ライフサイエンスコーパス: TCF7L2

1 romoter of the increased target genes (i.e., TCF7L2).

2 gate mechanisms of target gene regulation by TCF7L2.

3 ated translation of the transcription factor TCF7L2.

4 ibility in conjunction with gene variants in TCF7L2.

5 (4EBP1) resulted in decreased expression of TCF7L2.

6 nriched in the sites bound by both GATA3 and TCF7L2.

7 -specific pattern of alternative splicing of TCF7L2.

8 lation of the metabolic transcription factor TCF7L2.

9 , and beta2 (ADRB2) and transcription factor TCF7L2.

10 g T2D or glycemic traits, including DGKB and TCF7L2.

11 n with heavy polysomes, probably through the TCF7L2 5'-untranslated region (UTR), as determined by po

12 cence staining and coimmunoprecipitated with Tcf7l2, a canonical Wnt signaling transcription factor.

13 Polymorphism in TCF7L2, a component of the canonical Wnt signaling pathw

14 ymmetry, we identified two mutant alleles of tcf7l2, a gene that encodes a transcriptional regulator

15 ved intronic region within the gene encoding Tcf7l2, a key mediator of canonical Wnt signaling.

16 e that the MUC1-C oncoprotein contributes to TCF7L2 activation and thereby promotes cyclin D1 express

17 potential mechanism through which pericytic Tcf7l2 activity affects beta-cells.

18 Here, we show that Tcf7l2 activity in pancreatic pericytes is required for

19 al cellular mechanism through which abnormal TCF7L2 activity predisposes individuals to diabetes and

20 Tcf7l2 acts cell automously in nascent equipotential neu

21 However, the mechanisms by which TCF7L2 affect insulin secretion are still unclear.

22 ith opposing effects (eg, the same rs7901695/TCF7L2 allele is associated with increased odds of high

23 We show that a null Tcf7l2 allele leads, in a dose-dependent manner, to lowe

24 iabetes incidence in carriers of the at-risk TCF7L2 alleles.

25 A cluster of genes regulated by GSK3beta-TCF7L2 also displayed promoter hypomethylation.

26 Transcription factor 7-like 2 (TCF7l2), also known as TCF4, is a Wnt effector induced t

27 loss on transcription factor 7-like 2 gene (TCF7L2) alternative splicing in adipose tissue and liver

28 Variants near TCF7L2 and ADRA2A were associated with reduced glucose-i

29 2D by genome-wide association studies (e.g., TCF7L2 and CDKN2B).

30 CRISPR/Cas9 knockout of TCF7L2 and JMJD6 depleted their levels, inducing loss of

31 Our GWAS identified two known loci (TCF7L2 and KCNQ1) reaching genome-wide significance leve

32 also downregulated the transcription factor TCF7L2 and markedly reduced WNT signaling.

33 TCF7L2 and MUC1-C form a complex on the cyclin D1 gene p

34 ISL1 is a primary target of TCF7L2 and regulates proinsulin production and processin

35 UC1-C inhibitor blocked the interaction with TCF7L2 and suppressed cyclin D1 levels.

36 Two of these loci map to genes (TCF7L2 and TGFB1) with established roles in colorectal t

37 MUC1-C blocks the interaction between TCF7L2 and the C-terminal-binding protein (CtBP), a supp

38 heterozygous for null alleles of Cacna1c and Tcf7l2 and wild-type females from 30 inbred laboratory s

39 We conclude that TCF7L2 and Wnt signaling control gut and brain gcg expre

40 The mechanisms by which Tcf7l2 and Wnt/beta-Catenin signalling elicit such a div

41 ween variants rs1799884 (GCK) and rs7903146 (TCF7L2) and OGTT outcomes at 24-32 weeks' gestation in 3

42 entially bind transcription factor 7-like 2 (TCF7L2) and that the risk region physically interacts wi

43 1 gene (rs4689388 and rs1801214), rs7903146 (TCF7L2), and 3 SNPs in the KCNQ1 gene (rs231362, rs22378

44 loci with known islet function, e.g., PDX1, TCF7L2, and ADCY5 Importantly, binding sites previously

45 nal evidence of pleiotropy for APOE, TOMM40, TCF7L2, and CETP variants, many with opposing effects (e

46 -onset type 1 diabetes loci and FCRL3, GAD2, TCF7L2, and FTO.

47 esenting 7,046 genes including PPARG, KCNQ1, TCF7L2, and IRS1, showed differential DNA methylation in

48 trate a novel relationship between GATA3 and TCF7L2, and reveal important insights into TCF7L2-mediat

49 3, ENPP1, FTO, LEP, PPARG, PPARGC1A, SLC2A2, TCF7L2, and UCP2) associated with type 2 diabetes or obe

50 rphism in Wnt-regulated transcription factor TCF7L2 are associated with dysregulation of glucose meta

51 Common genetic variants in GCK and TCF7L2 are associated with higher fasting glucose and ty

52 The discovery of TCF7L2 as a global type 2 diabetes (T2D) gene has sparke

53 udes the transcription factor 7-like 2 gene (TCF7L2), as well as other type 2 diabetes mellitus-assoc

54 type 2 diabetic subgroup, and for rs7903146 (TCF7L2), association was observed for early-onset type 2

55 beta-catenin, transcription factor 7-like 2 (TCF7L2), attenuated insulin secretion, consistent with t

56 of 149 DEGs was suggested by strong proximal TCF7L2 binding (peak proximity score > 10) and early mRN

57 nformatic analysis of the cell type-specific TCF7L2 binding sites revealed enrichment for multiple tr

58 We identified 116,000 non-redundant TCF7L2 binding sites, with only 1,864 sites common to th

59 depleted GATA3 in MCF7 cells and showed that TCF7L2 binding was lost at a subset of sites.

60 only synthesis of proinsulin is regulated by TCF7L2 but also processing and possibly clearance of pro

61 etabolic effect of a functional knockdown of TCF7L2 by generating transgenic mice that express domina

62 zation of nuclear beta-catenin with TBL1 and TCF7L2 by the small-molecule inhibitor BC2059 combined w

63 asmic domain (MUC1-CD) binds directly to the TCF7L2 C-terminal region.

64 t that developmentally regulated splicing of tcf7l2 can influence the transcriptional output of the W

65 in 7 genes (APOA1, IL1alpha, IL1beta, TLR4, TCF7L2, CCK1Rec, and STAT3) after correction for phenoty

66 iobank participants, we observed three (near TCF7L2, CDKN2AB and CDKAL1) overestimated (body mass ind

67 recurrent mutations in the Wnt pathway gene TCF7L2, chromatin-remodelling genes such as TET2 and TET

68 ChIP-seq analysis revealed that TCF7L2 co-localizes with HNF4alpha and FOXA2 in HepG2 ce

69 Both SMAD1 and TCF7L2 co-occupy sites with master regulators adjacent t

70 Furthermore, phosphorylated residues in Tcf7l2 coded exon5 facilitate repressor activity.

71 TCF7L2 codes for the transcription factor TCF/LF, part o

72 transcriptional activity of the beta-catenin/TCF7L2 complex, whereas gamma-catenin down-regulates it.

73 f gene transcription beyond the beta-catenin/TCF7L2 complex.

74 he transcription factors ERG, SPI1, TCF4 and TCF7L2, components of the Ras signalling pathway, histon

75 t a highly conserved sequence in intron 5 of Tcf7l2 conceals an internal promoter region that, when a

76 Common variants in the gene TCF7L2 confer the largest effect on the risk of type 2 d

77 Although variants in TCF7L2 confer the strongest risk of T2D among common var

78 this study was to elucidate which variant in TCF7L2 confers diabetes susceptibility in African Americ

79 eviously that in gut endocrine L-cell lines, TCF7L2 controls transcription of the proglucagon gene (g

80 rvations, transgenic mice harboring multiple Tcf7l2 copies and overexpressing this gene display recip

81 ression may lead to diabetes, we developed a Tcf7l2 copy-number allelic series in mice.

82 One mechanism by which TCF7L2 could influence expression of genes involved in d

83 individual beta cells, were both lowered by Tcf7l2 deletion in islets from mice maintained on a high

84 oduce secreted factors, including BMP4, in a Tcf7l2-dependent manner to support beta-cell function.

85 In addition, we identified Tcf7l2-dependent pericytic expression of secreted factor

86 On the left, the parapineal prevents this Tcf7l2-dependent process, thereby promoting dHbl differe

87 icotine increases levels of blood glucose by TCF7L2-dependent stimulation of the mHb.

88 s a transcription factor 7-like 2-dependent (TCF7L2-dependent) enhancer element that functions to inc

89 rt that the diabetes-associated variation in TCF7L2 did not associate with fasting EGP, insulin-induc

90 In that context, Tcf7l2 directly activates cholesterol biosynthesis genes

91 expression of a dominant negative isoform of TCF7L2 (dnTCF7L2) in interzone progeny, which may accoun

92 hese data indicate that genetic variation at TCF7L2 does not predispose an individual to type 2 diabe

93 smosomal partners, and with beta-catenin and TCF7L2, effectors of the canonical Wnt pathway.

94 Although TCF7L2 encodes TCF4, which cooperates with beta-catenin

95 n pancreatic beta cells, despite evidence of TCF7L2 expression in various peripheral tissues importan

96 We define the effects of TCF7L2 expression level on mature beta-cell function and

97 Reducing TCF7L2 expression levels by RNAi decreased glucose- but

98 To further determine whether variation in Tcf7l2 expression may lead to diabetes, we developed a T

99 Restoring Tcf7l2 expression specifically in beta cells to endogeno

100 e of rs7903146 was associated with increased TCF7L2 expression, and decreased insulin content and sec

101 harbors cis-regulatory elements controlling TCF7L2 expression, we conducted in vivo transgenic repor

102 critical role for these enhancers in robust TCF7L2 expression.

103 In addition, both SMAD1 and TCF7L2 follow the binding of the predominant lineage reg

104 ing the fusion gene to be dependent on VTI1A-TCF7L2 for anchorage-independent growth using RNA interf

105 on proteins, including a fusion of VTI1A and TCF7L2 found in 3 out of 97 colorectal cancers.

106 al SNPs of BMI and diabetes in genes TFAP2B, TCF7L2, FTO and ZC3H4.

107 It is controversial whether Tcf4 (Tcf7L2) functions as an oncogene or tumor suppressor gen

108 ts in or near transcription factor 7-like 2 (TCF7L2), gastric inhibitory polypeptide receptor (GIPR),

109 Polymorphisms in the human TCF7L2 gene are associated with reduced insulin secretio

110 While deletion of the homologous murine Tcf7l2 gene throughout the developing pancreas leads to

111 TCF7L2 gene variants have been associated with increased

112 d by mutations in the TCF4 gene, but not the TCF7L2 gene.

113 ested for modulation by polymorphisms of the TCF7L2 gene.

114 o harbored diabetogenic polymorphisms of the TCF7L2 gene.

115 s) within the transcription factor 7-like 2 (TCF7L2) gene and Type 2 Diabetes (T2D) as well as additi

116 riants in the transcription factor 7-like 2 (TCF7L2) gene have been identified as the strongest genet

117 polymorphisms in the T-cell factor 7-like 2 (TCF7L2) gene, associated with T2D by genome-wide associa

118 ons were present within the ASTE1, HNF1A, or TCF7L2 genes, increasing even further when at least one

119 Effect modifications by TCF7L2 genetic polymorphisms are supported.

120 odds ratios (ORs) of T2D associated with the TCF7L2 genotype between high and low strata of GL (P = 0

121 ng and plasma glucose was independent of the TCF7L2 genotype.

122 SIGN AND Eight subjects with risk-conferring TCF7L2 genotypes (TT or TC at rs7903146) and 10 matched

123 n the group of subjects with risk-conferring TCF7L2 genotypes compared with control subjects.

124 n this population proved to be attenuated by TCF7L2 HapA (P-interaction = 0.01).

125 TCF7L2 HapA attenuates the positive association between

126 The objective was to investigate whether TCF7L2 HapA is associated with weight development and wh

127 y, these patterns of expression suggest that TCF7L2 has distinct functions within the brain, with a g

128 iple targets in key pathways may explain why TCF7L2 has emerged as the gene showing one of the strong

129 ymorphisms of transcription factor 7-like 2 (TCF7L2) have been associated with type 2 diabetes and BM

130 y and hepatic transcription factor 7-like 2 (TCF7L2) have generated opposing views.

131 es-associated variation at 20 loci including TCF7L2, HHEX-IDE, PPARG, KCNJ11, SLC30A8, IGF2BP2, CDKAL

132 To inactivate Tcf7l2 highly selectively in beta cells from the earlies

133 rs of oligodendrocyte differentiation (i.e., TCF7L2, ID2, and SOX2) and higher HAT transcript levels

134 s revealed an overlap of 20 genes, including TCF7L2, IGFBP2, CDKN2A, CDKN2B, GRB10, and PRC1.

135 d point to a previously unrecognized role of Tcf7l2 in control of cholesterol biosynthesis for CNS my

136 tests, no association between expression of TCF7L2 in eight types of human tissue samples and T2D-as

137 (rs7903146) for elevating the expression of TCF7L2 in human pancreas which may affect the regulation

138 Knockdown of TCF7L2 in MALAT1-overexpressing cells and HCC cell lines

139 erestingly, the persistent overexpression of Tcf7l2 in non-pancreatic tissues results in a significan

140 ced in understanding the functional roles of TCF7L2 in pancreatic beta cells, despite evidence of TCF

141 Alternative splicing of TCF7L2 in pancreatic islets warrants future studies.

142 We also reveal a novel role of TCF7l2 in repressing a bone morphogenetic protein signal

143 t this hypothesis, we performed ChIP-seq for TCF7L2 in six human cell lines.

144 results support a central role of CDKAL1 and TCF7L2 in T2DM susceptibility in Southwest Asian populat

145 of hepatocytes, but the precise role of the TCF7L2 in this process is unknown.

146 the spatial-temporal expression patterns of TCF7L2, including expression in tissues involved in the

147 ed expression of TCF7L2DN, but not wild-type TCF7L2, increased gluconeogenesis and gluconeogenic gene

148 The diabetes-associated allele in TCF7L2 increases the rate of conversion to diabetes; how

149 significant variants in two loci CDKAL1 and TCF7L2, independent of sex, age and BMI, with leading va

150 A well accepted dogma is that TCF7l2 inhibits oligodendrocyte differentiation through

151 At the differentiation onset, Tcf7l2 interacts with a transcriptional co-repressor Kai

152 In the absence of an androgen signal, TCF7L2 interacts with FOXA1 at AR-binding sites and repr

153 This TCF7L2 intronic region contains several SNPs (rs7901695,

154 o BMI-association signals are present in the TCF7L2 intronic region of Hispanics, one of which is tag

155 chromatin sites and found that rs7903146, a TCF7L2 intronic variant strongly associated with type 2

156 Our findings suggest TCF7L2 is an important regulator of the hepatic phenotyp

157 A common genetic variation in TCF7L2 is associated with type 2 diabetes.

158 re we show that the diabetes-associated gene Tcf7l2 is densely expressed in the medial habenula (mHb)

159 Tcf7l2 is essential for lateralized fate selection by ha

160 TCF7L2 is important in the development of peripheral org

161 TCF7L2 is involved in maintaining expression of beta-cel

162 The type 2 diabetes risk gene TCF7L2 is the effector of the Wnt signaling pathway.

163 TCF7L2 is the strongest type 2 diabetes (T2D) locus iden

164 We report that TCF7l2 is upregulated transiently in postmitotic, newly

165 factor Tcf4 (transcription factor 7-like 2; Tcf7l2) is strongly expressed in connective tissue fibro

166 ts donors', we also show that the identified TCF7L2-ISL1 transcriptional network is regulated in a ge

167 ives the expression of dnTcf7l2, a truncated Tcf7l2 isoform that cannot bind beta-catenin and that th

168 Knockdown of TCF7L2 isoforms in mouse chondrocytes rescued hedgehog s

169 gher messenger RNA and protein expression of TCF7L2, JMJD6, and c-Myc and following BETi washout exhi

170 th increased levels of nuclear beta-catenin, TCF7L2, JMJD6, and c-Myc in BETi-P/R sAML cells.

171 ing the mechanistic role of the beta-catenin-TCF7L2-JMJD6-c-Myc axis in BETi resistance.

172 multitargeted disruption of the beta-catenin-TCF7L2-JMJD6-c-Myc axis overcomes adaptive and innate BE

173 near 9 loci (NOTCH2, ADCY5, JAZF1, CDKN2A/B, TCF7L2, KCNQ1, MTNR1B, FTO, and HNF1B) were nominally as

174 (P(emp) < 0.05) at regional best SNPs in the TCF7L2, KLF14, and HMGA2 loci as well as suggestive sign

175 esults revealed that seven index SNPs at the TCF7L2, KLF14, KCNQ1, ADCY5, CDKAL1, JAZF1, and GCKR loc

176 hich were differentially expressed following Tcf7l2 knock-down.

177 Silencing Tcf7l2 led to a time-dependent appearance of 406 differe

178 Indirect gene regulation by TCF7L2 likely occurred via alternate transcription facto

179 y that a genetic variant harbored within the TCF7L2 locus impairs glucose tolerance through effects o

180 insulin secretion, genetic variation at the TCF7L2 locus may alter insulin action or directly modify

181 ly implicated noncoding variation within the TCF7L2 locus with type 2 diabetes (T2D) risk.

182 iation in the transcription factor 7-like 2 (TCF7L2) locus is associated with type 2 diabetes across

183 ypes as a result of manipulations leading to Tcf7l2 loss of function.

184 olymorphisms in 1 glucose and 4 lipids loci (TCF7L2, LPL, APOA5, CETP, and APOC1/APOE/TOMM40) signifi

185 ide insights as to how the overexpression of TCF7L2 may attenuate insulin secretion.

186 ociated variation (T allele at rs7903146) in TCF7L2 may impair the ability of hyperglycemia to suppre

187 d TCF7L2, and reveal important insights into TCF7L2-mediated gene regulation.

188 gulated SHROOM3 expression in a beta-catenin/TCF7L2-mediated manner, while SHROOM3 in turn facilitate

189 cyclin D1 gene promoter and MUC1-C promotes TCF7L2-mediated transcription by the recruitment of beta

190 inal-binding protein (CtBP), a suppressor of TCF7L2-mediated transcription.

191 nd miR-20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation.

192 Tcf7l2 mediates Wnt/beta-Catenin signalling during devel

193 genesis, a recent study using liver-specific Tcf7l2(-/-) mice suggested the opposite.

194 How Tcf7l2 modifies beta-catenin signalling and controls mye

195 Interestingly, in MCF7 cells the TCF7L2 motif is enriched in most TCF7L2 sites but is not

196 MALAT1 expression regulated TCF7L2 mRNA association with heavy polysomes, probably t

197 The expression of TCF7L2 mRNA in pancreas was also elevated (~23-fold) amo

198 Our study shows that the short TCF7L2 mRNA variant in subcutaneous fat is regulated by

199 d by Vax2, drives transcription of truncated Tcf7l2 mRNAs.

200 In tcf7l2 mutants, most neurons on both sides differentiate

201 Tcf7l2 null mice also display enhanced glucose tolerance

202 studies demonstrated a repressive effect of TCF7L2 on hepatic gluconeogenesis, a recent study using

203 ally opposing cell-type specific effects for Tcf7l2 on the maintenance of balanced glucose metabolism

204 LP-1 and GIP but rather due to the effect of TCF7L2 on the sensitivity of the beta-cell to incretins.

205 CRISPR/Cas9-mediated knockout of TCF7L2 or JMJD6 reversed BETi-P/R, whereas ectopic overe

206 se intolerance, to infer the contribution of Tcf7l2 overexpression in beta cells and in other tissues

207 n glucose tolerance in vivo, indicating that Tcf7l2 overexpression in beta cells does not account for

208 t account for the glucose intolerance in the Tcf7l2 overexpression mouse model.

209 variants in HMGA2 and replicated variants in TCF7L2 (p = 5.1 x 10(-15)).

210 6 x 10(-12)), KCNQ1 (P = 1.35 x 10(-4)), and TCF7L2 (P = 5.10 x 10(-4)) with study-wise statistical s

211 e-wide level with rs12772424 in an intron of TCF7L2 (P=2.85E-8).

212 regulation of a subset of metabolic genes by TCF7L2, particularly those involved in lipid and amino-a

213 These data demonstrate that Tcf7l2 plays a cell autonomous role in the control of be

214 Ac are also bound by TCF7L2, suggesting that TCF7L2 plays a critical role in enhancer activity.

215 These results directly demonstrate that Tcf7l2 plays a role in regulating glucose tolerance, sug

216 Collectively, these data posit that Tcf7l2 plays key roles in glucose metabolism through act

217 first hint that the well-known impact of the TCF7L2 polymorphism on type 2 diabetes risk may involve

218 The transcription factor 7-like 2 (TCF7L2) polymorphism rs7903146 is known to be tightly as

219 elevance of these findings for the action of TCF7L2 polymorphisms associated with Type 2 diabetes in

220 tion setting, we investigated the effects of TCF7L2 polymorphisms rs7903146 and rs12255372 and dietar

221 itional ablation, we found surprisingly that TCF7l2 positively regulates neonatal and postnatal mouse

222 The encoded Tcf7l2 protein binds to DNA, but not beta-catenin, and t

223 By contrast, mutant Tcf7l2 rats are resistant to these actions of nicotine.

224 During oligodendrocyte maturation, Tcf7l2 recruits and cooperates with Sox10 to promote mye

225 t downregulation of TCF7L1 and its paralogue TCF7L2 reduces tumor growth in a xenograft model of huma

226 Here we define a stage-specific Tcf7l2-regulated transcriptional circuitry in initiating

227 Using RNA-sequencing, we have identified a TCF7L2-regulated transcriptional network responsible for

228 Our findings suggest that TCF7L2 regulates the stimulatory actions of nicotine on

229 ansgenic reporter assays to characterize the TCF7L2 regulatory landscape.

230 Non-coding variation within TCF7L2 remains the strongest genetic determinant of type

231 RNA-seq analysis suggested that TCF7L2 represses transcription when tethered to the geno

232 y the physical interaction between CCAT2 and TCF7L2 resulting in an enhancement of WNT signaling acti

233 e use a humanized mouse model overexpressing Tcf7l2, resulting in glucose intolerance, to infer the c

234 eltaWC and DeltaWCBMI, regardless of FTO and TCF7L2 risk alleles.

235 Individuals with the TCF7L2 rs12255372 risk genotype may reduce body adiposit

236 Furthermore, the maternal genotype for TCF7L2 rs3814573 suggested an increased NTD risk among o

237 ation of four T2D susceptibility SNPS within TCF7L2 (rs7901695, rs7903146, rs11196205, and rs12255372

238 The strongest association was observed at TCF7L2 rs7903146 (odds ratio [OR] 1.30; P = 6.86 x 10(-)

239 ; HR, 5.70; 95% CI, 2.77-11.74; P < 0.0001), TCF7L2 rs7903146 (per each T allele; HR, 1.81; 95% CI, 1

240 TCF7L2 rs7903146 and rs10885406 were successfully genoty

241 In renal transplant patients, TCF7L2 rs7903146 is strongly and independently associate

242 We investigated whether FTO rs9939609 and TCF7L2 rs7903146 modified the association between the MD

243 significant interaction between the MDS and TCF7L2 rs7903146 on weight gain (P = 0.05), which sugges

244 less clear, but the effect may depend on the TCF7L2 rs7903146 variant.

245 The disease-associated variants in TCF7L2 (rs7903146) and WFS1 (rs10010131) have been shown

246 T16a insertion and the at-risk 'T' allele of TCF7L2 (rs7903146) for elevating the expression of TCF7L

247 8)), GCKR (rs1260326, P = 7.1 x 10(-11)) and TCF7L2 (rs7903146, P = 4.2 x 10(-10)) associated with 2-

248 TCF7L2(rs7903146) was identified as a complex effect or

249 luate whether transcription factor 7-like 2 (TCF7L2) rs7903146 gene polymorphism is associated with t

250 ng effects of transcription factor-7-like-2 (TCF7L2) rs7903146 polymorphism on these associations.

251 igher T2D risk in homozygous carriers of the TCF7L2-rs7903146 T-allele.

252 istage genome occupancy analyses reveal that Tcf7l2 serially cooperates with distinct co-regulators t

253 development of T2D through Wnt/beta-catenin/TCF7L2 signaling pathway.

254 ic attempts to enhance, rather than inhibit, TCF7l2 signaling to overcome arrested oligodendroglial d

255 Inhibition of TCF7L2 signalling in the mHb increases nicotine intake i

256 Gene expression profiling in TCF7L2-silenced cells revealed increased levels of mRNA

257 to examine gene expression 3-96 h following Tcf7l2 silencing in rat hepatoma cells, and combined thi

258 Tcf7l2-silencing enhanced the expression and chromatin o

259 7 cells the TCF7L2 motif is enriched in most TCF7L2 sites but is not enriched in the sites bound by b

260 isms (SNPs) in or near genes (KCNJ11, PPARG, TCF7L2, SLC30A8, HHEX, CDKN2A/2B, CDKAL1, IGF2BP2, ARHGE

261 A fourth cluster (TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was define

262 Taken together, we report association of TCF7L2 SNPs with amygdalar volume among T2D elderly Jewi

263 This association between TCF7L2 splicing and plasma glucose was independent of th

264 urthermore, we determined the association of TCF7L2 splicing with the levels of plasma glucose and se

265 y both H3K4me1 and H3K27Ac are also bound by TCF7L2, suggesting that TCF7L2 plays a critical role in

266 hologically docked vesicles was unchanged by TCF7L2 suppression, secretory granule movement increased

267 In 3 of the 14 regions, TCF7L2 (T2D), CTLA4 (Graves' disease) and CDKN2A-CDKN2B

268 Expression levels of canonical Wnt/Tcf7l2 targets bone morphogenetic protein 7 and Wnt5b, w

269 We show that Tcf3 and Tcf7L2 (Tcf4) are required for proper ventral patterning

270 godendrocyte-restricted transcription factor TCF7L2/TCF4 as a bipartite co-effector of beta-catenin f

271 ion abolished the injury-induced increase in TCF7L2/TCF4+ cells, and protected oligodendrocytes from

272 Tcf7l2/Tcf4, a beta-catenin transcriptional partner, is

273 ansgenic mice that express dominant-negative TCF7L2 (TCF7L2DN) specifically in gcg-expressing cells.

274 ed the liver-specific dominant-negative (DN) TCF7L2 (TCF7L2DN) transgenic mouse model LTCFDN.

275 , KCNQ1, LOC387761, MTNR1B, NOTCH2, SLC30A8, TCF7L2, THADA, and TSPAN8-LGR5.

276 light novel mechanisms of gene regulation by TCF7L2 that involve interplay between multiple hepatic t

277 so and Sox10 that sequentially interact with Tcf7l2 to coordinate the switch at the transitions of di

278 s analysis suggested that GATA3 might tether TCF7L2 to the genome at these sites.

279 erential binding of the transcription factor TCF7L2 to the rs6983267 risk allele over the non-risk.

280 The TCF7L2 transcription factor is linked to a variety of hu

281 erminal subunit (MUC1-C) associates with the TCF7L2 transcription factor.

282 MALAT1-enhanced TCF7L2 translation was mediated by upregulation of SRSF1

283 insulin secretion, consistent with the extra TCF7L2 translocating beta-catenin from the plasma membra

284 nvasion-driver genes, 17 of which, including TCF7L2, TWIST2, MSH2, DCC, EPHB1 and EPHB2 have been pre

285 Two vertebrate TCFs (TCF-1/TCF7 and TCF-4/TCF7L2) use the C-clamp as an alternatively spliced doma

286 that include exon five or an analogous human tcf7l2 variant can effectively provide compensatory repr

287 The TCF7L2 variant rs7903146 appears to affect risk of type

288 The TCF7L2 variant was associated with all three maternal gl

289 Maternal GCK and TCF7L2 variants are associated with glucose levels known

290 Knockdown of exon five specific tcf7l2 variants in tcf7l1a mutants also compromises eye

291 The diabetes risk allele at TCF7L2 was associated with a stronger effect on peak ins

292 Inactivation of pericytic Tcf7l2 was associated with impaired expression of genes

293 A previous association of CFRD with SNPs in TCF7L2 was replicated in this study (P = 0.004; combined

294 Transgenic mice in which Tcf7l2 was selectively inactivated in their pancreatic p

295 rs12255372 (in TCF7L2) was associated with lower BMI in both MESA (beta

296 ity variants near ADRA2A, KCNJ11, KCNQ1, and TCF7L2 were associated with reduced depolarization-evoke

297 in (TEAD) and transcription factor 7-like 2 (TCF7L2), which are transcription factors of the Hippo an

298 regulates beta-catenin and its binding with TCF7L2, which in turn is critical for the production of

299 ession of the Wnt pathway mediator Tcf4 (aka Tcf7l2) within OLPs is specific to lesioned-but not norm

300 Gata2, Gata3, Klf2, Lrp5, Ppargamma2, Sfrp1, Tcf7l2, Wnt10b, and Wnt3a.