ライフサイエンスコーパス: epistatic

1 Epistatic analyses demonstrate that Ccr7 acts downstream

2 Epistatic analyses demonstrate that Notch3 function lies

3 Moreover, epistatic analyses in vivo showed that dosage perturbati

4 gnaling is elevated in Pten cKO retinas, and epistatic analyses placed Pten downstream of TgfbetaRII

5 polymorphisms (SNPs), polygenic scores, and epistatic analyses.

6 Epistatic analysis indicates that DMAP1 acts in parallel

7 Epistatic analysis revealed a pathway in which Rho regul

8 cluster expression is controlled via complex epistatic and allelic interactions between rDNA haplotyp

9 eratively modulated Top1cc turnover in a non-epistatic and ATM kinase-independent manner.

10 TM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nucl

11 atic GSL defense genes to test the impact of epistatic and epistasis x environment interactions on ad

12 Here we examine whether epistatic and gene-by-environment interactions have shap

13 complex traits are found to be regulated by epistatic and polygenic variants.

14 sion during development, where gene-by-gene (epistatic) and gene-by-environment interactions can modi

15 ng of a combination of polygenetic, plastic, epistatic, and gene-environment interactive effects, as

16 a function of the ERAP1 context, explain the epistatic association of both molecules in ankylosing sp

17 We sought to determine independent and epistatic associations between filaggrin (FLG), serine p

18 ties and instead support an interchromosomal epistatic basis to hybrid female sterility.

19 m, the key enzyme(s) and its pleiotropic and epistatic behavior(s) responsible for low-molecular-weig

20 strong promoter, called "epistatic capture." Epistatic capture is the stabilization of a TFBS that is

21 transformed into a strong promoter, called "epistatic capture." Epistatic capture is the stabilizati

22 es, including Alzheimer's disease (AD), have epistatic causes, requiring more sophisticated analyses

23 with the polygenic score were tested for an epistatic component using a training set (n = 170), whic

24 nsidering a single final resistant genotype, epistatic contingencies among mutations restrict evoluti

25 Such a study is vital to identify epistatic couplings among residues that can provide usef

26 fitness landscape that both (i) features an epistatic distribution of fitness effects that agrees wi

27 An epistatic effect between CYP11A1 and VDR polymorphisms m

28 es, we demonstrate that D95E mutation has an epistatic effect on the motifs involved in Stl binding.

29 for kinship matrix calculations and main and epistatic-effect genome scanning employ parallel computi

30 sets showed both concordance of direction of epistatic effects (P = 5.56 x 10(-31)) and enrichment of

31 Analyses that incorporate sex-dependent and epistatic effects could reconcile past inconsistencies a

32 lts on the prediction of genetic values with epistatic effects for 280 accessions in the Nebraska Whe

33 However, estimating epistatic effects for quantitative traits is challenging

34 ng the prior knowledge on candidate SNPs for epistatic effects from biological experiments.

35 his study shows the necessity of considering epistatic effects in soybean SDS resistance breeding usi

36 loci may be considerably improved by taking epistatic effects into account.

37 of many quantitative trait loci (QTLs), the epistatic effects involving more than one QTLs, environm

38 owerful method that can handle both main and epistatic effects of a relatively large number of possib

39 l scan-revealing the individual and pairwise epistatic effects of every mutation to our model protein

40 e trait loci must consider both additive and epistatic effects of multiple candidate genotypes.

41 for robustness varied antagonistically with epistatic effects of mutations on viability and phenotyp

42 were the results of individual, additive and epistatic effects of the regulatory mutations.

43 nly 0.3% was contributed by the marginal and epistatic effects of the SNPs in the intergenic area.

44 a QTL model with a large number of main and epistatic effects on a personal computer, and outperform

45 ly cooccurring alleles at these loci display epistatic effects on herbivore resistance and fitness in

46 C, FACT, and TFIIS, resulting in synergistic/epistatic effects on plant growth/development.

47 osomes of 1, 3, 6, 8 and 10, and significant epistatic effects were found among the four pairs of ste

48 enetic architecture (additive, dominant, and epistatic effects) of potential QTLs for growth traits i

49 ion of patients would empower the search for epistatic effects, and how network and cellular models m

50 and gun1 mutations evoke similar patterns of epistatic effects.

51 ges in the magnitude and sign of fitness and epistatic effects.

52 tic effects (PEPIS), for analyzing polygenic epistatic effects.

53 gh breeding strategies based on additive and epistatic effects.

54 intly fitted all the additive, dominance and epistatic effects.

55 s geometric model is common in detecting the epistatic effects.

56 or binary traits that includes both main and epistatic effects.

57 nt analyses and genome scanning for main and epistatic effects.

58 ric functional map, allowing pleiotropic and epistatic enzymatic explanation of PAH metabolism.

59 is review discusses the current evidence for epistatic events and genetic interactions in neuropsychi

60 termining a recessive or dominant link among epistatic expression quantitative trait locus to enable

61 enotype ratio distortion represent loci with epistatic fitness effects; we conservatively estimate th

62 ells, we demonstrate that TDP1 and PARP1 are epistatic for the repair of Top1cc.

63 Based on prior data, we hypothesize that epistatic forces operate most strongly between residues

64 ty of LMW PAH-centric hydroxylation, and its epistatic functional contribution is also crucial for th

65 focal adhesion and secretion is affected by epistatic gene copy number variation and it is predictiv

66 esence of recombinational suppressors and/or epistatic gene interactions in the MAT-CEN intervening r

67 quantitative tools to make inferences about epistatic gene interactions when the fitness landscape i

68 study of functionally redundant genes and of epistatic gene interactions.

69 leneck frequently encountered in genome wide epistatic genetic effect analysis and enable accommodati

70 rver-based tool, the Pipeline for estimating EPIStatic genetic effects (PEPIS), for analyzing polygen

71 The epistatic genetic interactions observed among BEACH homo

72 ion was primarily influenced by additive and epistatic genetic variation, leaf damage was primarily i

73 Genome-wide association (GWAS) and epistatic (GWES) studies along with expression studies i

74 The dominance and epistatic hierarchies of key loci governing this diversi

75 oth local ruggedness and amino acid-specific epistatic hotspots and that inference is additionally co

76 Moreover, Tim and DDX11 are epistatic in promoting efficient resumption of stalled D

77 This epistatic influence manifested such that the cytoplasmic

78 epwise analysis failed to show a significant epistatic interaction among the variants analyzed; that

79 ting, we conducted exhaustive univariate and epistatic interaction association analyses.

80 ariants demonstrated independent effects and epistatic interaction at the locus, impacting the risk o

81 man genetic association analyses revealed an epistatic interaction between CYFIP1 and WAVE signaling

82 Epistatic interaction between FcGR polymorphisms and int

83 Our results show an epistatic interaction between IGHG1 and FCGR3A such that

84 The epistatic interaction between K33S and F427I thus may mi

85 cation and characterization of an intragenic epistatic interaction between the attenuating F427I muta

86 An epistatic interaction between the IL12RB2 risk locus at

87 Further analysis revealed an epistatic interaction between the UL and US regions.

88 t enrichment on the autosomes, supporting an epistatic interaction between the X Chromosome and autos

89 additional insights into virulence gene and epistatic interaction discovery in HSV-1.

90 Further analysis detected an epistatic interaction for neovascularization between a s

91 ases, we pairwise deplete them generating an epistatic interaction map, evaluate cell cycle perturbat

92 f spots in C. gracilis are determined by the epistatic interaction of alleles at two as yet unidentif

93 This epistatic interaction of rare and common variants define

94 This epistatic interaction together with varying frequencies

95 of sequence variants and the presence of an epistatic interaction were tested in a zebrafish model.

96 l possible combinations; and (2) how to test epistatic interaction when all potential combinations ar

97 .09; 95% CI, .01-.73), suggesting a negative epistatic interaction which contrasts previous findings.

98 e to alter phenotypic variation alone and in epistatic interaction with the nuclear genetic variation

99 well as a novel Parkinson's disease-specific epistatic interaction, all indicative of faster motor pr

100 nduced liver tumorigenesis, indicating their epistatic interaction.

101 g the functional and evolutionary effects of epistatic interactions across molecular interfaces.

102 In both scenarios, epistatic interactions affect the long-term response to

103 Epistatic interactions among genes can give rise to rugg

104 Epistasis analysis showed significant epistatic interactions among Pto-miR257 and its targets.

105 enhancing genes emphasized the importance of epistatic interactions among the targeted genes (synergi

106 integrated strains were used to characterize epistatic interactions among traits and to identify the

107 In addition, processes including epistatic interactions and compensatory evolution, cosel

108 ecent studies that have probed the extent of epistatic interactions and have begun to chart the fitne

109 nificant main effect loci and 24 significant epistatic interactions associated with SSR resistance, w

110 Our results indicate that epistatic interactions between alleles with both positiv

111 served across these systems, with a focus on epistatic interactions between beneficial mutations and

112 However, several studies have now identified epistatic interactions between common variants that incr

113 requires interactions between loci, negative epistatic interactions between divergent regulatory elem

114 inor changes in signal levels lead to strong epistatic interactions between EGF and Notch.

115 Negative epistatic interactions between genes from different pare

116 we investigate whether there is evidence for epistatic interactions between genetic variants within t

117 e patterns have locked in early (such as the epistatic interactions between groESL and a constellatio

118 Analysis of epistatic interactions between jazQ and phyB reveal that

119 sky-Muller (BDM) incompatibilities involving epistatic interactions between loci contributed to TRD a

120 ial cell modeling is a useful tool to assess epistatic interactions between multiple variants.

121 Epistatic interactions between mutant sites in the same

122 Epistatic interactions between mutations can make evolut

123 n results from the evolution of incompatible epistatic interactions between species: alleles that fun

124 We further identified 10 epistatic interactions between the vGWAS signals indepen

125 ndscapes were compared and used to calculate epistatic interactions between these mutations and the t

126 as well as provide a rationale to screen for epistatic interactions between variants in IRF6 and RTK

127 ic basis of canalization and speciation, and epistatic interactions can be used to infer genetic netw

128 Epistatic interactions can frustrate and shape evolution

129 dies showing that genotype x environment and epistatic interactions control fitness, the influences o

130 measured by fitness effects of mutations and epistatic interactions for TEM-1's original function.

131 Motivated by the problem of learning epistatic interactions from datasets developed in genome

132 Evidence of epistatic interactions has been reported in both humans

133 n the role of cis-QTLs, trans-QTLs and their epistatic interactions in gene expression.

134 quickly generated to study gain-of-function epistatic interactions in gene networks.

135 or the full-scale analysis of multiple-locus epistatic interactions in GWAS.

136 epistasis (CSE) for identifying significant epistatic interactions in population-based association s

137 ial new biology, including several plausible epistatic interactions in several diseases.

138 We observe that epistatic interactions increase rather than decrease the

139 a mouse backcross, thereby discovering novel epistatic interactions influencing phenotypes related to

140 ise association between genes, indicative of epistatic interactions involving components of the splic

141 Interpreting epistatic interactions is crucial for understanding evol

142 These results suggest that exploring epistatic interactions is valuable in uncovering the com

143 The epistatic interactions newly found by AprioriGWAS on AMD

144 landscapes due to changes in the fitness and epistatic interactions of some genotypes.

145 ndicating that plasmid-host coevolution, and epistatic interactions on fitness costs are likely to be

146 functional paralogous genes, suggesting that epistatic interactions or differential expression patter

147 ns of multiple mutations, possibly involving epistatic interactions or noncoding sequences, have been

148 Epistatic interactions play a fundamental role in molecu

149 the candidate genes and 75% of the candidate epistatic interactions tested.

150 onal residues comprise a network of strongly epistatic interactions that activate, suppress or reacti

151 Mutational analysis revealed specific epistatic interactions that explained the observed path

152 Underlying these relationships are the epistatic interactions that occur when the consequences

153 rther investigation of these loci reveals 57 epistatic interactions that replicated in a smaller data

154 ages, and is fixed in the ingroup because of epistatic interactions with derived TFBSs.

155 regularized polynomial regression to detect epistatic interactions with manageable complexity by exp

156 In addition, statistic tests for high order epistatic interactions with more than 2 SNPs propose com

157 a residue in terms of the importance of its epistatic interactions with neighbors, yielding better a

158 We used loss-of-function mutations to define epistatic interactions within the core JA signaling path

159 confounding due to population structure and epistatic interactions, are important to fully explain t

160 f SDS resistance, especially with respect to epistatic interactions, is still unclear.

161 kely than single-nucleotide variants to have epistatic interactions, reiterate the need for targeted

162 However, directional, epistatic interactions, which reflect regulatory relatio

163 pend on the viral sequence background due to epistatic interactions.

164 s to the topology of fitness landscapes with epistatic interactions.

165 R15 haplotype, or from their combinations or epistatic interactions.

166 computing to detect genome-wide multi-locus epistatic interactions.

167 ich are not shown up in detections of 2-loci epistatic interactions.

168 sed by transformed cells, due to ill-defined epistatic interactions.

169 and to directly measure fitness effects and epistatic interactions.

170 ach can effectively capture both genetic and epistatic interactions.

171 s and a tool to understand/define better the epistatic interactions.

172 iding a complementary excitability assay for epistatic interactions.

173 n of trait data, (shared) QTL positions, and epistatic interactions.

174 r regulatory models can guide the search for epistatic interactions.

175 ht be employed to further elucidate relevant epistatic interactions.

176 ent supplemented media, these results reveal epistatic intertwining of metabolism with gene expressio

177 sary for rapid adaptation, as in some highly epistatic landscapes the critical strength does not depe

178 en developed for efficient identification of epistatic loci do not systematically exploit linkage dis

179 in the order of millions), identification of epistatic loci is a statistically difficult and computat

180 Epistatic loci that are identified using data from Genom

181 These additive and epistatic loci together explained 24-52% of the phenotyp

182 enotypic manifestation of target genes in an epistatic manner.

183 Thus, detailed temporal, epistatic measurements of key TFs and VEGFA plus its rec

184 sults are consistent with the involvement of epistatic mechanisms in the manifestation of autoimmune

185 I point mutants, we generated a point mutant epistatic miniarray profile (pE-MAP) comprising approxim

186 mical level, genetic level (as assessed with epistatic miniarray profile screens), and phenotypic lev

187 model yeast Schizosaccharomyces pombe Using epistatic miniarray profiles (EMAPs) to survey the genet

188 uble mutant analysis disagreed with a simple epistatic model for HSP90 and AGO1 interaction; rather,

189 ble solution for various biological putative epistatic models in practice.

190 These data highlight the importance of epistatic models in understanding genetic association wi

191 and its targets under additive, dominant and epistatic models.

192 We show that epistatic modifiers of the cue polymorphism can evolve t

193 Permissive and restrictive epistatic mutations across the TF-RE interface opened an

194 to decipher and little has been achieved for epistatic mutations, especially at the metabolic level.

195 and other binding partners, due to a set of epistatic mutations.

196 fitness peak is reached via four positively epistatic mutations.

197 d phosphatases in S. cerevisiae we show that epistatic NEMs can point to modulators of genetic intera

198 c genetic variation was a central hub in the epistatic network controlling the plant metabolome.

199 Remarkably, this epistatic network of equivalent residues also controls c

200 Here we report the first discovery of an epistatic network of residues that controls the onset of

201 trait loci (QTL) that interact in a complex epistatic network.

202 types for multilocus genotype classes in the epistatic networks is often improved by accounting for t

203 Epistatic networks of three SNPs or more influence the e

204 Knowledge of epistatic networks will contribute to our understanding

205 y due to cultural or historical factors than epistatic or environmental constraints.

206 quate for shutting down its activity, and is epistatic over previously identified T271 autophosphoryl

207 Multi-SNP associations found 102 epistatic pairs associated with traits.

208 ul solution to map multiple QTL with complex epistatic pattern.

209 However, the fitness trajectories and epistatic patterns they predict are inconsistent with th

210 and stressed the potential importance of the epistatic pleiotropy and of the impact of host living co

211 In the third stage, new epistatic QTL are searched in pairs.

212 ond and third stages of analysis for mapping epistatic QTL can be maximized.

213 L is robust and does not bias the search for epistatic QTL due to a genetic property associated with

214 r of effects possibly including the main and epistatic QTL effects, environmental effects and the eff

215 No evidence for epistatic QTL pairs was found.

216 n impose a significant challenge for finding epistatic QTL reliably.

217 In the second stage, epistatic QTL that interact significantly with other ide

218 re are a number of difficulties for studying epistatic QTL.

219 to 42.33% phenotypic variation (PVE) and 10 epistatic QTLs (E-QTLs) up to 3.31% PVE for oil content

220 It is unknown whether such sign-epistatic recoveries are inconsequential events or an im

221 ycle and enucleation deficits are rescued by epistatic reintroduction of either of these 2 EKLF targe

222 hod has potential for detecting a meaningful epistatic relationship among the genes that influence br

223 This functional conservation of the epistatic relationship between BMP signaling and Blimp-1

224 Next, we determined the epistatic relationship between mecom and Notch signaling

225 Our findings establish an epistatic relationship between SWI/SNF chromatin remodel

226 Thus, the epistatic relationship is context dependent.

227 tory potential of SLP-2 suggest a functional epistatic relationship to Parkin and a protective role o

228 hich implicates BRCA1, PALB2 and BRCA2 in an epistatic relationship with one another.

229 eveloping computational methods for learning epistatic relationships among genetic markers.

230 chanistic effects of different mutations and epistatic relationships among loci that contribute to co

231 ding incorporating the environment, modeling epistatic relationships and using multilocus profiles.

232 etP (alr2818), asl1930, alr2902, and alr3234 Epistatic relationships between all four genes relating

233 YPOCOTYL IN FAR-RED (HFR1) proteins; and the epistatic relationships between cop1 and pif3, pif4, pif

234 We determine the epistatic relationships between the gfi factors and key

235 chanistic explanation of their dominance and epistatic relationships.

236 d cerebellar cell generation, arguing for an epistatic role of Pals1 in proliferation capacity.

237 a viral protein kinase encoded by HCMV, play epistatic roles in facilitating progression of the viral

238 cisplatin, suggesting that BER and MMR play epistatic roles in mediating cisplatin cytotoxicity.

239 CM and FAAP24 play multiple, while not fully epistatic, roles in maintaining genomic integrity.

240 demonstrating strong evidence of dispersive epistatic selection between populations.

241 omponents was originally used to investigate epistatic selection, we demonstrate that values of may a

242 tively corresponding to a selective sweep or epistatic selection.

243 We detect a complex epistatic sex system consisting of a major female hetero

244 of five SNPs with marginal effects and three epistatic SNP pairs in ARIC-three marginal SNPs were loc

245 plicated in the control of ciliogenesis, our epistatic studies suggest a more downstream function of

246 eral hemagglutinin substitutions required an epistatic substitution in the neuraminidase glycoprotein

247 miological studies suggest a polygenetic and epistatic susceptibility model involving the interaction

248 All the epistatic terms involving a particular locus appear in i

249 nositol-4-phosphate (PI-4P) phosphatase, was epistatic to agd1.

250 anthin-biosynthetic operon, crtOPQMN, but is epistatic to alternative sigma factor B.

251 Our analysis demonstrates that tmm-1 is epistatic to atgpi8-1, indicating that either TMM is a G

252 ed on the double mutant cgi-58 pxa1, PXA1 is epistatic to CGI-58 in all of these processes.

253 We report that DeltadivIVA mutations are not epistatic to DeltagpsB division-protein mutations in pro

254 ential roles in the release of seed dormancy epistatic to DOG1.

255 Jub is epistatic to EGFR and Ras for Yorkie regulation, Jub is

256 ubp7Delta mutants are epistatic to factors involved in histone maintenance and

257 d not protect, replication forks in a manner epistatic to FANCB.

258 Thus, CSF1 is epistatic to FLT1, establishing a link between FLT1 and

259 Brassinosteroid insensitive1 (BRI1) is epistatic to HXK1, as the Glc insensitive2bri1-6 double

260 another heterocyst patterning gene, patA, is epistatic to inactivation of patN, and transcription of

261 Therefore, JAK2 in adipose tissue is epistatic to liver with regard to insulin sensitivity an

262 Thus, loss of tsl is additive rather than epistatic to loss of tor.

263 Mutation of slrA was epistatic to mutation of pnpA for the motility-related p

264 ard to nucleotide selectivity, nsp14-ExoN is epistatic to nsp12-RdRp, consistent with its proposed ro

265 s acting early in a biosynthetic pathway are epistatic to other mutations that block downstream steps

266 TOR was epistatic to PKA components with respect to P-S6.

267 T KINASE A (CDKA);1 indicated that CDKA;1 is epistatic to RBR1 and controls endoreduplication through

268 RIN4 pT166 is epistatic to RIN4 pS141.

269 cholesterol, with mutations in Apoe and Ldlr epistatic to Sec24a, suggesting a receptor-mediated lipo

270 The cca1-1 lhy-20 double mutant is epistatic to sic-3, indicating the LHY and CCA1 splice v

271 n, and epistasis tests showed that baboon is epistatic to Smad2 for disc overgrowth.

272 Genetic analysis indicates that TGD4 is epistatic to TGD5 in ER-to-plastid lipid trafficking, wh

273 e proofreading activity of the nsp14-ExoN is epistatic to the function of the RdRp in fidelity.

274 , and suggest that the feminizing pathway is epistatic to the masculinizing pathway.

275 ation, which blocks disulfide formation, was epistatic to the R92A mutation.

276 r1 (P1; R2R3-MYB transcription factor) to be epistatic to the sm mutation.

277 t was established 60 y ago that tangerine is epistatic to yellow-flesh.

278 Epistatic transcriptional profiles mirrored these phenot

279 ectively neutral mutations, contributions of epistatic variance are always small.

280 As the magnitude of the epistatic variance depends critically on the heterozygos

281 determining the importance of epistasis and epistatic variance for complex traits, there is consider

282 ethods will be relevant to future studies of epistatic variance in founder populations and crosses.

283 experimental observations of low amounts of epistatic variance in outbred populations are concordant

284 bred populations, which helps in fitting the epistatic variance.

285 , focusing on the potential magnitude of the epistatic variance.

286 promising basis for network pharmacology of epistatic vulnerabilities as a promising therapeutic str

287 cally search for a comprehensive set of such epistatic vulnerabilities.

288 Both complexes are epistatic with BRCA2 and synthetically lethal with Rad52

289 dph3Delta was epistatic with dph1Delta for sensitivity to hydroxyurea

290 tably, for all traits examined, Helq was non-epistatic with Fancc, as Helq(gt)(/gt);Fancc(-)(/)(-) do

291 The effect of EGFR mutation was epistatic with FANCD2.

292 NA screen revealed that ERCC1 deficiency was epistatic with homologous recombination deficiency.

293 Strikingly, while Paxx loss is epistatic with Ku80, Lig4, and Atm deficiency, Paxx/Xlf

294 This pathway is epistatic with Rad5-mediated DNA damage bypass and disti

295 Moreover, FANCD2-mediated fork protection is epistatic with RAD51 functions, revealing an unanticipat

296 division, nod1Delta cells were elongated and epistatic with regulators of Wee1.

297 These genetic defects are epistatic with respect to each other, suggesting that th

298 suggestion we found that REV1 and FANCD2 are epistatic with respect to sensitivity to the double-stra

299 rsensitivity, and the gene encoding RNF4 was epistatic with the other genes encoding members of the F

300 This PrimPol UV lesion bypass pathway is not epistatic with the Pol eta-dependent pathway and, as a c