ライフサイエンスコーパス: modifier gene

1 occurs depends on genetic background (i.e., modifier genes).

2 ute to POAG and that WDR36 may be a glaucoma modifier gene.

3 nd, thus, it is proposed that Kif12 is a cpk modifier gene.

4 the identification of this elusive epistatic modifier gene.

5 n BRCA1 tumors and thought to harbor a BRCA1 modifier gene.

6 ntestinal tumorigenesis, but it may act as a modifier gene.

7 ostulated that it might harbor an autoimmune modifier gene.

8 at another locus, which is referred to as a modifier gene.

9 identified Anxa6, encoding annexin A6, as a modifier gene.

10 jection; therefore, NaStEP is a novel pistil-modifier gene.

11 tibility to determine whether Kitl is a TGCT modifier gene.

12 g growth factor-beta1 (TGFB1), a putative CF modifier gene.

13 ssociation study (GWAS) predicted additional modifier genes.

14 ore frequent mutations in RHOB and chromatin modifier genes.

15 ined by the underlying mutation and putative modifier genes.

16 y of SMA may be influenced by the actions of modifier genes.

17 members suggests the presence of additional modifier genes.

18 non-Mendelian inheritance patterns involving modifier genes.

19 er and chromosomal location of potential Ods modifier genes.

20 to tumor immunosurveillance is regulated by modifier genes.

21 ts the existence of trans-acting variants in modifier genes.

22 ations have revealed many possible candidate modifier genes.

23 netic background, suggesting the presence of modifier genes.

24 of strong genetic interactions between tumor modifier genes.

25 c map locations of the metastasis efficiency modifier genes.

26 titative trait that is strongly modulated by modifier genes.

27 screen using RNAi lines targeting known PEV modifier genes.

28 ential candidates for novel SCA causative or modifier genes.

29 fibrosis (CF) that is strongly influenced by modifier genes.

30 e the conflicting effect of 129SvEv-specific modifier genes.

31 of BLOC-1 function and its interactions with modifier genes.

32 e of additional causative, contributing, and modifier genes.

33 train-dependent, suggesting the influence of modifier genes.

34 arge extent by its genetic heterogeneity and modifier genes.

35 To date, two essential pistil-modifier genes, 120K and High Top-Band (HT-B), have been

36 s early as two weeks of age, suggesting that modifier genes act by influencing glomerular basement me

37 BC membrane characteristics are a target for modifier gene action.

38 It has now recognized that modifier genes affect the expression of cardiac phenotyp

39 Our results provide the first evidence of a modifier gene affecting the Tsc2 pathway in the progress

40 bred strains of mice can be used to identify modifier genes affecting the susceptibility to inherited

41 The mechanism by which modifier genes alter adenoma incidence can be readily st

42 This suggested that genetic background or modifier genes alter the clinical manifestations and pro

43 of ADR toxicity and identify Prkdc as a MDDS modifier gene and a component of the mitochondrial genom

44 ons, including potential roles for PON1 as a modifier gene and for PON1 protein as a regulator of nor

45 Because modifier genes and digenic inheritance are not always di

46 We propose testing specifically for modifier genes and protective alleles among at-risk indi

47 The mapping of these modifier genes and their eventual identification will he

48 r genetics and assess progress in studies of modifier genes and their targets in both simple and comp

49 region of the mouse genome is rich in tumor-modifier genes and this positioning of Ram1 may thus pro

50 ated opaque QPM variants to identify opaque2 modifier genes and to investigate deletion mutagenesis c

51 effect working alone or in combination with modifier genes and/or environmental factors.

52 among patients with HbSS suggests a role for modifier genes and/or environmental influences.

53 etween the causal genes, genetic background (modifier genes), and probably the environmental factors.

54 ncy will facilitate studies of pathogenesis, modifier genes, and testing of therapeutic approaches.

55 ential interactions with the environment and modifier genes, and the myriad of potential signaling pa

56 eractions among genetic etiology, background modifier genes, and/or hemodynamic factors.

57 establishes the principle that mouse cancer modifier genes are candidates for low penetrance human b

58 Mutations in chromatin modifier genes are frequently associated with neurodevel

59 We hypothesized modifier genes are partly responsible for the variation

60 Nuclear modifier genes are proposed to modify the phenotypic exp

61 t polymorphisms in some low-penetrance tumor modifier genes are reflected in the pattern of somatic a

62 mistry and genetics indicate that additional modifier genes are required.

63 The CFTR gene along with 2 or more modifier genes are the major determinants of intestinal

64 defects, modeling human HPE and implicating modifier genes as a cause of variability.

65 We attempted to map the modifier genes as quantitative trait loci (QTLs) using a

66 d suggests that it is suited for identifying modifier genes associated with Apc (Min/+) mutation, aft

67 e mutation, suggesting that Kitl is the TGCT modifier gene at the Steel locus.

68 me gene mutation has prompted the search for modifier genes at other loci, and for environmental fact

69 meiotic mutant desynaptic is a recombination modifier gene based on cytogenetic and segregation analy

70 (dy) was tested as a candidate recombination modifier gene because its effect is manifested in propha

71 elopment is regulated by products of several modifier genes, but instructions for their tumor-specifi

72 Alleles of modifier genes can either buffer perturbations on cardia

73 ated K8; and 4) higher production of the MDB-modifier gene CD73.

74 tion-based study that two previously studied modifier genes, coding for mannose-binding lectin 2 and

75 actors, either environmental or genetic (eg, modifier genes), contribute to the pathogenesis of XLP.

76 the etiology, identification of the specific modifier genes could have significant prognostic and the

77 ests that the common polymorphic variants of modifier genes could influence drug response in cardiova

78 1-null animals are influenced by one or more modifier genes, counterparts of which may play a similar

79 responses to epithelial damage, acting as a modifier gene determining the extent of the gut inflamma

80 Twin analysis suggested that modifier genes did not play a significant role because t

81 t stem cells, in silico variant modeling and modifier gene discovery, now in their earliest stages, w

82 Using a systematic approach toward modifier gene discovery, we have found five chromosome I

83 Interaction of the susceptibility genes with modifier genes, environmental factors, and conventional

84 idate for containing the first human nuclear modifier gene for a mitochondrial DNA disorder.

85 velopment and implicate Gata5 as a candidate modifier gene for congenital heart disease.

86 acid beta-galactosidase gene functions as a modifier gene for the phenotypic expression of genetic g

87 nsidering SDHx as candidate predisposing and modifier genes for CS/CSL-related malignancy risks, and

88 The individual modifier genes for HCM remain largely unknown, and a lar

89 Whole-exome sequencing identified candidate modifier genes for individuals with severe FD.

90 ro screen to triage and prioritize candidate modifier genes for more detailed future studies which is

91 causative genes of USH2, whereas PDZD7 is a modifier gene found in USH2 patients.

92 We show that while some modifier genes function similarly in SCA1 and HD Drosoph

93 led a second SJL-derived, GC tumor frequency modifier gene, Gct6, located 6.5 cM distal to Gct4 on Ch

94 ploring the role of genetics/genomics (e.g., modifier genes, gene-environmental interactions, and epi

95 omal loci: the melanosomal gene, SILV, and a modifier gene, harlequin (H), previously localized to ch

96 apeutic interventions aimed at targeting the modifier genes have shown salutary effects in animal mod

97 Three SUMO (small ubiquitin-related modifier) genes have been identified in humans, which ta

98 explaining dominance that renders Fisher's 'modifier genes' hypothesis otiose.

99 uable for quantitative trait locus (QTL) and modifier gene identification.

100 Modifier genes identified in our screen connect Ppt1 fun

101 tory increase in the expression of chromatin modifier genes implicated in X silencing is observed.

102 osphate kinase that has been implicated as a modifier gene in cystic fibrosis.

103 teracted by ADPRH, which could function as a modifier gene in disease.

104 Coincident mapping of a modifier gene in multiple experimental crosses using dif

105 cy, and the alpha1-ATZ mutation may act as a modifier gene in patients with concurrent cholestatic li

106 hlight the potential of Ras to function as a modifier gene in repressing mammary carcinogenesis.

107 es, and the KCC1 gene has been proposed as a modifier gene in sickle cell disease.

108 n some Heinz body hemolytic anemias and as a modifier gene in the beta-thalassemia syndromes.

109 a gene previously identified as a candidate modifier gene in the cpk mouse model of polycystic kidne

110 Studies of modifier genes in cystic fibrosis (CF) have often been p

111 ed pivotal roles in the expansion of histone modifier genes in F. vesca.

112 of additional potential histone acetylation modifier genes in human disease, we identified six histo

113 e conspired to focus interest on the role of modifier genes in humans.

114 We have mapped tumor-modifier genes in intraspecific crosses between transgen

115 Our results indicate that one or more modifier genes in Mh control the extent to which in vivo

116 ariation and that these hub genes may act as modifier genes in multiple, mechanistically unrelated ge

117 y interacting epigenetically with other TGCT modifier genes in previous generations.

118 addition, they demonstrate the importance of modifier genes in vertebrate axonal guidance.

119 Several potential modifier genes including genes encoding the components o

120 tients with GKD indicates the involvement of modifier genes, including other network partners.

121 and siblings (P = 1 x 10(-5)), showing that modifier genes independent of CFTR contribute substantia

122 We investigated the extent to which modifier genes influence nutrition in children with CF.

123 and class II modifiers enhance PEV when the modifier gene is present in fewer than two doses.

124 One potential modifier gene is represented by ZPR1, which is down-regu

125 eneous population, the predominant effect of modifier genes is health.

126 y and the role of environmental triggers and modifier genes is still not clear.

127 Linkage analysis identified potential modifier-gene loci.

128 Fine-mapping of this mutated modifier gene (M-locus) and the synteny analysis of the

129 This suggests that the MTO1-like modifier gene may influence the phenotypic expression of

130 This suggests that an MSS1-like modifier gene may influence the phenotypic expression of

131 ation of the disease phenotype by background modifier genes may be dependent upon the particular dise

132 w potential therapeutic targets, since these modifier genes may be more amenable to treatment than th

133 therefore expected that some of these prion-modifier genes may be of wider relevance in neurodegener

134 ndicating that environmental triggers and/or modifier genes may contribute to the disease.

135 Identification of these modifier genes may define the biological pathways that l

136 Human homologues of mouse cancer modifier genes may play a role in cancer risk and progno

137 "Psychosis-modifier genes" may act in the setting of neurodegenerat

138 We hypothesized that the modifier genes might be located in regions of allelic im

139 Although currently unidentified modifier genes might explain some of this heterogeneity,

140 Modifier genes might interact to determine the susceptib

141 Modifier-gene models for the evolution of genetic inform

142 Surprisingly, certain modifier genes modify SCA1 and HD models in opposite dir

143 s observation suggests that 129SvEv-specific modifier genes modulate the impact of Slc30a8 deletion.

144 However, it has been proposed that nuclear-modifier genes modulate the phenotypic manifestation of

145 ervations imply that human MTO2 may act as a modifier gene, modulating the phenotypic expression of t

146 complementary analyses such as searches for modifier genes, must be employed.

147 several are downstream targets of epigenetic modifier genes mutated in AML.

148 A major codominant modifier gene of embryo lethality was mapped to proximal

149 Our study reveals Nrf2 as a novel modifier gene of sepsis that determines survival by moun

150 Mon1a was originally identified as a modifier gene of vesicular traffic, as a mutant Mon1a al

151 Recent functional studies of modifier genes of hearing-loss loci have begun to refine

152 aling controls the expression of several key modifier genes of intestinal tumorigenesis and has a cri

153 iate linkage crosses and congenic lines, and modifier genes of large effect can be identified by posi

154 Yor1-DeltaF670 biogenesis identified several modifier genes of mRNA processing and translation, which

155 Recently, 'modifier' genes of the FCHL phenotype, such as the apoli

156 ses did not support the existence of a major modifier gene on chromosome 19 in a region previously li

157 eatitis, and the discovery of a pancreatitis modifier gene on the X chromosome that provides new clue

158 he possible effects of genetic background or modifier genes on PTEN-controlled tumorigenesis using ge

159 In summary, we have mapped two modifier genes on the mouse Chr X that cause high-freque

160 that could be ameliorated or exacerbated by modifier genes or environmental factors in different pop

161 e heterozygotes suggests important roles for modifier genes or environmental factors in RP1-related d

162 ain of function by mutant CLC5, an effect of modifier genes, or a secondary result of nonspecific ren

163 ic disorders and highlight the importance of modifier gene pathways as therapeutic targets.

164 nist paradox and identify a potential asthma modifier gene (phospholipase C-beta1), which may also be

165 ns with TSC, the present study suggests that modifier genes play a role in the variable expression of

166 strongly suggest that genetic background or modifier genes play an important role in the phenotypic

167 It is hypothesized that modifier genes play important roles in determining the s

168 s and genetic background, referred to as the modifier genes, play a significant role.

169 Twin and sibling analysis indicates that modifier genes, rather than allelic variation in CFTR, a

170 disrupts the SUMO1 (small ubiquitin-related modifier) gene, resulting in haploinsufficiency.

171 Our study was initiated to identify the modifier gene(s) encoded by the Pctm locus, in which mou

172 However, putative nuclear modifier gene(s) has been proposed to regulate the pheno

173 However, putative nuclear modifier gene(s) have been proposed to regulate the phen

174 sn-/- mice and appeared to be dependent on a modifier gene(s) in addition to the loss of gelsolin.

175 oma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in suscepti

176 background suggests the presence of a major modifier gene(s) that influences 4.1G function and is as

177 l evidence has suggested the role of nuclear modifier gene(s), but a genomewide search has indicated

178 f loss of heterozygosity (LOH) and potential modifier gene(s), we investigated the molecular basis of

179 Our studies suggest that in addition to modifier genes, SNPs may also contribute to the differen

180 livered within the tumor microenvironment by modifier genes, stromal and endothelial cells, and immun

181 gs from the CF Twin-Sibling Study, French CF Modifier Gene Study, and Canadian Consortium for Genetic

182 ese studies define what we believe to be new modifier gene targets for treatment of ALS.

183 s in the gene that causes CF (CFTR) and a CF-modifier gene (TGFbeta1) amplify the negative effects of

184 Nor can we rule out a prostate cancer-modifier gene that confers a lower-than-reported risk.

185 tagenesis screen, we identified Smarca4 as a modifier gene that exacerbates the phenotypic severity o

186 We originally isolated Scnm1 as a disease modifier gene that is required for efficient in vivo spl

187 Overall, rdSNVs were enriched in histone modifier genes that activate transcription (Fisher exact

188 (logarithm of the odds of linkage >2.0) for modifier genes that cause MI (chromosomes 4q35.1, 8p23.1

189 rare, indicating that the sets of background modifier genes that cause susceptibility to each disease

190 This suggests the existence of modifier genes that influence disease progression.

191 C mutations, providing no clear evidence for modifier genes that influence disease severity in this f

192 Modifier genes that influence the penetrance of mutation

193 Additional modifier genes that lie outside the SMA locus exist and

194 WY increased expression of stress modifier genes that maintain the health of the proteome,

195 ul for identification of TGCT susceptibility modifier genes that map to Chr 19 and also for studies o

196 Therefore, identification of modifier genes that might influence ALS survival could i

197 ait locus (QTL) analysis in mice to identify modifier genes that might influence the severity of huma

198 to facilitate the identification of germline modifier genes that promote the development of aggressiv

199 The primary and modifier genes that regulate normal maxillofacial develo

200 he data provide evidence for strain-specific modifier genes that support the survival of PWS-IC delet

201 Once the identities of modifier genes that suppress vision or hearing loss beco

202 s often result from the action of so-called "modifier genes" that modulate the phenotypic manifestati

203 n the frequency of white genes, according to modifier gene theory.

204 s and 2304 affected F2 animals localized the modifier gene to a 950-kb interval on mouse chromosome 3

205 ing the 10p13 locus restricted the candidate modifier genes to ITGA8, C10orf97 (CARP) and PTER.

206 revention and management strategies based on modifier genes, to pharmacogenetics, in which individual

207 Here, we identified the nuclear-modifier gene TRMU, which encodes a highly conserved mit

208 9.9%), and unique individual factors (e.g., modifier genes, unique exposures; 6.8%) (likelihood rati

209 the identification of three pistil essential modifier genes unlinked to the S-locus (HT-B, 120K, and

210 We hypothesize that "modifier" genes unlinked to Tsc2 affect its expressivity

211 The protein products of USH2 causative and modifier genes, USH2A, ADGRV1, WHRN and PDZD7, interact

212 One modifier gene was identified and highlights the importan

213 termine if PKD severity can be influenced by modifier genes, we carried out an intercross between DBA

214 high-frequency, low-penetrance breast cancer modifier genes, we have developed a rat genetic model th

215 genes, primarily immune response and immune modifier genes, were typed.

216 In summary, Scnm1 is the first example of a modifier gene which influences disease severity through

217 ity of our patient suggests the influence of modifier genes which exacerbated the testicular phenotyp

218 years have demonstrated how coinheritance of modifier genes, which alter the balance of alpha-like an

219 ions harboring "cryptic" tumor suppressor or modifier genes whose inactivation contributes to tumorig

220 Identification of the modifier genes will complement the results of studies of

221 The identification of these novel modifier genes will serve as strong candidates for the d

222 rk identifies 27-kD gamma-zein as an opaque2 modifier gene within the largest QPM quantitative trait

223 rain tumors 1) was identified as a candidate modifier gene within the SuprMam1 interval because it wa

224 confirmed mutations of one or more chromatin modifier genes within 96% of FL tumors and two or more i