ライフサイエンスコーパス: TCF-1

1 TCF-1 acted through both GATA-3-dependent and GATA-3-ind

2 TCF-1 and GATA3 were indispensable for the epigenetic pr

3 TCF-1 co-binds accessible regulatory regions containing

4 TCF-1 deficiency did not change the core T(reg) cell tra

5 TCF-1 has been recently shown to critically regulate mem

6 TCF-1 is a key transcription factor in progenitor exhaus

7 TCF-1 is highly expressed in the earliest thymic progeni

8 TCF-1 mediated a T-bet-to-Eomes transcription factor tra

9 TCF-1 mediated the bifurcation between divergent fates,

10 TCF-1 or stabilized beta-catenin greatly stimulated acti

11 TCF-1 thus has dual roles, i.e., acting cooperatively wi

12 TCF-1 used a pre-existing regulatory landscape establish

13 TCF-1 was directly associated with the Eomes allele and

14 TCF-1 was dispensable for the generation of specified EI

15 TCF-1 was intrinsically required for the differentiation

16 TCF-1+ stem cell-like memory CD8+ T (TSCM) cells are imp

17 TCF-1-deficient T(reg) cells strongly suppressed T cell

18 erentiation, was induced by T cell factor 1 (TCF-1) and its cofactor beta-catenin, mainly from the pr

19 expression of T cell transcription factor 1 (TCF-1) and promoted mitochondrial fitness, thereby facil

20 signaling in the intestine, T-cell factor 1 (TCF-1) and TCF-4, have opposing functions.

21 hancer factor 1 (LEF-1) and T cell factor 1 (TCF-1) are closely related transcription factors that ar

22 T cell factor 1 (TCF-1) is a transcription factor known to act downstream

23 T-cell factor 1 (TCF-1), a related transcription factor, contains a simil

24 t ILC2 development required T cell factor 1 (TCF-1, the product of the Tcf7 gene), a transcription fa

25 hat a transcription factor, T-cell factor 1 (TCF-1; also known as transcription factor 7, T-cell spec

26 study, we demonstrate that T cell factor 1 (TCF-1; encoded by Tcf7), a transcription factor also imp

27 identified, e.g., GATA3 and T cell factor-1 (TCF-1) (gene name Tcf7).

28 T cell factor-1 (TCF-1) and lymphoid enhancer factor-1 (LEF-1), members o

29 T cell factor-1 (TCF-1) and lymphoid enhancer-binding factor 1, the effec

30 characteristics, defined by T cell factor-1 (TCF-1) expression.

31 nscription factor 7 (TCF7) (T cell factor-1 (TCF-1)) are downstream effectors of the WNT signaling pa

32 anti-CTLA-4 preserves more T cell factor-1 (TCF-1)+ T cells during priming, while anti-PD-1 leads to

33 ression of CD27, CXCR3, and T cell factor-1 (TCF-1), each a marker that is individually correlated wi

34 T cell factor-1 (TCF-1), encoded by Tcf7, is a transcription factor and h

35 to impaired stimulation of TdLN CD8+ PD-1 + TCF-1+ T cells or an inability of PD-1+ TCF-1+ cells in

36 lyses, we identified a population of PD-1(+) TCF-1(+) CD4(+) T cells with memory-like features.

37 tumor-infiltrating antigen-specific PD-1(+) TCF-1(-) CD8(+) T cells express the immunosuppressive cy

38 Notably, PD-1(+)TCF-1(+) (Progenitor-exhausted) CD8(+) T cells shared cl

39 ifferentiation of antigen-experienced PD-1(+)TCF-1(+) stem-like CD8(+) T cells into effector cells is

40 More notably, HPV-specific PD-1(+)TCF-1(+) stem-like TILs proliferated and differentiated

41 e presence of functional HPV-specific PD-1(+)TCF-1(+)CD45RO(+) stem-like CD8 T cells with proliferati

42 These PD-1(+)TCF-1(+)TOX(+) stem-like CD8(+) T cells (also known as p

43 highlight the ability of these early PD-1(+)TCF-1(+)TOX(+) stem-like CD8(+) T cells to adapt their d

44 increase depends on trafficking of the PD-1+ TCF-1+ cells from the tumor-draining lymph node (TdLN) t

45 -1 + TCF-1+ T cells or an inability of PD-1+ TCF-1+ cells in the TdLN to traffic to the tumor.

46 nd differentiation of the TdLN derived PD-1+ TCF-1+ cells into TIM-3+ GZMB+ TCF-1- effector-like cell

47 Finally, we found that ablation of the PD-1+ TCF-1+ T cell population attenuates the enhanced tumor c

48 increases intra-tumor progenitor CD8+ PD-1+ TCF-1+ T cells.

49 mbination therapy enriches for a novel PD-1+ TCF-1+ TOX- LY6A+ subset with expression of a type I int

50 We examined the role of a LEF-1/TCF-1 binding site in the human adenosine deaminase (ADA

51 nalysis demonstrated that a functional LEF-1/TCF-1 binding site is not required for enhancer-mediated

52 Mutation of the LEF-1/TCF-1 site destroyed the ability of the ADA enhancer/loc

53 he hypothesis that factors binding the LEF-1/TCF-1 site play an architectural role during the in vivo

54 ncer in transgenic mice with a mutated LEF-1/TCF-1 site.

55 201-bp core promoter region and Sp1, NRE-2a, TCF-1/LEF-1, and Sp1/NF-AT binding sites in the upstream

56 c to the tumor and differentiate into TIM-3+ TCF-1- cells.

57 (scRNA-seq) and lineage tracing identified a TCF-1(+)Ly108(+)PD-1(+) CD8 T cell population that seeds

58 a stabilized beta-catenin (beta-cat(Tg)), a TCF-1 activator.

59 in loss of fumarate synthesis and abrogated TCF-1 expression via demethylation of the TCF-1 promoter

60 g site located within the enhancer abrogated TCF-1 and beta-catenin-mediated activation of CD4 report

61 In addition, TCF-1 as well as beta-catenin were able to stimulate tra

62 dampened expression of T-bet but not altered TCF-1 levels or T cell receptor signaling in CD8 T cells

63 Together, these data show that LEF-1 and TCF-1 are redundant in the regulation of T cell differen

64 LEF-1 and TCF-1 coordinated such differentiation by two general me

65 Thus, LEF-1 and TCF-1 differ in several aspects of nuclear localization.

66 t, the subcellular localization of LEF-1 and TCF-1 fused to green fluorescent protein (GFP)) was exam

67 LEF-1 and TCF-1 immunostaining can serve to identify specific subt

68 e evidence for a redundant role of LEF-1 and TCF-1 in Wnt signaling during mouse development.

69 CF-1 (P < 0.0001), suggesting that LEF-1 and TCF-1 transcription factor expression may be lost in Th2

70 been proposed for the HMG proteins LEF-1 and TCF-1.

71 model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upregulating e

72 wever, including E proteins, Myb, Gfi-1, and TCF-1.

73 2, Msx-1, serum response elements, SP-1, and TCF-1.

74 that most CD8 T cells were granzyme B(+) and TCF-1(-) To address if this phenotype is driven by CVT t

75 Cxcr5 expression and, together with Bcl6 and TCF-1, formed a transcriptional circuit that guided TFC

76 ing the interaction between beta-catenin and TCF-1.

77 tes the interaction between beta-catenin and TCF-1.

78 ired the transcription factors Bcl6, E2A and TCF-1 but was inhibited by the transcriptional regulator

79 e transcription factors RORalpha, GATA3, and TCF-1 and produce the type 2 cytokines IL-4, IL-5, IL-9,

80 expression of transcription factors such as TCF-1.

81 cases of T-ALL/LyL express LEF-1 as well as TCF-1, exhibiting uniform nuclear immunostaining for bot

82 ouse CVT gradually acquired a granzyme B(+), TCF-1(-) phenotype as seen in human CVT.

83 those encoding transcription factors Bcl11b, TCF-1 (Tcf7), and HEBalt, Notch target Deltex1, Deltex3L

84 and identified a distinct population of BCL6+TCF-1+PD1+CD4+ T cells in the spleen during helminth inf

85 Both TCF-1(-/-) and RORgammat(-/-) DP thymocytes underwent si

86 Because it interacts with beta-catenin, TCF-1 has been classically viewed as a downstream effect

87 d EBP50 stabilized conventional beta-catenin/TCF-1 complexes and connected beta-catenin to dnTCF-1 to

88 Moreover, beta-catenin/TCF-1 directly interacted with the RORgammat promoter re

89 ion and the development of TOX(+) and CD39(-)TCF-1(+) cells.

90 demonstrate that, like IL-7Ralpha and CD62L, TCF-1 and lymphoid enhancer-binding factor 1 exhibit dyn

91 In colon cancer cells, TCF-1 is predominantly cytoplasmic.

92 al, with limited impact on minimally cycling TCF-1(+) follicular helper T cells, despite high PD-1 ex

93 progenitor Tex cells to more differentiated TCF-1(-) Tex subsets.

94 on factor Zeb2, as well as multiple distinct TCF-1(+) stem/progenitor-like subsets in acute and chron

95 In contrast, CD4 levels were restored on DP TCF-1(-/-) cells by transgenic expression of a wild-type

96 o identify PD-1 as a protector of this early TCF-1 subset.

97 ic lymphoma (T-ALL/LyL) was found to express TCF-1, and we find that 9 of 10 cases of T-ALL/LyL expre

98 lations, non-effector subsets, which express TCF-1 and include memory and stem-like cells, were conti

99 rom apoptosis, whereas ectopically expressed TCF-1 was not able to rescue the defective T cell develo

100 her frequencies of memory T cells expressing TCF-1 and of SIV-specific CD4(+) and CD8(+) T cells in b

101 Despite Hmgb2(-/-) CD8(+) T cells expressing TCF-1 and TOX, these master regulators were unable to su

102 lls that develop from progenitors expressing TCF-1 lacking L1 exhibit lineage infidelity distinct fro

103 chromatin accessibility and gene expression, TCF-1 has the potential to reduce chromatin accessibilit

104 ally disordered region of the pioneer factor TCF-1 (termed L1) leads to an early developmental block

105 we demonstrate that the transcription factor TCF-1 (Tcf7) regulates CD8(+) T cell fate decisions in d

106 T cells expressing the transcription factor TCF-1 drives the response to immune checkpoint blockade.

107 owever, the role of the transcription factor TCF-1 in early fate decisions and initial generation of

108 gh mobility group (HMG) transcription factor TCF-1 is essential for early T cell development.

109 The transcription factor TCF-1 is essential for the development and function of r

110 We show that the transcription factor TCF-1 is required for the efficient generation of all kn

111 duced expression of the transcription factor TCF-1, and inhibited the dysfunctional phenotype, culmin

112 the long isoform of the transcription factor TCF-1.

113 EX) cells originated from the T cell factor (TCF-1(+)) T(EX) progenitor subset.

114 of CD8(+) T cells, the transcription factors TCF-1 and Blimp1 control progenitor and terminally diffe

115 The transcription factors TCF-1 and LEF-1 are essential for early T cell developme

116 tive expression of the transcription factors TCF-1 and T-bet, and by discrete levels of CD27 expressi

117 inhibit expression of transcription factors TCF-1, LEF-1, and RORgammat that are required for the IS

118 Whereas CD8+ effectors deficient for TCF-1 and LEF-1 retained the capacity to express IFN-gam

119 1 and 32 of 42 (76%) were immunoreactive for TCF-1, including most cases of angioimmunoblastic lympho

120 highlight recent reports showing promise for TCF-1 as a novel biomarker to identify recently characte

121 ngs demonstrate an essential requirement for TCF-1 in ILC2 differentiation and reveal a link among Tc

122 shing these lineages and the requirement for TCF-1 throughout lineage differentiation and maintenance

123 These data define a role for TCF-1 in early-fate-bifurcation-driving Tex precursor ce

124 ad decreased survival, suggesting a role for TCF-1 in promoting survival in the nonlymphoid tissues.

125 The complete spectra of regulatory roles for TCF-1 and LEF-1 in CD8+ T cell responses are yet unknown

126 igenetic and transcriptional transition from TCF-1(+) progenitor Tex cells to more differentiated TCF

127 in structure that allows the transition from TCF-1(+) progenitors to CX(3)CR1(+) effector cells.

128 Furthermore, TCF-1 blocked T(H)1 fate by negatively regulating interf

129 eadily localizes to the nucleus, whereas GFP-TCF-1 remains in the cytoplasm.

130 derived PD-1+ TCF-1+ cells into TIM-3+ GZMB+ TCF-1- effector-like cells in the tumor with further enh

131 Several reports now reveal how TCF-1 and GATA-3 are mobilized in early T cells and the

132 and RORgammat Overall, our study reveals how TCF-1 exerts central control of T cell differentiation i

133 Our studies thus identify TCF-1 as a critical player in a transcriptional program

134 ymocytes, we demonstrated that deficiency in TCF-1 and LEF-1 diminished the output of CD4(+) T cells

135 Mice deficient in TCF-1 displayed significantly reduced protein and mRNA l

136 RORgammat was significantly downregulated in TCF-1(-/-) thymocytes that underwent accelerated apoptos

137 ch reprogrammed cells included enrichment in TCF-1+ less-differentiated subsets, a superior response

138 depletion in the mice led to an increase in TCF-1(+)PD-1(+)Tim-3(-) stem-like memory CD8(+) T cells

139 +) ILC3 showed a dose-dependent reduction in TCF-1 expression.

140 erized.An intrinsically disordered region in TCF-1 has now been found to have an essential function i

141 s of other hematopoietic lineages, including TCF-1 and GATA-1.

142 strong evidence for beta-catenin-independent TCF-1 functions.

143 a suggest a model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upr

144 demonstrate that IL-7R signals also inhibit TCF-1 and LEF-1 expression in mature peripheral T cells.

145 Instead, TCF-1 physically interacted with Runx3 to cooperatively

146 Frequencies of PD-1(int) TCF-1(+) CD8(+) T cells decreased upon Il10rb or Stat3 d

147 sted CD8(+) T cells and functional PD-1(int) TCF-1(+) CD8(+) T cells is regulated by cell-intrinsic I

148 Two discrete intratumoral TCF-1(+) CD8(+) T cell subsets developed over time-a pro

149 (+) T cells revealed that while intratumoral TCF-1(+) CD8(+) T cells acquired dysfunctional features

150 phase, the Ag-specific CD8+ T cells lacking TCF-1 and LEF-1 exhibited an effector phenotype and were

151 is reveals increased proportion of stem-like TCF-1-expressing CD8(+) T cells among intra-tumoral CD3(

152 T cell responses in mild mpox and long-lived TCF-1(+) VACV/MPXV-specific CD8(+) T cells decades after

153 cell numbers, impaired maintenance of liver TCF-1+ progenitor-like T cells, and inhibition of GVHD.

154 patients with colorectal cancer showed lower TCF-1 expression and increased T(H)17 expression signatu

155 y and functionally distinct subsets: Ly108(+)TCF-1(+) progenitors, Ly108(-)CX(3)CR1(-) terminally exh

156 Mechanistically, TCF-1 and BATF are the targets for IKAROS and ETS1, resp

157 nt and independent of its role in modulating TCF-1 activity.

158 Moreover, TCF-1-deficient memory CD8(+) T cells were progressively

159 SL), GATA-3, E2A/HEB and Id proteins, c-Myb, TCF-1, and members of the Runx, Ets, and Ikaros families

160 4 enhancer was detected in wild-type but not TCF-1 null mice by chromatin-immunoprecipitation analysi

161 ter, and they severely impair the ability of TCF-1 to regulate growth in colon cancer cells.

162 Ablation of TCF-1 resulted in enhanced Tc17 cell development and exp

163 l Th1 differentiation even in the absence of TCF-1.

164 Furthermore, activation of TCF-1 by stabilized beta-catenin was able to enhance DP

165 ogenitors (EILPs) expressing high amounts of TCF-1.

166 ession circuits of Gfi1 against Egr-2 and of TCF-1 against PU.1 as proposed elsewhere, but requires a

167 In addition, the binding of TCF-1 bends the DNA and affects the chromatin conformati

168 is lineage diversion, L1 mediates binding of TCF-1 to its earliest target genes, which are subject to

169 CD8+ T cells in the peritoneal cavity of TCF-1-deficient mice had decreased survival, suggesting

170 a stabilized beta-catenin, a coactivator of TCF-1, resulted in up-regulation of CD4.

171 er nuclear organization, the contribution of TCF-1 on the control of three-dimensional (3D) genome st

172 and by combination with germline deletion of TCF-1, we found that loss of both factors completely abr

173 elity distinct from the lineage diversion of TCF-1-deficient cells.

174 indicating that RORgammat acts downstream of TCF-1 in the regulation of DP thymocyte survival.

175 nsion, maintenance and affinity evolution of TCF-1(+)PD-1(+)SLAMF6(high) stem-like CD8(+) T cells.

176 Forced expression of TCF-1 in bone marrow progenitors partially bypassed the

177 maintains a balance between the two forms of TCF-1 is unclear.

178 in this study we show additional function of TCF-1/beta-catenin pathway in the regulation of CD4 expr

179 program begins earlier with the induction of TCF-1 (Tcf7 gene product) and GATA-3.

180 colon cells, a dominant-negative isoform of TCF-1 (dnTCF-1) is expressed that is equally distributed

181 r example, alternatively spliced isoforms of TCF-1 and TCF-4 with a C-terminal "E" tail are uniquely

182 nce of crypt stem cells, whereas knockout of TCF-1 leads to adenomas.

183 cl-2 restored survival but not CD4 levels of TCF-1(-/-) DP cells.

184 Furthermore, loss of TCF-1 and LEF-1 unexpectedly caused derepression of CD4

185 Loss of TCF-1 expression impaired the capacity of these ILC subs

186 ents, we discovered that the co-occupancy of TCF-1 and the architectural protein CTCF altered the str

187 Finally, recruitment of TCF-1 to CD4 enhancer was detected in wild-type but not

188 , cDC1s in tumor dLN maintain a reservoir of TCF-1(+) CD8(+) T cells and their decrease contributes t

189 The role of TCF-1 and LEF-1 in the CD4-versus-CD8 lineage 'choice' w

190 Here, we investigated the role of TCF-1 in 3D genome reconfiguration.

191 view, we discuss the multifunctional role of TCF-1 in establishing these lineages and the requirement

192 lts are reminiscent of the critical roles of TCF-1 in early T cell development.

193 rrent understanding of the multiple roles of TCF-1 in T cell development and function and their mecha

194 their quantity, notably among the subset of TCF-1(+) self-renewing T cells.

195 t the intrinsically disordered N terminus of TCF-1 maintains T cell lineage fidelity.

196 Our results suggest that upregulation of TCF-1 expression denotes the earliest stage of ILC fate

197 early locus 'poising' function dependent on TCF-1 and GATA-3, a stochastic-permissivity function dep

198 but not the developmental block, depends on TCF-1, beta-catenin's DNA-binding partner.

199 l lymphoma, were immunoreactive for LEF-1 or TCF-1 (P < 0.0001), suggesting that LEF-1 and TCF-1 tran

200 ich encode the transcription factor LEF-1 or TCF-1, respectively) resulted in T(FH) cell defects, whi

201 The vast majority of LEF-1+ and/or TCF-1+ PTCL (34 of 39 or 87%) exhibit a composite Th1 T-

202 s (48%), are immunoreactive for LEF-1 and/or TCF-1, with 36 of 38 cases immunoreactive for both, indi

203 Enforced expression of a p45 TCF-1 isoform limited the expansion of Ag-specific CD8 T

204 inding of the B-catenin interacting partner, TCF-1, to DNA overlapped with Foxp3 binding at enhancer

205 lato et al. demonstrate that CXCR6 positions TCF-1(-) transitory CD8(+) cytotoxic lymphocytes (CTLs)

206 development within T cell factor 1-positive (TCF-1(+)) early innate lymphoid progenitors (EILPs), whi

207 nd decreased in number as tumors progressed, TCF-1(+) CD8(+) T cell frequency in the tumor draining L

208 layed improved survival, a higher proportion TCF-1+ Tox- stem-like cells, and greater antitumor and m

209 forced expression of Eomes partly protected TCF-1-deficient memory CD8(+) T cells from time-dependen

210 The T cell-specific DNA-binding protein TCF-1 is a central regulator of T cell development and f

211 nhances CD4 expression in vivo by recruiting TCF-1 to stimulate CD4 enhancer activity.

212 he activity of the transcriptional repressor TCF-1, we found that sustained IL-2 signals were still r

213 expression of RORgammat successfully rescued TCF-1(-/-) DP thymocytes from apoptosis, whereas ectopic

214 t with this, we identified a tissue-resident TCF-1(+) subpopulation that preferentially engrafted, ex

215 ns with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively u

216 ased the frequency of intratumoral SlamF6(+) TCF-1(+) CD8(+) T cells.

217 le-cell sequencing of tumor-antigen specific TCF-1(+) CD8(+) T cells revealed that while intratumoral

218 In mice with polyposis, T(reg) cell-specific TCF-1 deficiency promoted tumor growth.

219 Thus, T(reg) cell-specific TCF-1 expression differentially regulates T(H)17-mediate

220 ECSIT-mediated fumarate synthesis stimulates TCF-1 activity and memory CD8(+) T cell development duri

221 isolated a further member of this subfamily (TCF-1) from zebrafish.

222 In this study, we show that LEF1 and TCF7 (TCF-1) are not only expressed in thymocytes, but also in

223 y, we first identify Socs1, Socs3, and Tcf7 (TCF-1) as gene targets that are negatively regulated by

224 ads to the down-regulation of LEF1 and TCF7 (TCF-1) expression in human naive CD8 T cells.

225 erentially express inhibitory LEF1 and TCF7 (TCF-1) isoforms and that T cell activation changes the i

226 act ILC or NK cell development, GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are

227 soform balance in favor of stimulatory TCF7 (TCF-1) isoforms.

228 Two vertebrate TCFs (TCF-1/TCF7 and TCF-4/TCF7L2) use the C-clamp as an alter

229 We further demonstrated that TCF-1 directly repressed LEF-1 expression in early thymo

230 Therefore, our data demonstrated that TCF-1 enhances DP thymocyte survival through transcripti

231 We found that TCF-1 and GATA3 co-bound to the lineage-defining sites f

232 Unexpectedly, we found that TCF-1-deficient (Tcf7(-/-)) mice developed aggressive T

233 al Tcf7- or Tox-knockout mice highlight that TCF-1 is essential for the memory response generated by

234 These findings indicate that TCF-1 and Foxp3 together limit the expression of pro-inf

235 These data indicate that TCF-1 has a role in controlling global genome organizati

236 Here, we show that TCF-1 primarily suppresses transcription of genes that a

237 We also showed that TCF-1 and LEF-1 were dispensable for T cell lineage comm

238 Here we showed that TCF-1 deficiency limited proliferation of CD8(+) effecto

239 The TCF-1 and LEF-1 transcription factors are known to play

240 The TCF-1-dependent gain in long-range interactions was link

241 ed TCF-1 expression via demethylation of the TCF-1 promoter by the histone demethylase KDM5, thereby

242 Thus, the TCF-1+ CD8 T cell niche in tumors is highly dynamic, wit

243 and specificity for the LEF-1 NLS versus the TCF-1 NLS.

244 Further characterization of these TCF-1-induced cells revealed expression of many T-lineag

245 ex precursor cells, and PD-1 stabilized this TCF-1(+) Tex precursor cell pool.

246 Thus, TCF-1 and LEF-1 adopted distinct genetic 'wiring' to pro

247 Thus, TCF-1 and LEF-1 cooperatively regulate generation of mem

248 Thus, TCF-1 initiates T(H)2 differentiation of activated CD4(+

249 Thus, TCF-1-regulated survival and CD4 expression are two sepa

250 Transfer of the LEF-1 NLS to TCF-1 can confer pendulin/Rch1 binding, demonstrating th

251 Normal colonic epithelia express a truncated TCF-1 form, called dnTCF-1, that lacks the critical beta

252 on of a wild-type TCF-1, but not a truncated TCF-1 that lacks a domain required for interacting with

253 ells by transgenic expression of a wild-type TCF-1, but not a truncated TCF-1 that lacks a domain req

254 nto T(H)1-like cells, but instead upregulate TCF-1 expression and acquire stemness-associated feature

255 Most importantly, when TCF-1 is forcibly expressed in bone marrow (BM) progenit

256 suggest that TCF-4 is Wnt-promoting, whereas TCF-1 acts like a tumor suppressor.

257 provide insight into the mechanisms by which TCF-1 promotes developmental progression of ILC precurso

258 equence showed distinct subregions, in which TCF-1 sites and a conserved element were required for T-

259 ssion of MAF and RORgammat, in parallel with TCF-1-driven modulation of chromatin state.

260 associated with the Eomes allele and the Wnt-TCF-1 pathway was necessary and sufficient for optimal E

261 nt/transcription factor T cell factor 1 (Wnt/TCF-1) and mTORC through GSK3 inhibition to reprogram HI

262 Zebrafish TCF-1 is expressed throughout zebrafish embryonic develo

263 The protein product of zebrafish TCF-1 (zTCF-1), shares sequence similarity with the mamm