ライフサイエンスコーパス: RUNX1

1 PCTP is a direct transcriptional target of RUNX1.

2 ding in gel shift assay similar to wild-type Runx1.

3 essing the myeloid differentiation regulator RUNX1.

4 cells, indicating that PCTP is regulated by RUNX1.

5 rate amplitude-control function dependent on Runx1, a factor already present in multipotent progenito

6 Haplodeficiency of RUNX1, a major hematopoietic transcription factor, is as

7 samples with FLT3-ITD express high levels of RUNX1, a transcription factor with known tumor-suppresso

8 Direct interaction of HIRA and RUNX1 activates the downstream targets of RUNX1 implicat

9 These PTMs regulate RUNX1 activity either positively or negatively by alteri

10 the transcription factor RUNX1, deregulates RUNX1 activity in hematopoiesis, and induces AML.

11 Numerous studies have shown that RUNX1 activity is regulated by PTMs, including phosphory

12 Three mechanisms contribute to increased Runx1 activity upon tyrosine modification as follows: in

13 We predict that blocking RUNX1 activity will greatly enhance current therapeutic

14 Inhibition of RUNX1 activity with the Ro5-3335 small molecule resulted

15 FLT3-ITD directly impacts on RUNX1 activity, whereby up-regulated and phosphorylated

16 Reactivation of RUNX1 allowed exit from the bipotent state and subsequen

17 o new provisional entities, AML with mutated RUNX1 and AML with BCR- ABL1, have been included in the

18 rget genes strongly overlapped with those of RUNX1 and AML1-ETO and ASXL2 loss was associated with in

19 ity of its product to regulate genes such as RUNX1 and APOB.

20 onstrate an ER-dependent correlation between RUNX1 and AXIN1 in tumour biopsies.

21 matopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally distant lin

22 oiesis), as shown by decreased expression of runx1 and c-myb However, adtrp1 knockdown does not affec

23 at CHD7 enhanced transcriptional activity of RUNX1 and CBFbeta-SMMHC on Csf1r, a RUNX1 target gene.

24 RUNX1 and ER occupy adjacent elements in AXIN1's second

25 g induces transcription and translocation of RUNX1 and ETO fusion gene partners, opening a novel wind

26 reciprocal translocation t(8;21) that fuses RUNX1 and ETO genes.

27 g T cell gene expression programs is whether RUNX1 and ETS1 have independent functions in enhancer ac

28 tent progenitors to T lineage transition are RUNX1 and ETS1, which bind cooperatively to composite si

29 this paradox, we investigated the impact of RUNX1 and FLT3-ITD coexpression.

30 We identified Hhex as a direct target of RUNX1 and FLT3-ITD stimulation and confirmed high HHEX e

31 establish that SOX7 directly interacts with RUNX1 and inhibits its transcriptional activity.

32 A binding as well as the interaction between RUNX1 and its co-factor CBFbeta.

33 raaortic hematopoietic clusters that express Runx1 and Kit, but these clusters undergo apoptosis and

34 nstrate combinatorial regulation of AXIN1 by RUNX1 and oestrogen.

35 Our experiments reveal a novel function of RUNX1 and offer an explanation for the link between RUNX

36 We assessed the relationship between RUNX1 and PCTP in peripheral blood RNA and PCTP and deat

37 on factors (ERG, HOXA5, HOXA9, HOXA10, LCOR, RUNX1 and SPI1) that are sufficient to convert haemogeni

38 DNA-binding protein-7 (CHD7) interacts with RUNX1 and suppresses RUNX1-induced expansion of hematopo

39 t CHD7 interacted with CBFbeta-SMMHC through RUNX1 and that CHD7 enhanced transcriptional activity of

40 ued the hypothesis that PCTP is regulated by RUNX1 and that PCTP expression is correlated with cardio

41 four novel associations at LOC144817, COG6, RUNX1 and TP63, as well as three novel secondary associa

42 lthough runt-related transcription factor 1 (RUNX1) and its associating core binding factor-beta (CBF

43 expressed in HSPC downstream from Notch1 and runx1, and loss of Dnmt3bb.1 activity leads to reduced c

44 nscription-factor-encoding genes Fosb, Gfi1, Runx1, and Spi1 (collectively denoted hereafter as FGRS)

45 genes include HuR for miR-139-3p and Prdx6, Runx1, and Suz12 for miR-199a-3p.

46 The impact of ASXL1, RUNX1, and TP53 mutations on posttransplantation surviva

47 Somatic mutations of ASXL1, RUNX1, and TP53 were independent predictors of relapse a

48 acent elements in AXIN1's second intron, and RUNX1 antagonizes oestrogen-mediated AXIN1 suppression.

49 ce that RUNX1 has oncogenic roles and reveal RUNX1 as a novel therapeutic target in T-ALL.

50 Our data identified Runx1 as a novel therapeutic target with translational p

51 model of tissue morphogenesis and identified RUNX1 as a stem cell regulator.

52 ntified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31(+) vascular endothe

53 lasms and AML, and mutations in three genes- RUNX1, ASXL1, and TP53-have been added in the risk strat

54 us both repressor and activator functions of Runx1 at multiple hematopoietic stages and lineages like

55 We expect that the HIRA-RUNX1 axis might open up a novel approach in understandi

56 DNA-protein binding studies showed RUNX1 binding to consensus sites in approximately 1 kB o

57 We studied RUNX1 binding to the PCTP promoter using DNA-protein bin

58 ly, loss of Nf1 increased embryonic day 12.5 Runx1(+)/Blbp(+) progenitors that enable tumor formation

59 diting, ATAC-seq and ChIP-seq, that specific Runx1-bound enhancer elements critically modulate lineag

60 Mutation of the four Runx1 C-terminal tyrosines to aspartate or glutamate to

61 sized that the childhood affiliation of ETV6-RUNX1 cALL reflects its origins in a progenitor unique t

62 As few ETV6-RUNX1 carriers develop precursor B-cell acute lymphocyti

63 s was detected in 67% of young, asymptomatic RUNX1 carriers, providing a potential biomarker that cou

64 Mutations in mouse and human Nfe2, Fli1 and Runx1 cause thrombocytopenia.

65 Similar to the effect of Runx1/Cbfb deletion, PAR-1 overexpression induced CDKN1A

66 We recently showed that the combined loss of Runx1/Cbfb inhibited the development of MLL-AF9-induced

67 r, c-Kit(+)/Gr-1(-) cells remained viable in Runx1/Cbfb-deleted cells, indicating that suppressing RU

68 or PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted MLL-AF9 cells.

69 We show that the integrity of a Runx1/CBFbeta holocomplex is crucial for NGF-dependent n

70 acological inhibition of Runx1 function by a Runx1/Cbfbeta interaction inhibitor, Ro5-3335, decreased

71 Peripheral naive CD4(+) T cells from CD4-cre Runx1 cKO mice are phenotypically and functionally immat

72 loss of peripheral CD4(+) T cells in CD4-cre Runx1 cKO mice is not due to defects in homeostasis or d

73 PLZF-cre Runx1 cKO mice lack iNKT17 cells in the thymus, spleen a

74 Elevated adenosine levels increased runx1(+)/cmyb(+) HSPCs in the dorsal aorta, whereas bloc

75 r cell (HSPC) fate as part of an early Notch-runx1-cmyb HSPC specification pathway in the zebrafish.

76 In our model, ETV6-RUNX1 conferred a low risk of developing pB-ALL after ex

77 vity, and RHD-defective (K83N, N109D) mutant RUNX1 conferred resistance to ionizing radiation when ov

78 indels harbor putative de novo MYB, ETS1, or RUNX1 consensus binding sites.

79 ity, whereby up-regulated and phosphorylated RUNX1 cooperates with FLT3-ITD to induce AML.

80 phic factor NGF and the transcription factor Runx1 coordinate postmitotic differentiation of nonpepti

81 We demonstrate that a RUNX1 deficiency alters the expression of a crucial subs

82 Rather, immature Runx1-deficient CD4(+) T cells are eliminated in the per

83 Runx1-deficient granulocyte-macrophage progenitors are c

84 Here we show, counterintuitively, that Runx1-deficient hematopoietic stem and progenitor cells

85 resistance provides a selective advantage to Runx1-deficient HSPCs, allowing them to expand in the bo

86 Runx1-deficient iNKT cells have altered expression of se

87 oplasmic reticulum Ca(2+)-ATPase activity in Runx1-deficient mice increased sarcoplasmic reticulum ca

88 Runx1-deficient mice were protected against adverse card

89 expressing Meg markers was also increased in Runx1-deficient mice.

90 l tamoxifen-inducible cardiomyocyte-specific Runx1-deficient mouse.

91 se Cebpa and granulocyte colony formation by Runx1-deleted murine marrow.

92 We found that Runx1 deletion inhibits mouse leukemic growth in vivo an

93 required for lung cancer progression via the RUNX1-dependent CK1alpha repression, which activates TCF

94 l carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-like growth fac

95 are sequentially up-regulated in response to RUNX1 depletion, and their mutual interaction causes the

96 beta for binding to the transcription factor RUNX1, deregulates RUNX1 activity in hematopoiesis, and

97 sion of the RUNX1 promoter and the relief of RUNX1-directed growth repression.

98 interaction we demonstrate that SOX7 hinders RUNX1 DNA binding as well as the interaction between RUN

99 ents coupled with transcriptome analysis and Runx1 DNA-binding assays demonstrated that granulocytic/

100 Affinity for CBFbeta, the Runx1 DNA-binding partner, was not affected by these tyr

101 We also find that a RUNX1 domain, termed the negative regulatory domain for

102 Altogether, RUNX1 dosage could explain the differential phenotype ac

103 However, the regulation of RUNX1 during this developmental process is poorly unders

104 embryonic stem cells expressing an inducible RUNX1-ETO gene into blood cells as a model, combined wit

105 with a negative correlation in blood between RUNX1 expressed from the P1 promoter and PCTP expression

106 oform in adult hematopoiesis, present in all RUNX1-expressing populations, including the cKit(+) hema

107 the reuptake inhibitor fluoxetine increased runx1 expression and Flk1(+)/cMyb(+) HSPCs independent o

108 via the Notch pathway to fine tune RUNX3 and RUNX1 expression and manipulate B-cell growth.

109 Genetic inhibition of Runx1 expression by small hairpin RNA or pharmacological

110 Studies in 2 cohorts of patients showed that RUNX1 expression in blood correlated with PCTP gene expr

111 (-139 to -250 kb) that results in low-level RUNX1 expression in cells refractory to RUNX1-mediated g

112 mechanistically connecting preleukemic ETV6-RUNX1 expression in hematopoetic stem cells/precursor ce

113 RUNX1 expression is known to initiate at 2 alternative p

114 arget genes in HE, while having no effect on RUNX1 expression itself.

115 dothelial cells, which results in endogenous Runx1 expression.

116 l aorta that is in turn required to initiate runx1 expression.

117 cells and was associated with an increase in RUNX1 expression; the blockade was overcome by a RUNX1 i

118 esis, we generated Tal1/Lmo2/Rosa26-CreER(T2)Runx1(f/f) mice and examined leukemia progression in the

119 During the specification phase (days 8-20), RUNX1(+) FGRS-transduced endothelial cells commit to a h

120 , while enhancers that bind NF-E2 and either RUNX1, FLI1 or both TFs gave the highest signals for TF

121 Genome-engineered hPSCs expressing ETV6-RUNX1 from the endogenous ETV6 locus show expansion of t

122 hairpin RNA or pharmacological inhibition of Runx1 function by a Runx1/Cbfbeta interaction inhibitor,

123 1 neurofibroma initiation, and inhibition of RUNX1 function might provide a novel potential therapeut

124 To elucidate RUNX1 function(s) in leukemogenesis, we generated Tal1/L

125 utations of RUNX3 T173 and its equivalent in RUNX1 further corroborate the role of RUNX phosphorylati

126 gh-hyperdiploid and higher frequency in ETV6-RUNX1 fusion ALL.

127 Based on 1382 pre-B-ALL patients, the ETV6-RUNX1 fusion positive patients had over ten-fold elevati

128 Disrupting mutations of the RUNX1 gene are found in 10% of patients with myelodyspla

129 Mutations in the RUNX1 gene have been associated with chemotherapy resist

130 Mechanistically, p53 induced by RUNX1 gene silencing directly binds to CBFB promoter and

131 re associated with common aberrations in the RUNX1 gene.

132 These results suggest that Runx1 has an important role in Nf1 neurofibroma initiati

133 RUNX1 has been proposed to have tumor suppressor roles i

134 The transcription factor Runx1 has essential roles throughout hematopoiesis.

135 l roles in leukemogenesis, and inhibition of RUNX1 has now been widely recognized as a novel strategy

136 vide genetic and pharmacologic evidence that RUNX1 has oncogenic roles and reveal RUNX1 as a novel th

137 Expression of aortic runx1 has served as an early marker of HSC commitment in

138 creasing variant allele frequency in K/NRAS, RUNX1, IDH2, or NPM1 associated with progression in 7 pa

139 nd RUNX1 activates the downstream targets of RUNX1 implicated in generation of hematopoietic stem cel

140 thy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis.

141 nding sites and ChIP-seq implicated FLI1 and RUNX1 in activation of late MK, including NF-E2-dependen

142 date the unanticipated oncogenic function of RUNX1 in AML.

143 HHEX could replace RUNX1 in cooperating with FLT3-ITD to induce AML.

144 Thus, we describe a novel role of Runx1 in iNKT cell development and differentiation, part

145 orks with prognostic associations, including RUNX1 in kidney cancer.

146 In contrast, transcriptional initiation of Runx1 in nonpeptidergic nociceptor precursors is depende

147 Targeted genetic deletion of Runx1 in SCs and SCPs delayed mouse neurofibroma formati

148 ent studies also highlight the importance of RUNX1 in solid tumors both as a tumor promoter and a sup

149 Thus, we have defined independent roles for RUNX1 in the activation of a T cell developmental enhanc

150 us particularly on the biological effects of Runx1 in the generation of hematopoietic stem cells.

151 es after MI; however, the functional role of Runx1 in the heart is unknown.

152 The requirement for Runx1 in the normal hematopoietic development and its dy

153 ed a novel molecular complex between FAK and Runx1 in the nucleus of SCC cells and showed that FAK in

154 icantly contributes toward the regulation of RUNX1 in the transition of differentiating mouse embryon

155 Inactivating RUNX1 in tumors releases the differentiation block and d

156 n the context- and dosage-dependent roles of RUNX1 in various types of neoplasms.

157 re, by depleting mammary epithelial cells of RUNX1 in vivo and in vitro, we demonstrate combinatorial

158 6), NF1 (in 4), PMS2 (in 4), RB1 (in 3), and RUNX1 (in 3).

159 7 (CHD7) interacts with RUNX1 and suppresses RUNX1-induced expansion of hematopoietic stem and progen

160 ata indicate that the repressive function of RUNX1 influences the balance between erythroid and megak

161 ression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation,

162 could acquire the serious resistance against RUNX1-inhibition therapies and also whether CBFB could p

163 1 expression; the blockade was overcome by a RUNX1 inhibitor.

164 nant interleukin 32gamma (IL-32gamma), and a RUNX1 inhibitor.

165 nd that runt-related transcription factor 1 (RUNX1) inhibits erythroid differentiation of murine mega

166 Taken together, we show that RUNX1 is a key player within a network of transcription

167 n iNKT17 differentiation, demonstrating that Runx1 is a key regulator of several genes required for i

168 The transcription factor RUNX1 is a master regulator of hematopoiesis.

169 ETV6-RUNX1 is associated with childhood acute B-lymphoblastic

170 ETV6-RUNX1 is associated with the most common subtype of chil

171 Here, we demonstrate that Runx1 is critical for T cell maturation.

172 RUNX1 is crucial for the regulation of megakaryocyte spe

173 Here we explore the hypothesis that RUNX1 is directly involved in the response of hematopoie

174 monstrate that the transcriptional regulator Runx1 is essential for the generation of ROR-gammat expr

175 Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1

176 Collectively, our findings show that RUNX1 is required for mammary stem cells to exit a bipot

177 Moreover, RUNX1 is sufficient for long-range promoter-Ebeta loopin

178 We now show that RUNX1 is sufficient to activate the endogenous mouse Ebe

179 A potential strategy to target RUNX1 is through modulation of its posttranslational mod

180 Runt-related transcription factor 1 (RUNX1) is a potential miR-375 direct target, and its kno

181 cohorts, there were differential effects of RUNX1 isoforms on PCTP expression with a negative correl

182 d with RUNX1 overexpression and reduced with RUNX1 knockdown in human erythroleukemia cells, indicati

183 potent progenitor (MPP) cells in conditional Runx1-knockout (KO) mice, but the molecular mechanism is

184 rtment is increased by more than fivefold in Runx1 KO mice, with a prominent skewing toward megakaryo

185 Furthermore, knockdown of RUNX1, L-plastin, and vimentin resulted in significant r

186 Loss of Runx1 leads to a severe decrease in iNKT cell numbers in

187 Thus, loss of Runx1 leads to the earliest characterized block in post-

188 port a mechanism in which miR-375 suppresses RUNX1 levels, resulting in reduced vimentin and L-plasti

189 lacks RUNX1C expression but has normal total RUNX1 levels, solely comprising RUNX1B.

190 ting of cases with DUX4 rearrangements, ETV6-RUNX1-like gene expression, MEF2D rearrangements, and ZN

191 de-induced chromosomal breaks at the MLL and RUNX1 loci.

192 RUNX1 loss in ER(+) mammary epithelial cells increases b

193 Finally, RUNX1 loss-mediated deregulation of beta-catenin and mit

194 let expression profiling of a patient with a RUNX1 loss-of-function mutation revealed a 10-fold downr

195 ated Src synergizes with Runx1 to activate a Runx1 luciferase reporter.

196 evel RUNX1 expression in cells refractory to RUNX1-mediated growth inhibition.

197 either positively or negatively by altering RUNX1-mediated transcription, promoting protein degradat

198 However, mechanisms underlying the implied RUNX1-mediated tumour suppression remain elusive.

199 ata suggest that pharmacologic modulation of RUNX1 might be an attractive new approach to treat hemat

200 an neurofibroma initiation cells, suggesting RUNX1 might relate to neurofibroma formation.

201 medium-recurrence mutations in genes such as RUNX1, MTOR, CA3, PI3, and PTPN11, all mapping within cl

202 nd offer an explanation for the link between RUNX1 mutations and chemotherapy and radiation resistanc

203 operative interactions between Flt3(ITD) and Runx1 mutations are also blunted in fetal/neonatal proge

204 lymphoblastic leukemia (T-ALL) patients, and RUNX1 mutations are associated with a poor prognosis.

205 clinical variables, we identified DNMT3A and RUNX1 mutations as important predictors of shorter overa

206 RUNX1 mutations can be early events, creating preleukemi

207 how that Flt3(ITD) and cooperating Flt3(ITD)/Runx1 mutations cause hematopoietic stem cell depletion

208 t high-throughput studies revealed recurrent RUNX1 mutations in breast cancer, specifically in oestro

209 To explore how RUNX1 mutations predispose to leukemia, we generated ind

210 lain the differential phenotype according to RUNX1 mutations, with a haploinsufficiency leading to th

211 cells (iPSCs) from 2 pedigrees with germline RUNX1 mutations.

212 of the presence of BCR-ABL1 (n = 46) or ETV6-RUNX1 (n = 11).

213 , cytogenetic abnormalities and mutations in RUNX1, NRAS, SETBP1, and ASXL1 were independently associ

214 Unlike in the conditional adult Runx1 null models, megakaryocytic maturation is not affe

215 Src phosphorylates Runx1 on one central and four C-terminal tyrosines.

216 ute myeloid leukemia defined by mutations in RUNX1 or BCR-ABL1 translocations as well as a constellat

217 Enforced expression of Runx2, but not Runx1 or Runx3, in Smad2/Smad3 doubly deficient CD4 cell

218 Somatic mutation in ASXL1, RUNX1, or TP53 is independently associated with unfavora

219 PCTP expression was increased with RUNX1 overexpression and reduced with RUNX1 knockdown in

220 urofibroma Schwann cells (SCs) we identified RUNX1 overexpression in human neurofibroma initiation ce

221 Runx1 overexpression was confirmed in mouse Schwann cell

222 We generated a Runx1 P1 knock-in of RUNX1B, termed P1-MRIPV This mouse

223 on of RUNX1, thereby creating a compensative RUNX1-p53-CBFB feedback loop.

224 present results underscore the importance of RUNX1-p53-CBFB regulatory loop in the development and/or

225 Murine and human ETV6-RUNX1 pB-ALL revealed recurrent genomic alterations, wit

226 high Rag1/2 expression, known for human ETV6-RUNX1 pB-ALL.

227 avy chain (SMMHC; encoded by CBFB-MYH11) and RUNX1 plays a critical role in the pathogenesis of this

228 Patients with ETV6-RUNX1-positive ALL and patients 1 to 6 years of age perf

229 Runx1 possesses 2 promoters: the distal P1 and proximal

230 enetic basis for clonal evolution of an ETV6-RUNX1 preleukemic clone to pB-ALL after infection exposu

231 athway to promote expression of Cbfb but not Runx1 prior to maturation of nonpeptidergic nociceptors.

232 Murine preleukemic ETV6-RUNX1 pro/preB cells showed high Rag1/2 expression, know

233 leading to RUNX3-mediated repression of the RUNX1 promoter and the relief of RUNX1-directed growth r

234 Immunostaining confirmed RUNX1 protein overexpression in human plexiform neurofib

235 Consistent with this, two RHD-defective RUNX1 proteins lacked any antiproliferative or apoptotic

236 ersensitive sites (DHSs), enabling ETS-1 and RUNX1 recruitment to previously inaccessible sites.

237 015) show that loss-of-function mutations in RUNX1 reduce ribosome biogenesis and provide pre-LSCs a

238 RUNX1 regulation of PCTP may play a role in the pathogen

239 MYH11-induced leukemogenesis by facilitating RUNX1 regulation of transcription and cellular prolifera

240 showed that FAK interacted with a number of Runx1-regulatory proteins, including Sin3a and other epi

241 This unknown activity of RUNX1 required an intact runt homology domain (RHD), a d

242 ith cytarabine in vitro Upon overexpression, RUNX1 restricted proliferation, promoted apoptosis, and

243 endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glu

244 RUNX1 (Runt-related transcription factor 1) is indispens

245 acute myeloid leukemia patients bearing the RUNX1-RUNX1T1 (AML1-ETO) fusion.

246 ected by KDM1A inhibition, and cells bearing RUNX1-RUNX1T1 (AML1-ETO) translocations were especially

247 RUNX1-RUNX1T1 (formerly AML1-ETO), a transcription facto

248 adult (n = 78) samples, including cases with RUNX1-RUNX1T1 (n = 85) or CBFB-MYH11 (n = 80) rearrangem

249 tations are strong disease accelerators in a RUNX1-RUNX1T1 AML mouse model, suggesting that H3K27me2/

250 Outside of signaling alterations, RUNX1-RUNX1T1 and CBFB-MYH11 AMLs demonstrated remarkabl

251 hylase JMJD1C functions as a coactivator for RUNX1-RUNX1T1 and is required for its transcriptional pr

252 fferent spectra of cooperating mutations, as RUNX1-RUNX1T1 cases harbored recurrent mutations in DHX1

253 r growth in an AML xenograft model harboring RUNX1-RUNX1T1 translocations.

254 ate oncogenic fusion genes such as PML-RARA, RUNX1-RUNX1T1, and MLL-AF9.

255 used retroviral vectors to express PML-RARA, RUNX1-RUNX1T1, or MLL-AF9 in bone marrow cells derived f

256 l ex vivo and that DNMT3A is dispensable for RUNX1-RUNX1T1- and MLL-AF9-driven self-renewal.

257 KDM1A also effectively suppressed growth of RUNX1-RUNX1T1-containing cell lines.

258 genes encoding transcription factors such as RUNX1, RUNX2, and MEF2C in HCT116 cells.

259 The Runx family of transcription factors (Runx1, Runx2, and Runx3) are highly conserved and encode

260 In contrast, enforced expression of Runx1, Runx2, or Runx3 failed to restore differentiation

261 ional mutations (eg, in SRSF2, ASXL1, and/or RUNX1 [S/A/R(pos) in >60% of cases]).

262 c2 in T cells, such as Raptor, CHEK1, CREB1, RUNX1, SATB1, Ikaros, and Helios.

263 ATA2, as well as heterozygous alterations in RUNX1, SF3B1, and genes encoding epigenetic modifiers, f

264 Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FV

265 parison to low-risk MDS), TP53, GATA2, KRAS, RUNX1, STAG2, ASXL1, ZRSR2 and TET2 mutations (type 2) h

266 d step, we demonstrate EBNA2 activation of a RUNX1 super-enhancer (-139 to -250 kb) that results in l

267 EBNA2 activation of the RUNX1 super-enhancer is also dependent on RBP-J.

268 that these proteins negatively regulate the RUNX1 super-enhancer, curbing EBNA2 activation.

269 loss-of-function mutations, indicating that RUNX1 suppresses T-cell transformation.

270 ytic/monocytic (G/M) commitment is marked by Runx1 suppression of genes encoding adherence and motili

271 ivity of RUNX1 and CBFbeta-SMMHC on Csf1r, a RUNX1 target gene.

272 we show that SOX7 inhibits the expression of RUNX1 target genes in HE, while having no effect on RUNX

273 ns mostly through altering the expression of RUNX1 target genes.

274 gakaryopoiesis and deregulated expression of RUNX1 targets.

275 eractions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehens

276 in familial hematopoietic disorders (GATA2, RUNX1), telomeropathies (TERC, TERT, RTEL1), ribosome di

277 acts as a platform for the stabilization of RUNX1, thereby creating a compensative RUNX1-p53-CBFB fe

278 suppression of rad21a reduced expression of runx1; this phenotype was corrected by injection of huma

279 We find that activated Src synergizes with Runx1 to activate a Runx1 luciferase reporter.

280 ngly, besides this key repressor function of Runx1 to control lineage decisions and cell numbers in p

281 es to aspartate but not phenylalanine allows Runx1 to increase Cebpa and granulocyte colony formation

282 ndergoing EHT, as identified by the ratio of RUNX1 to SOX17 immunofluorescence levels, and the morpho

283 owever, the underlying mechanisms connecting RUNX1 to the success of therapy remain elusive.

284 Expression of the Runx1 transcription factor is increased in adult cardiom

285 The gene encoding the RUNX1 transcription factor is mutated in a subset of T-c

286 sociated Epstein-Barr virus (EBV), RUNX3 and RUNX1 transcription is manipulated to control cell growt

287 ting a unique activator protein 1 (AP-1) and runx1 transcription program autonomous to the haemogenic

288 oderm (PLM), well before aorta formation and runx1 transcription.

289 AI-10-49 restores RUNX1 transcriptional activity, displays favorable pharm

290 nd other epigenetic modifiers known to alter Runx1 transcriptional function through posttranslational

291 ally, further supporting a positive role for Runx1 tyrosine phosphorylation during granulopoiesis, mu

292 Mutation of the five modified Runx1 tyrosines to aspartate markedly reduced co-immunop

293 oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal ang

294 h the translated phenylalanine and aspartate Runx1 variants.

295 e correlation between miR-375 expression and RUNX1, vimentin, and L-plastin RNA expression.

296 RUNX1 was upregulated posttranscriptionally by cytotoxic

297 ions in NRAS, KRAS, PTPN11, GATA2, TP53, and RUNX1 were found in <5% of patients.

298 enhancer express canonical motifs for the TF Runx1, which is essential for the development of these l

299 , KIT, and TP53) and a MEGS (NPM1, TP53, and RUNX1) whose mutation status was strongly associated wit

300 ce that SOX7 is broadly expressed across the RUNX1(+) yolk sac HE population compared with SOX17.