ライフサイエンスコーパス: TAL1

1 role of T-cell acute lymphocytic leukemia 1 (TAL1).

2 GATA2) and erythro-megakaryocytic (GATA2 and TAL1).

3 transcription factor stem cell leukemia (SCL/Tal1).

4 ey transcription factors including GATA1 and TAL1.

5 en combined with overexpression of GATA-4 or TAL1.

6 Sirt1 playing a role upstream of GATA-4 and TAL1.

7 ding order) as follows: LDB1 > SSBP > LMO2 > TAL1.

8 nt of those regulated by the GATA factors or TAL1.

9 ss wild-type Tal1 or a DNA-binding mutant of TAL1.

10 ents were occupied by neither GATA-2 nor Scl/TAL1.

11 egulatory loop with the transcription factor TAL1.

12 4,000 locations were bound by both GATA1 and TAL1.

13 three transcription factors: GATA1, FLI1 and TAL1.

14 pisomal reintegration in a single site 5' to TAL1.

15 responses to three TALs expressed in worms (TAL1, -3, and -5) became more prevalent with age.

16 gene regulation of the transcription factor TAL1, a critical regulator of hematopoiesis, at multiple

17 previously unaligned reads corresponding to TAL1, a human TF involved in lineage specification of he

18 sing knockout mice, we study the function of Tal1, a key haematopoietic transcription factor, and dem

19 In this study, we demonstrate that Tal1, a Lyl1-related basic helix-loop-helix transcriptio

20 SCL/TAL1, a tissue-specific transcription factor of the basi

21 d that erythroid master regulators GATA1 and TAL1 act cooperatively within active enhancers but confe

22 e leukemic prone promoter IV interaction for TAL1 activation in T-ALL.

23 mechanistic diversity, the mode of oncogenic TAL1 activation, rather than expression levels, impact o

24 d enhancer/promoter interaction required for TAL1 activation.

25 Dysregulation of TAL1 activity has been associated with T-cell leukemogen

26 ating endocardial extension, suggesting that Tal1 activity influences the behavior of individual endo

27 tream effector of NOTCH1, and preventing SCL/TAL1 activity.

28 we demonstrate that the transcription factor Tal1 (also known as Scl) is indispensable for the establ

29 tical factors that are directly activated by TAL1 and contribute to T-ALL pathogenesis are largely un

30 remains unclear how the interactions between TAL1 and corepressors versus co-activators are properly

31 TRIB2 gene, which is oppositely regulated by TAL1 and E2A/HEB and is essential for the survival of T-

32 ion analysis demonstrated the association of Tal1 and E47, one of its E protein DNA-binding partners,

33 ding the basic helix-loop-helix proteins SCL/TAL1 and E47, the zinc finger protein GATA-1, and LIM-do

34 o erythropoietin with concomitantly elevated TAL1 and EPO-R expression.

35 A link between elevated TAL1 and excessive erythrocytosis is suggested by erythr

36 l alterations in the binding patterns of SCL/TAL1 and FLI1.

37 plex that contains the transcription factors Tal1 and GATA-1, the LIM domain protein Lmo2, and Ldb1 a

38 We show that TAL1 and GATA1 form a precisely organized complex at a c

39 Both TAL1 and GATA1 generated distinct characteristic ChIP-ex

40 LR, Fcgamma and SIGLEC receptors, as well as TAL1 and IFI16, regulators of proliferation and cell cyc

41 The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the

42 id-important transcription factors Gata1 and Tal1 and is essential for terminal erythropoiesis.

43 We found that TAL1 and its heterodimerization partner E47 regulate miR

44 ified the miRNA genes directly controlled by TAL1 and its regulatory partners HEB, E2A, LMO1/2, GATA3

45 scriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1/2, GATA3

46 RID5B positively regulates the expression of TAL1 and its regulatory partners.

47 pre-LSCs, which were induced here by the SCL/TAL1 and LMO1 oncogenes.

48 /LDB1 complex is observed in human T-ALL and Tal1 and Lmo2 expression in mice results in disease acce

49 Thymic expression of the Tal1 and Lmo2 oncogenes in mice results in rapid develop

50 y reveal a basis for the unique functions of Tal1 and Lyl1 in T acute lymphoblastic leukemia.

51 These findings redefine how TAL1 and neighboring genes communicate within the nucleu

52 fically, we identify UTX as a coactivator of TAL1 and show that it acts as a major regulator of the T

53 d, intriguingly, loops occurring between the TAL1 and STIL genes at the common TAL1/STIL breakpoints

54 ion of GATA-4 and the basic helix-loop-helix TAL1 and that knockdown of both factors promotes differe

55 t disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important ste

56 emia (T-ALL), often due to deletions between TAL1 and the neighboring STIL gene.

57 em cell enhancer located 19 Kb downstream of TAL1 and this interaction is disrupted by the -31CBS inv

58 derexpression of leukemia-associated (MLLT3, TAL1) and erythropoiesis-associated (GATA3, EPOR, ANK1,

59 Runx1, Scl (Tal1) and Hhex expression is upregulated within 3 hours

60 Numerous TFs, including Scl (Tal1) and PU.1 (Spi1), are known regulators of developme

61 regulators of hematopoiesis (GATA-1 and Scl/TAL1) and the non-DNA binding components ETO2, the LIM d

62 of the endothelium is known to require SCL (TAL1), and an SCL-E12 (SCL-Tcfe2a) heterodimer can bind

63 T cell acute lymphocytic leukemia 1 protein (Tal1), and Erythroid Kruppel-like factor (EKLF; hencefor

64 tose phosphate pathway enzyme transaldolase (TAL1), and the transcription factor vitamin H response t

65 poietic transcription factors (GATA1, GATA2, TAL1, and FLI1) and three diagnostic histone modificatio

66 A-binding complex containing LMO2, LDB1, SCL/TAL1, and GATA-1.

67 m of cloche and the transcription factor Scl/Tal1, and is maintained by Hedgehog and vascular endothe

68 ing strong functional synergy between Gata1, Tal1, and Klf1.

69 ineage-specific transcription factors Gata1, Tal1, and Klf1.

70 TA1-occupied segments that are also bound by TAL1, and show evolutionary constraint on the GATA1-bind

71 These data suggest that GATA-4, TAL1, and Sirt1 cross-talk each other to regulate myogen

72 alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and

73 and GATA-2 function combinatorially with Scl/TAL1, another key regulator of hematopoiesis.

74 How GATA1 and TAL1 are juxtaposed along the DNA and their cognate DNA

75 Genes flanking TAL1 are partly dependent on hub integrity for their tra

76 entified binding of the transcription factor TAL1 as a potential mediator of the increased expression

77 ith the dual roles of TAL1 in transcription, TAL1-associated LSD1 is decreased while recruitment of h

78 Furthermore, we demonstrate that the TAL1-associated LSD1, HDAC1, and their enzymatic activit

79 n and suggest that the dynamic regulation of TAL1-associated LSD1/HDAC1 complex may determine the ons

80 tors appears to be a stronger determinant of TAL1 binding to chromatin than the canonical E-box bindi

81 These data suggest that TAL1 binds to the EPO-R promoter to activate EPO-R expre

82 ining the EPO-R transcription start site and TAL1 binds to the flanking 5' GATA and 3' E-box regions

83 fic regions of open chromatin pinpointed two TAL1-bound endothelial enhancers, which we validated usi

84 shifting has been demonstrated to facilitate TAL1 but not GATA-1 binding to regulate target gene expr

85 shifting specifically facilitates binding of TAL1 but not GATA1 and is linked to subsequent transcrip

86 Finally, wild-type Tal1, but not a DNA binding-defective mutant, rescued th

87 Gata1 and Tal1 can assemble within higher-order protein complexes

88 Yet, over half of the TAL1(+) cases lack TAL1 lesions, suggesting unrecognized

89 e, we use single-cell profiling to show that Tal1(-/-) chimeric embryos display defects in early meso

90 ings into close physical proximity all known TAL1 cis-regulatory elements including CTCF-bound insula

91 The TAL1 complex coordinately regulates the expression of AR

92 atory loop with GATA3 and RUNX1 and that the TAL1 complex directly activates the MYB oncogene, formin

93 ormal thymocytes, while it is induced by the TAL1 complex in human T-ALL cells.

94 the same amino acid can selectively inhibit TAL1 complex or FOG1 binding, producing distinct cellula

95 Diminished TAL1 complex recruitment mainly impairs transcriptional

96 ALL, deacetylated LMO2 induces expression of TAL1 complex target genes HHEX and NKX3.1 as well as LMO

97 loci encoding multiple components of the Scl/TAL1 complex, a master regulator of hematopoiesis and le

98 ather, one of these disrupted binding to the TAL1 complex, implicating it in diseases caused by GATA1

99 ocess that depends on gene activation by the TAL1 complex.

100 ound at its promoter and up-regulated by the TAL1 complex.

101 t with LIM domain binding 1 and activate the TAL1 complex.

102 Scl/Tal1 confers hemogenic competence and prevents ectopic c

103 y erythroid transcription factors, GATA1 and TAL1, cooperate, along with other proteins, to regulate

104 Consistent with the rapid changes of TAL1-corepressor complex during differentiation, TAL1 re

105 The defects in endocardial behavior in tal1-deficient embryos originate during the earliest ste

106 earliest steps of endocardial morphogenesis: tal1-deficient endocardial cells fail to generate a cohe

107 r time, a progressively increasing number of tal1-deficient endocardial cells initiate myocardial gen

108 In addition, we find that the tal1-deficient endocardium fails to maintain its identit

109 junction protein ZO-1 is mislocalized in the tal1-deficient endocardium, indicating a defect in inter

110 of ectopic myocardial gene expression in the tal1-deficient endocardium.

111 The sequence responsible for Tal1 degradation was localized to a region in the C term

112 biquitination and degradation, CHIP promoted Tal1 degradation with both chaperone binding and ubiquit

113 own double- or single-E-box binding factors (TAL1, deltaEF1, E2A, HEB, etc.) failed to identify this

114 egulated T-ALL, and PIK3R1/PTEN mutations in TAL1 deregulated ALL, which suggests that different sign

115 D1 plays an important role in repressing the TAL1-directed transcription of GAL4 reporter linked to a

116 with T cell acute lymphoblastic leukemia 1 (TAL1), directly activates AURKB transcription, constitut

117 The GATA1 coregulators FOG1 and TAL1 dissociate from mitotic chromatin, suggesting that

118 ighly sensitive to BCL-2 inhibition, whereas TAL1 driven tumors mostly showed poor ABT-199 responses.

119 leading to inhibition of TAL1 expression and TAL1-driven leukemogenesis.

120 transcriptional complex consisting of LMO2, TAL1, E47, GATA1 and LDB1 that recognizes bipartite E-bo

121 Similarly, a TAL1/E47/LMO2/LDB1 complex is observed in human T-ALL an

122 tube formation: in zebrafish embryos lacking Tal1, endocardial cells form a disorganized mass within

123 In TAL1-expressing erythroid cells, the locus adopts a loop

124 We identified looping patterns unique to TAL1-expressing T-ALL cells, and, intriguingly, loops oc

125 However, in TAL1-expressing T-ALL cells, the leukemia-prone TAL1 pro

126 a to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplant

127 looping facilitates both normal and aberrant TAL1 expression and may predispose to structural rearran

128 d CTCF-mediated TAD leading to inhibition of TAL1 expression and TAL1-driven leukemogenesis.

129 nd molecular consequences of inactivation of Tal1 expression ex vivo.

130 Deleted or inverted -31CBS impairs TAL1 expression in a context-dependent manner.

131 and TAL1 promoter-1 leading to inhibition of TAL1 expression in erythroid cells, but not T-ALL cells.

132 To better understand the events that lead to TAL1 expression in hematopoiesis and in T-ALL, we studie

133 ATA-4 binds to the TAL1 promoter to regulate TAL1 expression positively.

134 Sirt1 knockdown reduced GATA-4 and TAL1 expression, impaired EPO effect on delayed myogenic

135 ruvate carboxykinase (encoded by ICL1, MAS1, TAL1, FBP1, and PCK1 respectively), suggestive of increa

136 ic transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members.

137 ence of RUNX1, haematopoietic genes bind SCL/TAL1, FLI1 and C/EBPbeta and that this early priming is

138 ed transcription factor heptad (GATA2, LYL1, TAL1, FLI1, ERG, RUNX1, LMO2) binding to MEG-associated

139 Comparison of Lmo2-/- with Tal1-/- Flk-1+ cells further showed that TAL1 was requir

140 We show that TAL1 forms a positive interconnected autoregulatory loop

141 ARID5B and TAL1 frequently co-occupy target genes and coordinately

142 tory shear stress, the transcription factors Tal1, Gata2, and Ets1/2 physically interacted with and r

143 The Scl (Tal1) gene encodes a helix-loop-helix transcription fact

144 We therefore propose a model in which Tal1 has distinct roles in regulating the formation of e

145 ATA-1 target genes, that the presence of SCL/TAL1 helps distinguish transcriptional activation versus

146 cases generally lacked overexpression of the TAL1, HOX11, HOX11L2, or the HOXA cluster genes, which h

147 has implicated the bHLH transcription factor Tal1 in endocardial tube formation: in zebrafish embryos

148 a-globin genes, we reduced the expression of TAL1 in erythroid K562 cells using lentiviral short hair

149 h insights into the context-specific role of TAL1 in erythropoiesis.

150 To explore the role of TAL1 in transcription activation of the human gamma-glob

151 Consistent with the dual roles of TAL1 in transcription, TAL1-associated LSD1 is decreased

152 r binding of LMO2 to its partner protein SCL/TAL1 in vitro and for the function of this complex in vi

153 In addition, overexpression of TAL1 increased the gamma-globin transcription and increa

154 TAL1 increases association of the GATA-1.TAL1.LMO2.LDB1

155 ptional program by positively regulating the TAL1-induced regulatory circuit and MYC in T-ALL, thereb

156 of ARID5B, thereby positively regulating the TAL1-induced transcriptional program and the MYC oncogen

157 r and represses myogenin expression, whereas TAL1 inhibits myogenin expression by decreasing MyoD bin

158 activity in vivo, we treated near-end-stage Tal1/Ink4a/Arf+/- leukemic mice with vehicle or with a G

159 e A (PKA)-mediated phosphorylation regulates TAL1 interaction with the lysine-specific demethylase (L

160 The human oncogene SCL/TAL1 interrupting locus (Stil) is highly conserved in ve

161 Here, we demonstrate that the SCL/TAL1 interrupting locus (STIL) protein interacts via its

162 that nbb is a homolog of the vertebrate SCL/TAL1 interrupting locus (Stil).

163 f mRNA for polo-like kinase 4 (Plk4) and SCL/Tal1-interrupting locus gene (Stil), key regulators of c

164 TAL1 is a critical transcription factor required for hem

165 nd CRISPR/Cas9 genome editing, we found that Tal1 is a direct NANOG target.

166 TAL1 is a key hematopoietic transcription factor that bi

167 TAL1 is amongst the most frequently deregulated oncogene

168 TAL1 is an important regulator of hematopoiesis and its

169 Here, we show that TAL1 is associated with histone demethylase complexes co

170 Aberrant activation of the TAL1 is associated with up to 60% of T-ALL cases and is

171 We show that transcription factor Scl/Tal1 is essential for both establishing the hematopoieti

172 ence of LMO2, the target site recognition of TAL1 is impaired.

173 trate that aberrant miR-223 up-regulation by TAL1 is important for optimal growth of TAL1-positive T-

174 Here we show that TAL1 is normally silenced in the T-cell lineage, and tha

175 demonstrate that the DNA-binding activity of Tal1 is not required to cooperate with Lmo2 to cause leu

176 (LCR) and active globin genes, and although TAL1 is one of the two DNA-binding complex members, its

177 ession of the oncogenic transcription factor TAL1 is uniquely sensitive to variations in the dosage a

178 ription factor (TF) stem cell leukaemia (Scl/Tal1) is crucial for development of these adult haemangi

179 gulator T-cell acute lymphocytic leukemia-1 (TAL1) is involved in regulating H3K27me3 variations in c

180 nal complex that contains RUNX1, GATA-3, and TAL1 itself.

181 In the TAL1 knockdown cells, the gamma-globin transcription was

182 miR-223 partially rescues T-ALL cells after TAL1 knockdown.

183 s performed using retrospective assays, that Tal1 knockout does not immediately bias precursor cells

184 While Tal1 knockout had minimal effects on cell survival and s

185 ap with the interactomes of GATA1, GATA2, or TAL1, leading to a model in which EKLF directs programs

186 XW7 protein expression, whereas knockdown of TAL1 leads to up-regulation of FBXW7 protein levels, wit

187 Yet, over half of the TAL1(+) cases lack TAL1 lesions, suggesting unrecognized (epi)genetic dereg

188 how that it acts as a major regulator of the TAL1 leukemic gene expression program.

189 miR-223 expression mirrors TAL1 levels during thymic development, with high express

190 We demonstrate that Tal1 limits the expression of multiple E2A target genes

191 tial haematopoietic regulators including Scl/Tal1, Lmo2 and PU.1.

192 sion by an enhancer complex including GATA1, TAL1, LMO2, LDB1 and Pol II at least, in erythroid cells

193 the use of tiling arrays we detected the SCL/TAL1, LMO2, Ldb1, E2A complex at all positively acting G

194 TAL1 increases association of the GATA-1.TAL1.LMO2.LDB1 transcription activation complex to the r

195 Tal1/Lmo2 and MutTAL1/Lmo2 bitransgenic mice exhibit per

196 The Ldb1/GATA-1/TAL1/LMO2 complex mediates long-range interaction betwee

197 cells indicate that LDB1, as part of a GATA1/TAL1/LMO2 complex, brings erythroid-expressed genes into

198 To address the mechanism(s) of Tal1/Lmo2 synergy in leukemia, we generated Lmo2 transge

199 into direct gene contact by the LDB1/GATA-1/TAL1/LMO2-containing complex.

200 at the haemangioblast stage to position the TAL1/LMO2/LDB1 complex to regulatory elements that are i

201 function(s) in leukemogenesis, we generated Tal1/Lmo2/Rosa26-CreER(T2)Runx1(f/f) mice and examined l

202 mately 10,000 GATA1 and approximately 15,000 TAL1 locations, which were essentially confirmed by ChIP

203 CTCF-mediated genome organization within the TAL1 locus, suggesting that CTCF boundary plays a pathog

204 -ALL, we studied looping interactions at the TAL1 locus.

205 ne 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermeth

206 TAL1, LYL1, HOX11 and other transcription factors essent

207 el interplay between PKA phosphorylation and TAL1-mediated epigenetic regulation that regulates hemat

208 ine demethylase LSD1 may negatively regulate TAL1-mediated transcription and suggest that the dynamic

209 We conclude that TAL1-mediated up-regulation of miR-223 promotes the mali

210 ukemia maintenance in TAL1-positive (but not TAL1-negative) T-ALL.

211 mutant, rescued the proliferative defect in Tal1-null MM precursors.

212 ccupied segments, and a subset shows reduced TAL1 occupancy and increased H3K27me3 at the transcripti

213 TAL1, together with genome-wide analysis of TAL1 occupancy by chromatin immunoprecipitation coupled

214 Furthermore, shifts in TAL1 occupancy during erythroid differentiation are asso

215 ristic molecular hallmarks, specifically Scl/TAL1 occupancy, a specific epigenetic signature, specifi

216 Genes near the GATA-2-Scl/TAL1-occupied composite elements were regulated by GATA-

217 tronic variant predicted to cis-activate the TAL1 oncogene, a finding validated in vivo by chromatin

218 ich creates a super-enhancer upstream of the TAL1 oncogene.

219 mated them with mice that express wild-type Tal1 or a DNA-binding mutant of TAL1.

220 LDB1, E2A, HEB, Lyl1, ETO2, and SP1, but not TAL1 or GATA proteins.

221 ate with the TALLMO subtype characterized by TAL1 or LMO2 rearrangements.

222 Knockdown of TAL1 or LSD1 led to a derepression of the TAL1 target ge

223 topoietic basic helix-loop-helix factors Scl/Tal1 or Lyl1.

224 y key erythroid transcription factors GATA1, TAL1, or KLF1.

225 Sequencing reveals that >20% of monoallelic TAL1(+) patients without previously known alterations di

226 ugh blastomere transplantation, we find that tal1 plays a cell-autonomous role in regulating endocard

227 These results indicate that TAL1 plays a critical role in chromatin loop formation b

228 factor essential for leukemia maintenance in TAL1-positive (but not TAL1-negative) T-ALL.

229 demethylase inhibitor that efficiently kills TAL1-positive primary human leukemia.

230 cursor, HOXA-positive, LEF1-inactivated, and TAL1-positive subtypes, which have differentiation arres

231 n by TAL1 is important for optimal growth of TAL1-positive T-ALL cells and that sustained expression

232 During organogenesis of the kidney, SCL/Tal1(+) progenitors gave rise to endothelium and blood p

233 Overall, these results show that SCL/Tal1(+) progenitors with hemogenic capacity originate an

234 te GATA-4 expression and GATA-4 binds to the TAL1 promoter to regulate TAL1 expression positively.

235 ction between the +51 erythroid enhancer and TAL1 promoter-1 leading to inhibition of TAL1 expression

236 1-expressing T-ALL cells, the leukemia-prone TAL1 promoter-IV specifically interacts with the +19 ste

237 O-R transcription start site suggesting that TAL1 promotes accessibility of this region.

238 The stem cell leukemia (Scl or Tal1) protein forms part of a multimeric transcription f

239 -Seq indicates that most DNA-bound Gata1 and Tal1 proteins are contained within higher order complexe

240 trolled by HLH inhibitors such as Id and SCL/TAL1 proteins, which recently have been suggested to pla

241 Primary and secondary xenotransplantation of TAL1-rearranged leukemia allowed development of leukemic

242 -corepressor complex during differentiation, TAL1 recruits LSD1 to the silenced p4.2 promoter in undi

243 progenitor cells, while the USF proteins and Tal1 regulate genes that specify the differentiated phen

244 tory loop that reinforces and stabilizes the TAL1-regulated oncogenic program.

245 We found that TAL1 regulates EPO-R expression mediated via three conse

246 f additional proteins lead to the model that TAL1 regulates expression after being directed to a dist

247 The oncogenic transcription factor TAL1 regulates the transcriptional program in T-ALL.

248 echanisms may facilitate the conservation of TAL1 regulation despite cis-regulatory remodeling during

249 TAL3 IgE responders, themselves a subset of TAL1 responders.

250 initial wave of mesoderm, Mesp1 binds to the Tal1 (Scl) +40 kb enhancer and generates Flk-1+ precurso

251 ignaling also accelerated the degradation of Tal1/SCL (T cell acute leukemia 1/stem cell leukemia) pr

252 ligase activity of CHIP was dispensable for Tal1/SCL binding but essential for degradation.

253 Although the TPR domain was not involved in Tal1/SCL binding, it was required for enhancing its degr

254 gous to the situation for E47, Notch-induced Tal1/SCL degradation not only required Skp2, a substrate

255 Notch-induced Tal1/SCL degradation was mediated by ubiquitination and

256 The oncogenic transcription factor TAL1/SCL induces an aberrant transcriptional program in

257 TAL1/SCL is a hematopoietic-specific oncogene and its ac

258 The oncogenic transcription factor TAL1/SCL is aberrantly expressed in 60% of cases of huma

259 The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of

260 basic helix-loop-helix transcription factor TAL1/SCL plays a critical role in other hematopoietic li

261 lexes and potential means by which Notch and Tal1/SCL regulate eukaryotic development.

262 les include comparative DHS mapping of known TAL1/SCL regulatory elements between human embryonic ste

263 basic helix-loop-helix transcription factor, TAL1/SCL, is required for normal erythropoiesis.

264 largely caused by aberrant activation of the TAL1/SCL, LMO1/2, and NOTCH1 oncogenes.

265 tion factors--GATA1, GATA2, RUNX1, FLI1, and TAL1/SCL--in primary human megakaryocytes.

266 elements with the blood stem cell regulator TAL1/SCL.

267 hematopoiesis-specific transcription factor Tal1/SCL.

268 ells expressing hemangioblast markers (Flk1, Tal1/Scl1, platelet endothelial cell adhesion molecule 1

269 regulator of hematopoiesis, SCL (also called TAL1), Snai1 and Snai2.

270 Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction

271 SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leuk

272 etween the TAL1 and STIL genes at the common TAL1/STIL breakpoints found in T-ALL.

273 specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer

274 a MYB interaction with an 18-bp indel in the TAL1 superenhancer.

275 ated that ARIEL is specifically activated in TAL1 (+) T-ALL cases, and its expression is associated w

276 me3-repressive mark is focally diminished in TAL1(+) T-ALLs.

277 Manipulation of CTCF boundary can alter TAL1 TAD and oncogenic transcription networks in leukemo

278 in MEL cells resulted in derepression of the TAL1 target gene accompanied by increasing dimeH3K4 at t

279 of TAL1 or LSD1 led to a derepression of the TAL1 target genes in T-cell acute lymphoblast leukemia (

280 ile recruitment of hSET1 is increased at the TAL1 targets during erythroid differentiation.

281 Flk-1+ precursors expressing Etv2 (ER71) and Tal1 that undergo hematopoietic differentiation.

282 eveal that it functions upstream of etv2 and tal1, the earliest expressed endothelial and haematopoie

283 y by an enhancer of Gata2 transcription, Scl/TAL1, thereby repressing Gata2 transcription.

284 findings reveal a novel role for GATA-4 and TAL1 to affect skeletal myogenic differentiation and EPO

285 ice and suggest that Lmo2 may cooperate with Tal1 to interfere with E47/HEB function(s).

286 through de novo recruitment of the activator TAL1 to promote chromatin looping of distal enhancers to

287 sively parallel DNA sequencing) to GATA1 and TAL1 to study their positional organization across the m

288 the tegumental-allergen-like protein family (TAL1 to TAL13).

289 RNA) expression profiling after depletion of TAL1, together with genome-wide analysis of TAL1 occupan

290 ncer (Samd14-Enh), occupied by GATA2 and SCL/TAL1 transcription factors, reduces SAMD14 expression in

291 or LIM domain only 2 (LMO2), a member of the TAL1 transcriptional complex, plays an essential role du

292 directly leads to decreased stability of the TAL1 transcriptional complex.

293 Translocations involving LMO2, TAL1, Ttg-1, and Hox11, as well as a recurrent interstit

294 ove background levels in cell culture (LMO2, TAL1, Ttg-1, and SIL) are also cleaved by the RAG protei

295 ith Tal1-/- Flk-1+ cells further showed that TAL1 was required to initiate or sustain Lmo2 expression

296 SOX18 and TAL1 were the strongest EC barrier-inducing TFs, upregul

297 completely abrogated binding of the cofactor TAL1, which binds to a separate motif.

298 is one of the critical downstream targets of TAL1, which further activates the oncogenic regulatory c

299 s localized to a region in the C terminus of Tal1, which is evolutionarily conserved, thus suggesting

300 adigm, one would predict that GATA-2 and Scl/TAL1 would commonly co-occupy such composite elements in