci (eQTLs) at these loci.
162 nd trans expression Quantitative Trait Loci (eQTLs) demonstrating 2 trans eQTL 'hotspots' associated
163 udies of expression quantitative trait loci (eQTLs) from a broad range of tissues by using a Mendelia
164          Expression quantitative trait loci (eQTLs) help to explain the regulatory mechanisms underly
165 of known expression quantitative trait loci (eQTLs) impact expression of local genes (cis-eQTLs).
166 pped cis expression quantitative trait loci (eQTLs) in 13 tissues via joint analysis of SVs, single-n
167 talog of expression quantitative trait loci (eQTLs) in a nonhuman primate model.
168 files to expression quantitative trait loci (eQTLs) in a wide range of human tissues/cell types, we i
169 coded by expression quantitative trait loci (eQTLs) is a key to construct the genotype-phenotype map
170 k across expression quantitative trait loci (eQTLs) of a gene and use this approach to identify asthm
171 lysis of expression Quantitative Trait Loci (eQTLs) provides modest support for altered regulation of
172 pping of expression quantitative trait loci (eQTLs) revealed that genetic factors had a stronger effe
173 e to map expression quantitative trait loci (eQTLs) that affect the expression of individual genes.
174 or these expression quantitative trait loci (eQTLs) that disrupt transcription factor binding and val
175 pping of expression quantitative trait loci (eQTLs) with WGS and RNA-seq, and found that lead eQTL va
176 ne, i.e. expression quantitative trait loci (eQTLs), can help us understand how genetic variants infl
177          Expression quantitative trait loci (eQTLs), genetic variants associated with gene expression
178 known as expression quantitative trait loci (eQTLs), may improve understanding of the functional role
179 ks using expression quantitative trait loci (eQTLs), methylation quantitative trait loci (meQTLs), ch
180 s act as expression quantitative trait loci (eQTLs), suggesting that modulation of transcript abundan
181 iched in expression quantitative trait loci (eQTLs), thus suggesting that most risk variants alter ge
182 ing many expression quantitative trait loci (eQTLs).
183 f 20 206 expression quantitative trait loci (eQTLs).
184  such as expression quantitative trait loci (eQTLs).
185 apped as expression quantitative trait loci (eQTLs); however, a major limitation of eQTLs is their lo
186 rformed expression quantitative trait locus (eQTL) analyses by using abdominal subcutaneous adipose t
187   Using expression quantitative trait locus (eQTL) analyses, we constructed bipartite networks in whi
188    Gene expression quantitative trait locus (eQTL) analysis in 1,425 normal lung tissue samples highl
189         Expression quantitative trait locus (eQTL) analysis in multiple cell types of the melanocytic
190         Expression quantitative trait locus (eQTL) analysis showed suggestive eQTL signals at rs14466
191 WAS and expression quantitative trait locus (eQTL) data with RNA-seq data from the RISK study, an inc
192 4 as an expression quantitative trait locus (eQTL) for IFITM3, with the risk allele associated with l
193 -acting expression quantitative trait locus (eQTL).
194 for whole blood, which can be used to lookup eQTLs more accurately than in standard unconditional who
195                           We identified many eQTL genes (eGenes) not observed in the comparably sized
196                                         Many eQTLs operate in a tissue- and condition-specific manner
197 ts of post-transcriptional events in mapping eQTL.
198  of DNA (in this case, CpG sites) on mapping eQTLs.
199                                   While most eQTL studies focus on identifying mean effects on gene e
200                    In recent years, multiple eQTL (expression quantitative trait loci) catalogs have
201                           Detecting multiple eQTLs simultaneously in a population based on paired DNA
202 nts the existing methods, and identifies new eQTLs with heterogeneous effects across different quanti
203 the expression of 4105 genes, including nine eQTLs regulating genes associated with flavonoid biosynt
204 E scores discriminate cis-eQTL SNVs from non-eQTL SNVs in the training set with a cross-validated are
205 x populations of different ancestry from non-eQTL SNVs with an AUC of 0.939.
206  approach for investigating novel aspects of eQTL data sets.
207 ntify technical and biological correlates of eQTL effect size.
208                            Our dissection of eQTL effects may be used to distinguish genes whose asso
209                        While the majority of eQTL identified in genome-wide analyses impact a single
210 formation available to maximize the power of eQTL mapping.
211 estimated that SVs are causal at 3.5-6.8% of eQTLs-a substantially higher fraction than prior estimat
212 loci (eQTLs); however, a major limitation of eQTLs is their low resolution, which precludes investiga
213 tial to discover a more comprehensive set of eQTLs and illuminate the underlying molecular consequenc
214 t that determines the nature and strength of eQTLs may help identify cell types relevant to pathophys
215 ative individual peaks for networks based on eQTL, mQTL or pQTL information.
216 that most haplotypes associated with GWAS or eQTL phenotypes are located outside of DNase-seq footpri
217 own as expression quantitative trait loci or eQTLs) is important in unravelling the genetic basis of
218 ore enriched in GWAS associations than other eQTLs.
219               We illustrate the value of our eQTL database in the context of a recent GWAS meta-analy
220 at rs715212 may influence AREG expression (P eQTL = 0.035), although further functional studies are n
221  attributed to the presence of 'third-party' eQTLs that influence the gene expression mean in a fract
222 eated with interferon (IFN)-beta and perform eQTL analysis on 23 pooled samples.
223 clinical strains-which allowed us to perform eQTL mapping with 50-fold higher resolution than previou
224                                 We performed eQTL analysis by correlating genotype with RNA-seq-based
225                    Furthermore, we performed eQTL and co-expression analyses in lung tissue.
226   Finally, our results suggest the placental eQTLs may mediate the function of GWAS loci on postnatal
227 nstrate it by analyzing the cross-population eQTL data from the GEUVADIS project and the multi-tissue
228 dentified ceruloplasmin (Cp) as a positional eQTL in macrophages but not in serum.
229      The small sample sizes of some previous eQTL studies have limited their statistical power.
230  cis- and/or trans-eQTLs across 16 published eQTL studies.
231  SMR analyses performed with expression QTL (eQTL) data.
232 ntegration with genome-wide expression QTLs (eQTLs) from the same BC population identified ceruloplas
233 antification type to detect disease relevant eQTLs and eGenes.
234 iological inferences based on these reported eQTL.
235 lts demonstrate the power of high-resolution eQTL mapping in understanding the molecular mechanisms o
236 stimuli and provide a time-resolved response eQTL map.
237  trait loci (eQTL), we identify 417 response eQTLs (reQTLs) with varying effects between conditions.
238                               These response eQTLs were enriched in disease-associated variants, part
239                         Although large-scale eQTL mapping studies routinely identify many local eQTLs
240 S SNPs, 48% are identified to be significant eQTLs in our study.
241 sible loci and identify a set of significant eQTLs modulating differentiation and function of gene ex
242 atalog contains more genome-wide significant eQTLs per sample than comparable human resources and ide
243 s) at any genomic loci, including GWAS SNPs, eQTLs and cis-regulatory elements, facilitating the unde
244 ative trait loci (cis-eQTLs) and/or splicing eQTLs.
245 ing applications of transcriptomics to study eQTLs, B and T cell repertoire diversity, and isoform us
246 actor analysis methods when identifying such eQTL.
247 rait locus (eQTL) analysis showed suggestive eQTL signals at rs1446669, rs699664 and rs1078004 for CA
248                   Our results reveal that TE-eQTL are involved in population-specific gene regulation
249  also more likely to be tissue specific than eQTLs identified by linear regression.
250 lated cardiomyopathy phenotype we found that eQTL variants are also enriched for dilated cardiomyopat
251 relevance of these genes is supported by the eQTL analyses and co-expression of PTTG1lP with vimentin
252 pecific transcription factors binding to the eQTL SNPs.
253                                          The eQTLs are predominantly under negative selection, partic
254                                          The eQTLs that regulate the expression levels of Egfr betwee
255                    Notably, we show that the eQTLs identified by QRank but missed by linear regressio
256           We show, in 13 tissues, that these eQTL networks are organized into dense, highly modular c
257                                Many of these eQTLs were found to influence the expression of several
258 nd computational analyses revealed that this eQTL is linked to an unannotated alternate MFN2 start si
259 sis is superior to normal hippocampal tissue eQTL analyses for identifying the variants and genes und
260 ng standard tissue-by-tissue or joint tissue eQTL mapping techniques.
261 om the GEUVADIS project and the multi-tissue eQTL data from the GTEx project.
262                         Current multi-tissue eQTL mapping techniques are limited to only exploiting g
263                                  Traditional eQTL mapping is to associate one transcript with a singl
264 ive Trait Loci (eQTLs) demonstrating 2 trans eQTL 'hotspots' associated with expression of hundreds o
265 polyTE loci correspond to both cis and trans eQTL, and their regulatory effects are directly related
266          In addition, we identified 13 trans-eQTL hotspots, affecting from ten to hundreds of genes,
267 antitative trait loci (eQTL) and 6,695 trans-eQTL associated with the 433 significant insulin-associa
268               Of note, we identified a trans-eQTL (rs592423), where the A allele was associated with
269  analyses identified both cis-eQTL and trans-eQTL impacting individual genes, and CONFETI had better
270  the observed patterns of cis-hubs and trans-eQTL regulation across tissue types.
271  attributed to all identified cis- and trans-eQTL.
272                                   Four trans-eQTL hotspots coincided with GLS disease QTLs mapped in
273 tion testing suggested that for 35% of trans-eQTL-trans-eGene pairs in different chromosomes and 90%
274 n and between populations and a strong trans-eQTL hotspot at TLR1 that decreases expression of pro-in
275                                  These trans-eQTL signals confirmed and extended the previously repor
276         We discovered 3218 cis- and 35 trans-eQTLs at </=10% false discovery rate in human placentas.
277                    We identified 2,350 trans-eQTLs (at p < 10(-7)); more than 80% of them were found
278 tatistics; (2) considers both cis- and trans-eQTLs; (3) incorporates eQTLs identified in different ti
279                             One common trans-eQTLs mechanism is "mediation" by a local (cis) transcri
280 articular, how genetic variants (i.e., trans-eQTLs) affect expression of remote genes (i.e., trans-eG
281 of genetic variation on distant genes (trans-eQTLs) and understand their biological mechanisms.
282 s-eQTLs and over 6000 independent lead trans-eQTLs, targeting over 10,000 gene targets (eGenes), with
283 ultaneously and found that hundreds of trans-eQTLs each affect hundreds of transcripts in lymphoblast
284 ranscripts of a high-confidence set of trans-eQTLs encode proteins that interact more frequently than
285 tify 59 distinct blocks or clusters of trans-eQTLs, each targeting the expression of sets of six to 2
286 ranscripts that are "cis-mediators" of trans-eQTLs, including those "cis-hubs" involved in regulation
287 es that were found to have cis- and/or trans-eQTLs across 16 published eQTL studies.
288 cting local, cis-eQTLs is now routine, trans-eQTLs, which are distant from the genes of origin, are f
289                                   Some trans-eQTLs point toward novel mechanistic explanations for th
290              We hypothesized that some trans-eQTLs regulate expression of distant genes by altering t
291                                  These trans-eQTLs target the same genes across the three populations
292 gests biological mechanisms underlying trans-eQTLs, both of which are relevant for understanding susc
293 498 genes) was enriched for genes with trans-eQTLs in hotspots coinciding with GLS resistance QTLs on
294 Y-s module was enriched for genes with trans-eQTLs in hotspots on chromosomes 9 and 10, which also co
295 Ex and show that in nearly all cases the two eQTLs act independently in regulating gene expression.
296  We generalize aFC to analyze genes with two eQTLs in GTEx and show that in nearly all cases the two
297                                        Using eQTLs from three major immune subpopulations, we found s
298 tions, several studies investigated variance eQTLs.
299              These enriched loci, along with eQTL associations, were unexpectedly present in non-neur
300 ther combined DXME gene expression data with eQTL data from the GTEx project and with allele frequenc

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