ライフサイエンスコーパス: RUNX1

1 tions in RUNX family transcription factor 1 (RUNX1).

2 ey TFs of macrophages (IRF8, JUNB, CEBPA and RUNX1).

3 anscription factors such as CEBPA, PU.1, and RUNX1.

4 a region spanning the PBX1 homeodomain, with RUNX1.

5 essing the myeloid differentiation regulator RUNX1.

6 cells, indicating that PCTP is regulated by RUNX1.

7 B-MYH11, is a dominant negative repressor of RUNX1.

8 multilayered interplay between E2A-PBX1 and RUNX1.

9 to LEN harbour recurrent variants of TP53 or RUNX1.

10 In contrast, overexpression of Runx1, a cellular binding partner of CBFbeta, phenocopie

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

12 Thus, Runx1, acting at the URE, and Pu.1 itself directly regul

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 PCs during development through modulation of RUNX1 activity.

16 Runt-related transcription factor 1 (RUNX1) acts as a mediator of aberrant retinal angiogenes

17 210143 in BAK1, P = 2.21 x 10(-8)), and ETV6-RUNX1 ALL at 17q21.32 (rs10853104 in IGF2BP1, P = 1.82 x

18 cies and specific effects of IGF2BP1 on ETV6-RUNX1 ALL evidenced by both germline and somatic genomic

19 Using the Leucegene RUNX1 AML patient group, we sought to investigate the pr

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

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

22 y among downregulated genes, suggesting that RUNX1 and CBFbeta-SMMHC mainly function together as acti

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

24 tients (mother and son) had co-occurrence of RUNX1 and CEBPA germline mutations, with variable AML di

25 d E2A as critical regulators of the ASE, and Runx1 and E2A as critical regulators of the Rag1 promote

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

27 expression-mimickers (EMs), which repressed RUNX1 and exerted in vitro and in vivo efficacy against

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

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

30 granulosa cell identity and combined loss of RUNX1 and FOXL2 results in masculinization of fetal ovar

31 ccupancy in the fetal ovary, suggesting that RUNX1 and FOXL2 target common sets of genes.

32 Similarly, DEL-1 increased RUNX1 and FOXP3 expression in human conventional T cells

33 ed the transcriptional activity of wild-type RUNX1 and functioned as a dominant negative form of RUNX

34 ly binds to a subset of gene loci cobound by RUNX1 and gene-activating machineries (p300, MED1, and H

35 AML1-ETO-activated gene, we demonstrate that RUNX1 and HDAC3 collaboratively repress AML1-ETO-depende

36 L have favourable genetic subtypes (eg, ETV6-RUNX1 and high hyperdiploidy), which confer a superior o

37 s of AML expressing mtRUNX1 versus wild-type RUNX1 and improved survival of mice engrafted with mtRUN

38 BET-proteolysis targeting chimera) repressed RUNX1 and its targets, inducing apoptosis and improving

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

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

41 The importance of down-regulation of Runx1 and Pu.1 in erythropoiesis is further supported by

42 In this study, we identify the actions of Runx1 and Pu.1 itself at the Pu.1 gene Upstream Regulato

43 During early erythropoiesis, Runx1 and Pu.1 levels decline, and chromatin accessibili

44 ly regulating transcription factors Irf4 and Runx1 and receptor Il12rb1 expression, in turn promoting

45 NX1 target genes by competitively displacing RUNX1 and recruiting corepressors such as histone deacet

46 linical models established the importance of RUNX1 and RUNX2 in ccRCC.

47 The LH surge increases the expression of Runx1 and Runx2 in ovulatory follicles, while Cbfb is co

48 matopoietic transcription factors, including Runx1 and Spi1.

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

50 CHD7 physically interacts with RUNX1 and suppresses RUNX1-induced expansion of HSPCs du

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

52 RUNX1 and the AML1-ETO fusion protein are coexpressed in

53 Patients with high RUNX1 (and RUNX2) expression exhibited significantly poo

54 main of Runt-related transcription factor 1 (RUNX1) and almost all of ETO.

55 d by reciprocal mutations in the epithelium (Runx1) and endothelium (Alk1) in adult mice, and is acco

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

57 k gene mutation (ie, in SRSF2, ASXL1, and/or RUNX1), and presence of two or more high molecular risk

58 scription factors TCF1, GATA3, PU.1, Bcl11b, Runx1, and E proteins in the primary establishment of T-

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

60 d by reducing the levels of RORgammat, IRF4, RUNX1, and T-bet, thereby reducing the number of pathoge

61 SM cases, particularly those carrying ASXL1, RUNX1, and/or DNMT3A (A/R/D) pathogenic variant allele f

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

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

64 ntified Runt-related transcription factor 1 (RUNX1) as a gene highly expressed in surgically-removed

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

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

67 We thus uncovered a DEL-1/alphavbeta3/RUNX1 axis that promotes Treg responses at barrier sites

68 nged CTCF binding in AML, as well as loss of RUNX1 binding at RUNX1/CTCF-binding sites.

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

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

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

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

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

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

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

76 say, we observed a significant enrichment of RUNX1/CBFbeta-SMMHC target genes in Runx1f/fMx1-CreCbfb+

77 ons in genes encoding transcription factors (RUNX1, CEBPalpha), signaling molecules (FTL3-ITD, RAS) a

78 colony-forming assays showed that gata2a(-) runx1(+) cells abundantly contain erythroid- and/or myel

79 anscriptome analysis revealed that gata2a(+) runx1(+) cells showed typical molecular signatures of HS

80 Consequently, the RUNX1:CHD7 axis provides proper timing and function of H

81 nd corepressor functions across the AML1-ETO/RUNX1 cistrome.

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

83 ber as assessed by in situ hybridization for runx1/cmyb and flow cytometry.

84 Recent studies have shown that AML1-ETO and RUNX1 co-occupy the binding sites of AML1-ETO-activated

85 Furthermore, nuclear CBFB/RUNX1 complex transcriptionally represses the oncogenic

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

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

88 e translocated into the nucleus and bound to RUNX1 consensus motifs.

89 Our findings suggest that Runx1 controls the regenerative response of multiple car

90 HSV-1 infection, we found that overexpressed RUNX1 could bind putative binding sites in the HSV-1 gen

91 Transcriptional profiling of RUNX1-CRISPR-deleted cells revealed a gene signature dom

92 in AML, as well as loss of RUNX1 binding at RUNX1/CTCF-binding sites.

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

94 Runx1-deficient iNKT cells have altered expression of se

95 Runx1-deficient mice were protected against adverse card

96 Finally, RUNX1 deletion in a genetic mouse model of kidney cancer

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

98 vbeta3 integrin, DEL-1 promoted induction of RUNX1-dependent FOXP3 expression and conferred stability

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

100 ion of this gene network was associated with RUNX1 DNA binding and triggered a transcription cascade

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

102 al bottleneck separates pre-HE from HE, with RUNX1 dosage regulating the efficiency of the pre-HE to

103 CRISPR/Cas9-mediated editing-out of RUNX1 enhancer (eR1) within its intragenic super-enhance

104 A distal candidate Runx1 enhancer exhibits high chromatin accessibility spe

105 ular recomposition with protein domains from RUNX1, ETO, BCR and N-CoR without any NHR2 and NHR4 sequ

106 not have irreplaceable functions concerning RUNX1/ETO activity for the establishment of human CD34+

107 A C-terminally NHR3 + 4 truncated RUNX1/ETO containing a heterologous, structurally highly

108 Furthermore RUNX1/ETO interacts with ETO-homologous proteins via NHR

109 As shown recently, RUNX1/ETO retains oncogenic activity upon either deletio

110 We could resemble the function of RUNX1/ETO through modular recomposition with protein dom

111 ures expressing the NHR2 exchanged truncated RUNX1/ETO.

112 ncode transcription factors, such as GATA-2, RUNX1, ETV6, and C/EBPalpha, which establish and maintai

113 Here, we report that RUNX1, expressed highly in DRG, binds HSV-1 genome, repr

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

115 Furthermore, runx1 expression depends on prior arterial programming b

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

117 This study demonstrates RUNX1 expression in critical cell types involved in a la

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

119 e Yap overexpression significantly increased runx1 expression in vivo and the number of CD41(+) HSPCs

120 RUNX1 expression is known to initiate at 2 alternative p

121 determined that in HRMECs, TNF-alpha-induced RUNX1 expression occurs via JNK activation, while NF-kap

122 embranes (FVMs) taken from patients with PDR RUNX1 expression was increased in the vasculature, while

123 We demonstrate that ginger can induce scl/runx1 expression, and that rescued HE fate is dependent

124 ECs), TNF-alpha stimulation causes increased RUNX1 expression, which can be modulated by RUNX1 inhibi

125 lpha and D-glucose had an additive effect on RUNX1 expression, which was downregulated by VEGF modula

126 ective at stopping high D-glucose-stimulated RUNX1 expression.

127 appaB and p38/MAPK inhibition did not affect RUNX1 expression.

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

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

130 predisposition to hematologic malignancies (RUNX1-FPD, FPD/AML, FPDMM); ~44% of affected individuals

131 Cs were highly enriched within the gata2a(+) runx1(+) fraction.

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

133 Here we show that RUNX1 functions as a bona fide repressor of transcriptio

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

135 ition to pB-ALL (Pax5 heterozygosity or ETV6-RUNX1 fusion) shaped a distinct gut microbiome.

136 cell ALL [B-ALL] with the TCF3-PBX1 or ETV6-RUNX1 fusions), and 2 subtypes had higher MTXPG levels (

137 The RUNX1(G60C) mutation abolished the transcriptional activ

138 somatic MEK2(P128L) mutation and a germline RUNX1(G60C) mutation in two patients with iMCD-TAFRO, re

139 s in the myeloid transcription factors (TFs) RUNX1, GATA2, and CEBPA.

140 t LEN-induced degradation of IKZF1 enables a RUNX1-GATA2 complex to drive megakaryocytic differentiat

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

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

143 us signaling pathways in these patients with RUNX1 germline-mutated AML.

144 RUNX1 has been proposed to have tumor suppressor roles i

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

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

147 Runt-related transcription factor 1 (RUNX1) has been identified as an important mediator of a

148 pecific deletion of the transcription factor RUNX1, identified by RNA sequencing analysis of the DEL-

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

150 ations in these diseases (for example, TP53, RUNX1, IKZF1 and ETV6) are the same as those that harbou

151 molecular insights into the requirement for Runx1 in a mouse model of inv(16) acute myeloid leukemia

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

153 date the unanticipated oncogenic function of RUNX1 in AML.

154 Ectopic expression of Runx1 in BFUe lacking a URE fails to block terminal eryt

155 To definitively address the role of Runx1 in CBFB-MYH11-induced leukemia, we crossed conditi

156 is was functionally relevant, as deletion of RUNX1 in ccRCC cell lines reduced tumor cell growth and

157 hese data suggest that the downregulation of RUNX1 in conjunction with anti-VEGF agents may be import

158 tory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.

159 In sum, these data support a novel role for RUNX1 in directly binding herpesvirus genome, silencing

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

161 In contrast, knockdown of RUNX1 in neuroblastoma cells induced viral gene expressi

162 This work shows a critical role for RUNX1 in PVR and supports the feasibility of targeting R

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

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

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

166 y of Ro5-3335, a small molecule inhibitor of RUNX1, in experimental CNV is reported.

167 Knockdown or inhibition of RUNX1 induced more apoptosis of AML expressing mtRUNX1 v

168 7 (CHD7) interacts with RUNX1 and suppresses RUNX1-induced expansion of hematopoietic stem and progen

169 ysically interacts with RUNX1 and suppresses RUNX1-induced expansion of HSPCs during development thro

170 D4 depletion by short hairpin RNA, repressed RUNX1, inhibited cell growth, and induced cell lethality

171 These data suggest that RUNX1 inhibition alone or in combination with anti-VEGF

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

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

174 RUNX1 inhibitor Ro5-3335, aflibercept-an FDA-approved va

175 ulated Ro5-3335, a lipophilic small molecule RUNX1 inhibitor, into a nanoemulsion that when administe

176 1 expression; the blockade was overcome by a RUNX1 inhibitor.

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

178 RUNX1 expression, which can be modulated by RUNX1 inhibitors.

179 inding to gene enhancers is dependent on the RUNX1 interaction but not the DNA-binding activity harbo

180 Mechanistically, we show that RUNX1 is a component of the HDAC3 corepressor complex an

181 ltiple cardiac cell types and that targeting Runx1 is a novel therapeutic strategy for inducing endog

182 Runx1 is a transcription factor that plays a key role in

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

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

185 RUNX1 is crucial for the regulation of megakaryocyte spe

186 that expression of the transcription factor RUNX1 is enriched in the fetal ovary in rainbow trout, t

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

188 In t(8;21)+ acute myeloid leukemia, RUNX1 is fused to nearly the entire ETO protein, which c

189 These data indicate that Runx1 is indispensable for Cbfb-MYH11-induced leukemogen

190 RUNX1 is mutated in ~10% of adult acute myeloid leukemia

191 a possible explanation as to the reason that RUNX1 is recurrently found translocated to ETO family me

192 Here, we report how Runx1 is specifically upregulated at the injury site dur

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

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

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

196 sets queried with messenger RNA signature of RUNX1 knockdown identified novel expression-mimickers (E

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

198 H11-induced leukemia, we crossed conditional Runx1 knockout mice (Runx1f/f) with conditional Cbfb-MYH

199 e, compound-mediated YAP activation enhanced RUNX1 levels and hematopoietic colony-forming potential.

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

201 at regulate leukemia-specific genes, such as RUNX1-linked regulatory elements proximal to the marker

202 Notably, the RUNX1 locus itself is also directly activated by E2A-PBX

203 ere, we report that the transcription factor RUNX1 marks a specific subpopulation of proximal luminal

204 In the mouse, RUNX1 marks the supporting cell lineage and becomes pre-

205 e double-positive fraction of gata2a:GFP and runx1:mCherry (gata2a(+) runx1(+)) was detected at appro

206 f two HSC-related transgenes, gata2a:GFP and runx1:mCherry.

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

208 Finally, overexpression of Runx1 mimicked the effect of D/N Vif mutants and inhibit

209 that were also enriched for Gata1, Ets, and Runx1 motifs.

210 Interestingly, the RUNX1 mRNA, which encodes the transcriptional partner of

211 firmed that mouse DRG neurons highly express Runx1 mRNA.

212 Somatic or germline mutant RUNX1 (mtRUNX1) is associated with poorer outcome in acu

213 th these populations cannot be identified in runx1 mutant wounds that contain less collagen and fibri

214 Runx1(-/-) mutants fail to downregulate arterial genes i

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

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

217 ther highlight the importance of testing for RUNX1 mutations in instances in which allogeneic stem ce

218 Our results showed that 30% of RUNX1 mutations in our AML cohort are germline.

219 igher than anticipated frequency of germline RUNX1 mutations in the Leucegene cohort and further high

220 igate the proportion of germline vs acquired RUNX1 mutations in this cohort.

221 Although most RUNX1 mutations in this disease are believed to be acqui

222 Indeed, germline RUNX1 mutations result in the well-described autosomal-d

223 analysis, age, ASXL1, CBL, DNMT3A, NRAS, and RUNX1 mutations retained significance.

224 lonal inflammatory disorders bearing MEK and RUNX1 mutations such as histiocytoses and myeloid neopla

225 ers of this complex such as Gata1, Fli1, and Runx1, mutations of Scl have not been observed as a caus

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

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

228 hed at sites occupied by CHD7, and decreased RUNX1 occupancy correlated with loss of CHD7 localizatio

229 At the chromatin level, RUNX1 occupancy overlaps partially with FOXL2 occupancy

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

231 Ectopic expression of Runx1 or Pu.1, both of which bind the URE, prevents Pu.1

232 2 restored LEN sensitivity in the context of RUNX1 or TP53 mutations by enhancing LEN-induced megakar

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

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

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

236 1 gene (Runx1t1, also called Mtg8) or CBFA2/RUNX1 partner transcriptional co-repressor 3 (Cbfa2t3, a

237 CBFA2/RUNX1 partner transcriptional co-repressor 3 (CBFA2T3, a

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

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

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

241 RUNX1 plays complementary/redundant roles with FOXL2 to

242 ng and genetic lineage tracing, we show that RUNX1(+) PLCs are unaffected by androgen deprivation, an

243 Collectively, our results reveal that RUNX1(+) PLCs is an intrinsic castration-resistant and s

244 demonstrate that a transcriptionally similar RUNX1(+) population emerges at the onset of embryonic pr

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

246 d that the wild-type injury site consists of Runx1-positive endocardial cells and thrombocytes that i

247 y patient samples from hyperdiploid and ETV6/RUNX1-positive pediatric ALL.

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

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

250 LEN upregulated RUNX1 protein and function in a CRBN- and TP53-dependent

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

252 mplex and that HDAC3 preferentially binds to RUNX1 rather than to AML1-ETO in t(8;21) AML cells.

253 The inhibition of RUNX1 reduced proliferation of human C-PVR cells in vitr

254 mic analysis of these populations identifies Runx1-regulated genes and shows that HE initially expres

255 Conversely, the HFSC activator Runx1 regulates secreted proteins with previously demons

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

257 otein 1 (AP-1) and investigated the JNK-AP-1-RUNX1 regulatory feedback loop, which can be modulated b

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

259 5q) cells, and mutation or downregulation of RUNX1 rendered cells resistant to LEN.

260 Here, we present a transgenic zebrafish runx1 reporter line to isolate HE and aortic roof endoth

261 ns integrated within the DA, suggesting that Runx1 represses the pre-existing arterial programme in H

262 However, recent findings challenge the RUNX1-repression model for CBFbeta-SMMHC-mediated leukem

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

264 ation assays further establish a significant RUNX1 requirement for E2A-PBX1-mediated target gene acti

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

266 nd functioned as a dominant negative form of RUNX1, resulting in enhanced self-renewal activity in he

267 fish heart regeneration, and that absence of runx1 results in increased myocardial survival and proli

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

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

270 (AML) patients that carry the fusion protein RUNX1-RUNX1T1 produced by t (8;21) (q22;q22).

271 but its prognostic impact was outweighed by RUNX1-RUNX1T1 TLs during treatment.

272 of patients exceeding a cutoff value of 150 RUNX1-RUNX1T1 TLs in BM, and in 84% of patients exceedin

273 d in 84% of patients exceeding a value of 50 RUNX1-RUNX1T1 TLs in PB.

274 We assessed both reduction of RUNX1-RUNX1T1 transcript levels (TLs) and achievement of

275 les of 155 intensively treated patients with RUNX1-RUNX1T1+ AML, using a qRT-PC-based assay with a se

276 ed practical guideline for MRD assessment in RUNX1-RUNX1T1+ AML.

277 hallmarks of the three mammalian RUNX genes, RUNX1, RUNX2 and RUNX3, and discuss the regulation of th

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

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

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

281 AML1-ETO represses transcription of RUNX1 target genes by competitively displacing RUNX1 and

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

283 led to interact with ETO-homologues, repress RUNX1 targets, and transform progenitors.

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

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

286 We further linked JNK to RUNX1 through Activator Protein 1 (AP-1) and investigate

287 How this joined binding allows RUNX1 to antagonize AML1-ETO-mediated transcriptional ac

288 thway in which E2A-PBX1 acts in concert with RUNX1 to enforce transcriptome alterations for the devel

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

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

291 RUNX1 transcription factor regulates normal and malignan

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

293 e data attest to the validity of targeting a RUNX1-transcriptional program in ccRCC.

294 ine tissues from mice with disruption of the RUNX1 translocation partner 1 gene (Runx1t1, also called

295 RUNX1 upregulation was a hallmark of EMT in primary cult

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

297 RUNX1 was upregulated posttranscriptionally by cytotoxic

298 n of gata2a:GFP and runx1:mCherry (gata2a(+) runx1(+)) was detected at approximately 0.16% in the kid

299 These findings identify RUNX1, with an ovary-biased expression pattern conserved

300 VR and supports the feasibility of targeting RUNX1 within the eye for the treatment of an EMT-mediate