ライフサイエンスコーパス: genetic model

1 this tradeoff using a stochastic population-genetic model.

2 genic contaminants of food, and an important genetic model.

3 oms by logistic regression using an additive genetic model.

4 in a sample with 97% power for the additive genetic model.

5 toward the establishment of a tractable fern genetic model.

6 ion procedure is employed to help choose the genetic model.

7 the incidence of neural tube defects in some genetic models.

8 epithelial barrier has not been addressed in genetic models.

9 rphism and oral cancer susceptibility in all genetic models.

10 lack the flexibility of incorporating other genetic models.

11 enomic data under non-equilibrium population genetic models.

12 atasets simulated under classical population genetic models.

13 ve been evaluated mostly for linear additive genetic models.

14 e exact p-value for each SNP using different genetic models.

15 in the Finnish population across a range of genetic models.

16 pically test each of the SNPs using multiple genetic models.

17 a outcomes using both additive and recessive genetic models.

18 reatitis, have been investigated using novel genetic models.

19 complexity in channel types and scarcity of genetic models.

20 edical research as an activator of inducible genetic models.

21 gnificantly associated with GD in all of the genetic models.

22 d distributions, time series, and population genetics models.

23 e conidiation signaling was conserved in the genetic model A. nidulans and mediated by NapA, a homolo

24 n rs1061170 and ocular sarcoidosis in 2 of 3 genetic models (additive, P = .0078; recessive, P = .001

25 n using logistic regression with an additive genetic model adjusting for age, gender, average intraoc

26 An array of genetic models allows analysis of integrated receptor fu

27 ustness against variations in the underlying genetic model and expression trait distribution, but tes

28 ole of HuR in intestinal homeostasis using a genetic model and further defined its target mRNAs.

29 In this study, using a population genetic model and the chicken transcriptome, we assess w

30 ular plant Arabidopsis thaliana is a central genetic model and universal reference organism in plant

31 Finally, we discuss general concepts in genetic modeling and the current state-of-the-art techno

32 Here, using murine genetic models and cell ablation strategies, we have dem

33 ative contributions of STAT1 and STAT3 using genetic models and chromatin immunoprecipitation-sequenc

34 utilizing a range of multilocus quantitative genetic models and gene frequency distributions, focusin

35 Furthermore, through the use of genetic models and inhibitors, we have found that select

36 to build upon the combination of population genetic models and molecular biological knowledge.

37 al framework for the development of faithful genetic models and new therapeutic approaches.

38 ion of these fat cells and critically review genetic models and other experimental tools currently av

39 cannot be explained by classical population genetics models and is irreconcilable with the current v

40 election (GWS) involves reliable statistical genetics models and methods.

41 interval [CI] = 1.02-1.42) under a dominant genetic model, and this risk was more evident in subgrou

42 vely according to mathematically intractable genetic models, and to assist the validation, statistica

43 pressure, and that explicitly (quantitative) genetic models are able to provide us with an understand

44 Simple population genetic models are not sufficient to explain the high le

45 -cycle-specific gene-silencing system in the genetic model Aspergillus nidulans.

46 also be adapted to the growing repertoire of genetic models available in the mouse, and it provides a

47 selective pharmacological tool compounds and genetic models available to study these receptors, and p

48 at the molecular level and applying improved genetic models based on Deltaku80 Toxoplasma strains wil

49 eports on this topic are common for additive genetic models but not for additive-dominance models.

50 m the three tests corresponding to the three genetic models, but such an approach inherently leads to

51 hus, even specific partial failures of mouse genetic modeling can be instructive to human tumor biolo

52 If the genetic model, defined according to the mode of inherita

53 A genetic model depicting regulation of conidiation in A.

54 neralize to all non-EA populations assessed, genetic models derived from GWAS findings in EA may gene

55 to the same genome (recipient or donor) and genetic model (dominant, recessive, or allelic) reported

56 In conditional genetic models, enforced expression of a LIN28-resistant

57 Furthermore, current quantitative genetic models fail to fully capture the heritable varia

58 A genetic model for ALS was developed to determine whether

59 We update the two-class risk genetic model for autism, especially in regard to childr

60 ge, sugar, and lignocellulosic biomass and a genetic model for C4 grasses due to its relatively small

61 potentially using the Hungarian Vizsla as a genetic model for comparative studies with human myositi

62 The fly's power as a genetic model for disease and neuroscience can be augmen

63 ral cases and provide a two-locus population genetic model for each.

64 r support for investigations of 22q11DS as a genetic model for elucidating neurobiological mechanisms

65 to the human disease, it provides a valuable genetic model for elucidating the pathogenic mechanism o

66 Zea mays is an important genetic model for elucidating transcriptional networks.

67 miR-431 transgenic mice are a unique genetic model for investigating the cellular features an

68 e procedure to handle the uncertainty of the genetic model for non-normal quantitative trait genetic

69 cidosis of dRTA patients, they provide a new genetic model for nonsyndromic deafness with enlarged ve

70 The established genetic model for Primula heterostyly involves a diallel

71 light-induced photoreceptor injury and for a genetic model for RP.

72 r results highlight C. elegans as a powerful genetic model for studying the effects of biogenic and s

73 Nras(LSL-G12D); Cbfb(56M) mice as a valuable genetic model for the study of inversion(16) AML-targete

74 We develop a spatially explicit population genetic model for these clines based on the known geneti

75 melanogaster, has been used for decades as a genetic model for unraveling mechanisms of development a

76 centres in India, we built population-based genetic models for 14 Indian regions to model Indian reg

77 ood-unit registry, we built population-based genetic models for 21 U.S. racial and ethnic groups to p

78 Furthermore, studies in genetic models for adenosine receptors implicated the A2

79 We review these developments in light of genetic models for ASDs.

80 l provide opportunities to better understand genetic models for diseases and molecular mechanisms of

81 the genetic features of seed characters, two genetic models for mapping quantitative trait loci (QTLs

82 dormancy and the applicability of the novel genetic models for reversible metastatic PDAC to elucida

83 Genetic models for studying localized cell suicide that

84 Through bivariate genetic modeling, genetic and environmental influences o

85 Inclusion of cytoplasmic variation into the genetic model greatly increased the explained phenotypic

86 SSO) for estimating the sparse oversaturated genetic model greatly reduces the computational costs of

87 Under a variety of genetic models, gTDT showed increased power compared wit

88 Lack of a suitable genetic model has impaired further translational researc

89 ty of pharmacological tools as well as mouse genetic models has revealed several physiological action

90 Earlier studies that used a mouse genetic model have shown that a deletion of laminin alph

91 However, we also emphasize that primate genetic models have great potential to address many fund

92 lar disease (CVD) at baseline using additive genetic models (hazard ratio 1.17 [95% CI 1.01-1.36]; P

93 In genotoxic and genetic models, HCCs arose exclusively from hepatocytes

94 Using the Drosophila visual system as a genetic model, here we show that a multicellular glial n

95 We assumed an additive genetic model in an association analysis of imputed 2.5

96 In this study, we took advantage of a genetic model in which LyC6(-) circulating monocyte deve

97 Here, we have developed a genetic model in which neurons of the dorsal medial habe

98 Such links have benefited from genetic modeling in the mouse, and in this review we hig

99 gard to fitness and that standard population genetic models in fact well predict observed levels of b

100 ptake of miRNAs in newborn mice, we employed genetic models in which newborn miR-375 and miR-200c/141

101 ith exceptional longevity, under a recessive genetic model, in 3 independent populations.

102 In females, the best genetic model included substantial effects of direct add

103 the hypothesis that a combined clinical and genetic model incorporating atrial fibrillation risk SNP

104 Consistent with data, population genetics models incorporating the trade-offs successfull

105 Recent mouse genetic models indicate that chromosomal breakage is com

106 Results from a bivariate genetic model indicated that genetic factors explain a s

107 the pedigree information from the Mendelian genetic model into variant calling.

108 Using a genetic model involving constitutive activation of Hh pa

109 However, in practice, the genetic model is often unknown beforehand.

110 e, is known, the NPT derived under the given genetic model is optimal.

111 When the underlying genetic model is unknown, a robust test is preferred to

112 mputing the likelihood of complex population genetic models is often infeasible.

113 assuming an additive, dominant, or recessive genetic model, is commonly performed.

114 his outcome has been proven for a variety of genetic models, it has not been proven in general for mu

115 n of the optic vesicle, but due to a lack of genetic models, its role in mammalian retinal developmen

116 Using a compelling array of genetic models, Kim et al. report in this issue of the J

117 minority and did not change post-stress in 2 genetic models lacking either Spi-C or VCAM-1 with impai

118 olution through time-dependent analysis, the genetic model maintained its prognostic relevance at any

119 In particular, the use of non-additive genetic models may uncover new information about the gen

120 Together, this work provides a genetic model of a fracture nonunion and demonstrates th

121 es obtained from BS/Orl mice, which is a new genetic model of absence epilepsy.

122 thalamic astrocytes from a well-established genetic model of absence seizures, the genetic absence e

123 Here we use a simple genetic model of Alexander disease, a progressive and se

124 igh Drinking in the Dark (HDID-1) mice are a genetic model of AUD risk that have been selectively bre

125 uscle-specific Pgc-1alpha transgenic mice, a genetic model of augmented mitochondrial biogenesis.

126 tion effects are important components of the genetic model of body composition traits.

127 We examined the genetic model of brd2 lo mice, a BET protein hypomorph,

128 s using transgenic (Tg)Notch3(R169C) mice, a genetic model of CADASIL, revealed functional defects in

129 Using a genetic model of cardiomyocyte ablation, we demonstrated

130 Importantly, when crossbred into a mouse genetic model of CHF (alpha-myosin heavy chain-calseques

131 lly restore SPINK1 function, present a novel genetic model of chronic pancreatitis.

132 Drosophila border cells represent a genetic model of collective migration within a cell-dens

133 The present study used a genetic model of CRF overexpression to test the hypothes

134 ke social deficits in a well-validated mouse genetic model of Dravet syndrome (DS), a severe childhoo

135 e (Mn) export using flatiron (ffe/+) mice, a genetic model of Fpn deficiency.

136 etic mapping were used to analyze the murine genetic model of HIT.

137 ted sodium channels, is widely regarded as a genetic model of human pain.

138 utionary model for aging with a quantitative genetic model of indirect genetic effects.

139 We pharmacologically activated SERCA2b in a genetic model of insulin resistance and type 2 diabetes

140 blocked spontaneous seizures in R6/2 mice, a genetic model of juvenile Huntington's disease known to

141 Here, we develop a population genetic model of malaria including these variations, and

142 ch responses and extend these results into a genetic model of MMP7 deficiency and gastric cancer.

143 PI3Kgamma ablation in db/db diabetic mice, a genetic model of obesity-driven beta-cell failure and di

144 ntrols in the diet-induced compared with the genetic model of obesity.

145 ased FPN and increased TFR1 is observed in a genetic model of ovarian cancer tumor-initiating cells (

146 We used a genetic model of PAH, the Bmpr2 mutant mouse, to study t

147 an tumor xenografts, syngeneic tumors, and a genetic model of pancreatic cancer.

148 In a genetic model of pancreatic carcinoma, vaccination with

149 We recently showed in a genetic model of pancreatic ductal adenocarcinoma that p

150 MitoPark mice are a recently developed genetic model of PD that lacks the gene for mitochondria

151 The MitoPark mouse is a genetic model of PD that mimics many of the key characte

152 In a rat genetic model of PD, PLK2 overexpression reduces intrane

153 productive variance, we present a population-genetic model of phenotypic evolution in a dioecious pop

154 Previously, we have generated a genetic model of PKD using human pluripotent stem cells

155 Our results establish a genetic model of primary dystonia that is overtly sympto

156 n alterations to cSCC development by using a genetic model of RDEB and organotypic skin cultures.

157 rigin of epileptiform activity in a targeted genetic model of SBH in rats.

158 Our analysis is based on a quantitative genetic model of sexual conflict, in which genes control

159 In a genetic model of spontaneous CKD, therapeutic delivery o

160 ulin dysfunction on tau phosphorylation in a genetic model of spontaneous type 1 diabetes: the nonobe

161 Here we present a genetic model of spontaneous, early-onset metabolic synd

162 cular phenotype akin to a channelopathy in a genetic model of SVD.

163 Fruit flies are a far cry from the quaint genetic model of the past, but rather, continue to evolv

164 sion changes in the retinas of Akita mice, a genetic model of type 1 diabetes, and investigated the p

165 ted mutagenesis can be an effective tool for genetic modeling of human disease in nonhuman primates.

166 during other conditions, similar to multiple genetic models of 5-HT system dysfunction in mice.

167 behavioral measures of neural dysfunction in genetic models of Alzheimer's disease.

168 Using multiple genetic models of breast cancer, we demonstrated that en

169 tation into immunodeficient mice to generate genetic models of clonal hematopoiesis and neoplasia.

170 litis and adenomatous polyps in chemical and genetic models of colon carcinogenesis.

171 ein hyperacetylation, previously observed in genetic models of defective mitochondrial function, also

172 breeding load in small populations, assuming genetic models of deleterious mutations which account fo

173 ted, and reversed established nephropathy in genetic models of diabetes.

174 We show how to embed quantitative genetic models of inheritance of labile traits into age-

175 lecular imaging probe in both orthotopic and genetic models of MB.

176 neuron (MN) survival following trauma and in genetic models of MN disease.

177 not been proven in general for multiallelic genetic models of mutation, migration, and recombination

178 posed animals to cyst development, either in genetic models of polycystin-1/2 reduction or in respons

179 Our methodology combines quantitative genetic models of social interactions with stochastic pr

180 cy on rodent neurons using pharmacologic and genetic models of the disease.

181 ly with regard to including recombination in genetic models of the divergence process.

182 (Biston betularia), the classical ecological genetics model of industrial melanism, aimed both at loc

183 genetic variation, using a simple population genetics model of mutational effects on fitness componen

184 + IA or proven/probable IA using a different genetic model or time to IA (3 months vs 2 years) compar

185 Activating or suppressing Hh signaling, with genetic models or pharmacological agents used in cancer

186 Here, we utilize the genetic model organism Caenorhabditis elegans to elucida

187 of asexual nematodes closely related to the genetic model organism Caenorhabditis elegans.

188 rom larvae of the very small but widely used genetic model organism Drosophila.

189 nsory feedback shapes active locomotion in a genetic model organism exhibiting simple locomotion-the

190 ruses, Aedes aegypti has a long history as a genetic model organism for other bloodfeeding mosquitoes

191 More complex mammalian brains and genetic model organisms including zebrafish have been st

192 ished in the early 1900s as one of the first genetic model organisms owing to its short generation ti

193 Recent studies from two genetic model organisms, Caenorhabditis elegans and Dros

194 ditional gene silencing is possible in other genetic model organisms, this technology is largely unav

195 Despite recent advances in human genetics, model organisms are indispensable for human di

196 Several quantitative genetics models predict that species escaping extinction

197 ls rise during obesity, recent studies using genetic models provide conflicting evidence as to whethe

198 hat vitamin B12 (B12) deficiency in a murine genetic model results in severe postweaning growth retar

199 Multivariate genetic modeling revealed that global FA contributed ind

200 Quantitative genetic models revealed significant additive genetic var

201 Univariate quantitative genetic models revealed that all phenotypes (schizophren

202 erformed under the assumption of an additive genetic model, revealed several imputed SNPs (eg, rs1152

203 terization of a LMBR1/LIMR-type protein in a genetic model reveals an important role in modulating BM

204 Under the quantitative genetic model, sampling from the high extreme of the dis

205 Using a genetic model, sequence variant data can be generated ei

206 Population genetic models show that senescence for these maternal e

207 A mathematical population-genetics model showed how tolerance boosts the chances f

208 Different strains of one genetic model species after another are turning out to h

209 ) that is flexible to encompass a variety of genetic models such as additive, dominant and compound h

210 Other genetic models such as recessive, dominant, or overdomin

211 nomalies in relation to classical population genetic models such as the Wright-Fisher model and the K

212 xpectation derived from a neutral population genetic model suggests that the lineage was copying unti

213 Population genetic modeling suggests that at least some of these in

214 gether, the results from our study in murine genetic models support the notion that infection may rep

215 maging at the cellular level in roots of the genetic model system Arabidopsis (Arabidopsis thaliana).

216 ing GPCR-mediated behaviors, we utilized the genetic model system Caenorhabditis elegans Our studies

217 er as an inexpensive, flexible, and powerful genetic model system for NIHL.

218 t of Fanconi Anemia (FA) signaling, a unique genetic model system for studying human aging or cancer,

219 review the recent history of zebrafish as a genetic model system for understanding how and why tissu

220 Here, we exploit a genetic model system to establish a mechanistic link bet

221 network collapse, validating Drosophila as a genetic model system to investigate keratin dynamics.

222 ng so, FA provides researchers with a unique genetic model system to study cancer etiology.

223 ly, we claim that Drosophila, an established genetic model system, can be well utilized for further u

224 butterflies and unlock their potential as a genetic model system.

225 r bedding plant that has a long history as a genetic model system.

226 hototaxis using Drosophila melanogaster as a genetic model system.

227 Using static and inducible genetic model systems and chromatin studies, we develope

228 Work on genetic model systems such as Drosophila and mouse has s

229 s been the limited availability of effective genetic model systems that could be used to identify the

230 one of the best-understood and most powerful genetic model systems.

231 We developed a murine genetic model that allows for inducible and reversible V

232 Furthermore, a polygenic genetic model that explains adaptation to contrasting be

233 The zebrafish is a powerful genetic model that has only recently been used to dissec

234 etic property associated with the orthogonal genetic model that the additive and additive by additive

235 and population genetics can be reconciled by genetic models that include the complexities of social s

236 cological ERK/MAPK inhibitors and the use of genetic models that only partially reduce total ERK/MAPK

237 We analyze a population genetics model that incorporates purifying selection, re

238 Using a dominant genetic model, the 4q25 SNP, rs2200733, predicted a 1.4-

239 Combining two tractable genetic models, the bacterium E. coli and the nematode C

240 ur distinct implementations of the Mendelian genetic model: the Bayesian network algorithm, a graphic

241 ls and present Dictyostelium as a convenient genetic model to characterize these pathways.

242 Even though addition of this limited genetic model to COMPASS did not improve prediction of p

243 Here, we present a genetic model to differentiate the roles of these two fu

244 stem cells, we developed a Keratin 15-driven genetic model to directly perturb molecular signaling in

245 are specifically impaired, and utilized this genetic model to directly test the role of glutamatergic

246 and that flatiron mice provide an excellent genetic model to explore the role of this exporter in Mn

247 after laser injury: i) by using an inducible genetic model to inhibit specifically proliferating PDGF

248 Using a genetic model to rapidly inhibit Zap70 catalytic activit

249 Our approach uses a population genetic model to relate effective migration rates to exp

250 anogaster egg-laying site selection offers a genetic model to study a simple form of value-based deci

251 We develop an individual-based, eco-genetic model to study how mating systems and fitness tr

252 hus, Nedd4-2 heterozygous mice provide a new genetic model to study inflammatory pain.

253 enorhabdus nematophila, and is emerging as a genetic model to study symbiosis and pathogenesis.

254 therefore, represents an excellent molecular-genetic model to study the biosynthesis and modification

255 or pronephros, is a simplified yet conserved genetic model to study this renal development process be

256 endelian disorders, and we use probabilistic genetic modeling to demonstrate that Mendelian variants

257 Finally, we use population genetic modeling to show that the relative contributions

258 We used two complementary genetic models to address this important biological ques

259 n now present the opportunity to develop new genetic models to assess ILC2 immune function and to inv

260 It is hardly surprising that matching genetic models to computational constraints has limited

261 We use population genetic models to examine the ability of Fisherian sexua

262 Recent applications of population genetic models to human craniodental traits have reveale

263 suggesting potential for developing clinical-genetic models to identify patients with PD at increased

264 has made possible the generation of targeted genetic models to interrogate uniplex function in vivo.

265 ns controversial, not least because suitable genetic models to probe their function in developing org

266 Here, we use mouse genetic models to reveal a mechanism by which Sox2 coope

267 Here we used two genetic models to show that continuous transforming grow

268 We use population genetic models to show that recent human demography has

269 We previously described the development of genetic models to study the in vivo functions of the hep

270 Here we utilize multiple mouse genetic models to uncover a role for PI3KC2alpha in regu

271 a haplotype method based on the quantitative genetics model towards the utilization of functional and

272 morphocline for domesticated rice, propose a genetic model underlying complex panicle traits, and dem

273 n these empirical results and the population genetic models used to interpret them.

274 Similarly, a genetic model using Myd88/Trif-deficient mice, which lac

275 By constructing genetic models via frequentist and Bayesian association

276 An additive genetic model was applied to 2.5 million imputed SNPs fo

277 anoids propagated from primary tumors in the genetic model was further developed.

278 Quantitative genetic modeling was used to decompose the cross-disorde

279 Multivariate quantitative genetic modeling was used to estimate common genetic inf

280 Using a mouse genetic model, we also showed that the combined loss of

281 Using a double mutant genetic model, we confirm that DBC1 suppresses B cell ac

282 Importantly, using a second genetic model, we were able to attribute all altered beh

283 Using genetic models, we demonstrate that inactivation of phos

284 veloped humanized antibodies and conditional genetic models, we demonstrate that Notch1/Notch2 recept

285 Using murine genetic models, we demonstrated that GP96 is required fo

286 Specifically, using murine genetic models, we determined that SEC63 deficiency sele

287 ecific loss-of-function and gain-of-function genetic models, we determined that this in vivo toxin se

288 Here, using murine genetic models, we determined that USP28 antagonizes the

289 sed on evidence gained from studies on mouse genetic models, we have identified tyrosine phosphorylat

290 In additive genetic models, we identified nonsignificant association

291 oaches along with loss- and gain-of-function genetic models, we identified OCT4-dependent mechanisms

292 lung adenocarcinoma mouse models, including genetic models, we show that autochthonous tumors that l

293 Using gain- and loss-of-function murine genetic models, we show that beta-catenin controls ventr

294 Using several genetic models, we show that macrophage FLT1 signaling i

295 Using pharmacological and genetic models, we show that the selective loss of adren

296 T in humans is directly mirrored in a murine genetic model, where inbred mouse strains are differenti

297 d overall survival (OS) using a log-additive genetic model with adjustment for age, sex, and age-adju

298 ndii using a strategy that weds a population genetic model with field data.

299 We used additive genetic models with adjustment for sex, age, and BMI, fo

300 nt (interaction parameter = 1.54, p = 0.001) genetic models without any heterogeneity (I(2) = 0.0%);