ライフサイエンスコーパス: FOXM1

1 rative transcription factor Forkhead box M1 (FoxM1).

2 the phosphorylated, likely active, forms of FoxM1.

3 et genes, including the transcription factor FOXM1.

4 activity reverses OGT-mediated regulation of FOXM1.

5 ture expression via induction and binding of FOXM1.

6 itor PF-4942847 and heat shock also suppress FOXM1.

7 hereby deubiquitination and stabilization of FoxM1.

8 M1, it also led to enhanced transcription of FOXM1.

9 ant, significantly enhances the half-life of FOXM1.

10 tion of Lys48-linked ubiquitin-conjugates on FOXM1.

11 gh mechanisms that depend in part on Src and FoxM1.

12 ing of IGF-1R and HER2 reduced expression of FoxM1.

13 beta suppresses tubular repair by inhibiting FoxM1.

14 g the nuclear and mitochondrial functions of FOXM1.

15 sites recognized by forkhead box protein M1 (FoxM1), a key transcription factor in the control of mit

16 Forkhead box M1 (FOXM1), a nuclear transcription factor that activates ce

17 bited expression of forkhead box protein M1 (Foxm1), a reparative transcription factor.

18 e of an autoinhibited NRD-TAD complex within FoxM1, a critical activator of mitotic gene expression.

19 In this study, we examined the role of FoxM1, a forkhead box family member transcription factor

20 ur study found that heightened expression of FoxM1, a Forkhead box transcription factor, is regulated

21 TCPOBOP-driven induction of FOXM1, a key transcriptional regulator of cell cycle pro

22 FOXM1, a known transcription factor, promotes cell proli

23 HIF2alpha), which controls the expression of FoxM1, a recognized proliferative factor of Club cells.

24 lial Brg1 or FoxM1 or chemical inhibition of FoxM1 abolishes the stress-induced Ace2-to-Ace switch an

25 These data suggest that FoxM1 abundance and activity are controlled by VprBP and

26 FoxM1 accumulation in the nucleus promotes recruitment o

27 We identify FoxM1 activation in islets from neuronal relay-stimulate

28 on the RN in view of the whole GEP, whereas FOXM1-activation could be an interesting way to perturb

29 hat the substrate receptor VprBP is a potent FoxM1 activator.

30 We showed that JUN/FOS and FOXM1 activities are altered in almost all MM patients a

31 iven metastatic melanoma cells impaired both FOXM1 activity and cell survival.

32 FOXM1 activity correlated with expression of the enzyme

33 We hypothesized that increased FoxM1 activity in aged beta-cells would rejuvenate proli

34 These data suggest that elevated basal FOXM1 activity predisposes HPV+ HNSCC to WEE1i-induced t

35 ments, Pin1 proved to be a main regulator of FOXM1 activity through MEK-dependent physical regulation

36 Reducing expression of FOXM1 also decreased the quiescence of human CD34(+) HSC

37 FOXM1 also upregulated ZEB1, which could act as a feedba

38 on and improving glucose homeostasis, making FoxM1 an attractive therapeutic target for diabetes.

39 onstrate a molecular interaction of Brg1 and FoxM1 and an endothelial mechanism of modulating Ace/Ace

40 Moreover, both FOXM1 and AURKA were essential for maintaining the BCSC

41 correlation between the expression levels of FOXM1 and AURKA.

42 Interestingly, the repression of FOXM1 and CENPF by these miRNAs occurs through COUP-TFII

43 cell invasion and inhibit the expression of FOXM1 and CENPF, two master regulators of metastasis in

44 xin complex and leads to interaction between FoxM1 and deubiquitinating enzyme USP5, thereby deubiqui

45 n conclusion, these results demonstrate that FOXM1 and EGFR/ERBB2 pathways are key points of vulnerab

46 of neurosphere stemness in conjunction with FOXM1 and EZH2.

47 FOXM1 and FOXF1 improved elastin fiber organization, dec

48 dentified a positive feedback loop formed by FOXM1 and HGF/Met and revealed that this loop is a poten

49 ctivity of FOXM1, and the cross talk between FOXM1 and HGF/Met signaling promoted PDA growth and resi

50 1 expression, and simultaneous inhibition of FOXM1 and HSP70 increases the sensitivity of human cance

51 s showed increased expression levels of both FOXM1 and its proliferation-associated target genes.

52 The downregulation of FoxM1 and its target genes preceded mitotic arrest.

53 Our regulatory network analysis identified FOXM1 and KDM4E as signature transcription factor of AF

54 strong and significant correlations between FOXM1 and KIF20A expression in breast cancer patient sam

55 and mitotic catastrophe and that deregulated FOXM1 and KIF20A expression may confer paclitaxel resist

56 ith poor survival, consistent with a role of FOXM1 and KIF20A in paclitaxel action and resistance.

57 Statistical analysis reveals that both FOXM1 and KIF20A protein and mRNA expression significant

58 esembling paclitaxel treatment, silencing of FOXM1 and KIF20A similarly promotes abnormal mitotic spi

59 eased expression of the transcription factor FOXM1 and members of the E2F family.

60 that function in G1/S of the CC while B-MYB, FOXM1 and MuvB control G2/M gene expression.

61 on studies for TP53, RB1, E2F, DREAM, B-MYB, FOXM1 and MuvB.

62 ored by the significant correlations between FOXM1 and OTUB1 expression in breast cancer patient samp

63 ure of patients with PAH, where it regulates FoxM1 and PLK1, proteins implicated in the DNA damage re

64 hways, potentially through interactions with FoxM1 and PLK1.

65 ranked target gene maps for TP53, DREAM, MMB-FOXM1 and RB-E2F and enables prediction and distinction

66 , the essential mitotic transcription factor FoxM1 and RNA polymerase II were found to occupy the cyc

67 Transcription factors FOXM1 and STAT3, which function to activate and promote

68 Elevated FOXM1 and TYMS expression was also observed in acquired

69 er tissue specimens, a strong correlation of FOXM1 and TYMS staining was observed.

70 t expression of these genes was regulated by FOXM1 and/or p38 MAPK.

71 role of cross talk between Forkhead box M1 (FOXM1) and HGF/Met signaling in promotion of PDA growth

72 , which could act as a feedback inhibitor of FOXM1, and caused the transition of adherent cells to no

73 eration-promoting factors, including NFATC1, FOXM1, and CCNA1.

74 oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen recept

75 cantly associated with increased ERalpha and FOXM1, and significantly associated with tamoxifen resis

76 e expression and transcriptional activity of FOXM1, and the cross talk between FOXM1 and HGF/Met sign

77 TK-RAS-PI3K pathways and upregulation of the FOXM1- and E2F2-mediated cell cycle transitions, as well

78 ycle regulators E2F1, MYC, MYBL2 (B-Myb) and FOXM1 are among the DREAM targets that are diminished by

79 Moreover, we establish FOXM1 as a critical downstream target of PRRX1 in pancre

80 es reveal a previously unrecognized role for Foxm1 as a critical regulator of the quiescence and self

81 yclin B1 protein and RNA levels, implicating FoxM1 as a critical target for cyclin B1 inhibition duri

82 both cyclin B1 protein and RNA, implicating FoxM1 as a critical target mediating MVM-induced cyclin

83 Here, we identified FoxM1 as a novel target of Wnt signaling, which is essen

84 an be recruited by Forkhead box subclass M1 (FOXM1) as a co-factor to transactivate FOXM1 target gene

85 Further analysis revealed forkhead box M1 (FOXM1) as a key effector of the p300-MITF axis driving c

86 and epirubicin resistance through targeting FOXM1, as OTUB1 has little effect on FOXM1-deficient cel

87 Depleting ALKBH5 and FOXM1-AS disrupted GSC tumorigenesis through the FOXM1 a

88 e, a long non-coding RNA antisense to FOXM1 (FOXM1-AS) promotes the interaction of ALKBH5 with FOXM1

89 Subsequently, the USP5-FoxM1 axis abolishes the inhibitory effect of ICAT and i

90 a confirm the critical role of the p300-MITF-FOXM1 axis in melanoma and support p300 as a promising n

91 age and provide evidence of a possible PRRX1-FOXM1 axis that is critical for PDAC cells.

92 These findings indicate that the AhR-FoxM1 axis, at least in part, mediates colonic stem/prog

93 1-AS disrupted GSC tumorigenesis through the FOXM1 axis.

94 to invasion and metastasis via an SIRT1/ERK/FOXM1 axis.

95 K3) was found to be an upstream regulator of FoxM1 because GSK3 inhibition or renal tubular GSK3beta

96 Furthermore, knockdown of FoxM1 blocked IGF-1-mediated invasion, and dual targetin

97 Importantly, cell-permeable Pin1-FOXM1-blocking peptides repressed the proliferation of m

98 aired expression of the transcription factor Foxm1, both G1/S and G2/M cyclins, tryptophan hydroxylas

99 Mechanistically, FOXM1 bound to the promoter region of the Met gene and t

100 physiological relevance of the regulation of FOXM1 by OTUB1 is further underscored by the significant

101 through a Forkhead response element, whereas FOXM1 can activate AURKA expression at the transcription

102 and global ChIP-seq data also confirms that FOXM1 can also potentially regulate other 5-FU targets,

103 gent WEE1i treatment through activation of a FOXM1-CDK1 circuit that drives mitotic gene expression a

104 ly correlates with the increase of COUP-TFII-FOXM1-CENPF activity in clinical PCa data sets, implicat

105 RNAs through the regulation of the COUP-TFII-FOXM1-CENPF cascade in PCa metastasis and drug resistanc

106 Most importantly, this miRNA-COUP-TFII-FOXM1-CENPF regulatory axis is also involved in the deve

107 nctional DNA binding domain is essential for FOXM1 chromatin recruitment.

108 Targeting of a constitutively active FoxM1 construct or the activation domain of FoxM1 to the

109 Recruiting a constitutively active FoxM1 construct or the activation domain of FoxM1 to the

110 verning the protein synthesis of ERalpha and FOXM1 contributes to anti-estrogen insensitivity in ER(+

111 e feedback signalling loop between AURKA and FOXM1, crucial for BCSC self-renewal.

112 Inducible beta-cell-specific FoxM1 deficiency also blocks compensatory beta-cell prol

113 rgeting FOXM1, as OTUB1 has little effect on FOXM1-deficient cells.

114 Foxm1-deficient islets indeed displayed reduced insulin

115 Tamoxifen-inducible Foxm1 deletion suppressed the capacity of AtoMs to diffe

116 peptide-recapitulate the findings of genetic FOXM1 deletion.

117 ly promote beta-cell proliferation through a FoxM1-dependent mechanism.

118 roximal tubule repair, and we reveal an EGFR/FOXM1-dependent signaling pathway that drives proliferat

119 between PRRX1 and FOXM1 in the regulation of FOXM1-dependent transcriptional activity.

120 kinesis in keratinocytes via activation of a FoxM1-dependent transcriptional program, suggesting new

121 In here, we show that FOXM1 depletion can sensitize breast cancer cells and mo

122 Mitochondrial FOXM1 did not change cellular proliferation.

123 nome Atlas (TCGA) data revealed an activated FOXM1-directed promitotic transcriptional signature in H

124 In mitochondria, the FOXM1 directly bound to and increased the pentatricopept

125 g proteotoxic stress and that HSP70 inhibits FOXM1 DNA-binding ability.

126 B1), transcription factors (Myc, E2F1, TBX2, FOXM1), DNA replication regulators (CDKN1A, EZH2, RRM2),

127 FOXM1 drives expression of lactate dehydrogenase (LDH) b

128 The combination of HOTAIR and FOXM1 enables greater discrimination of endocrine therap

129 Thus, activation of p110gamma-FoxM1 endothelial regeneration may represent a novel str

130 Increased expression of FOXM1 enhanced the activation of HGF/Met signaling and i

131 We show here that persistent FOXM1 expression following drug treatment is a biomarker

132 ients with TP53 mutations and high levels of FOXM1 expression have the poorest survival outcomes.

133 Renal FoxM1 expression increased after renal ischemia/reperfus

134 In human hypertrophic hearts, BRG1 and FOXM1 expression is also activated in endothelial cells;

135 oprecipitation experiments demonstrated that FOXM1 expression is associated with OTUB1 binding but in

136 ut the posttranslational mechanisms by which FOXM1 expression is regulated by genotoxic agents and ho

137 ern blot analysis showed that both OTUB1 and FOXM1 expression reduced upon genotoxic agent treatment

138 FOXM1 expression reduced upon OTUB1 depletion by siRNA a

139 with p53 mutations exhibit higher levels of FOXM1 expression than patients with wild-type p53, but a

140 K3beta gene deletion significantly increased FoxM1 expression, and improved tubular repair and renal

141 In addition, HSP70 suppression elevates FOXM1 expression, and simultaneous inhibition of FOXM1 a

142 Therapeutic restoration of endothelial Foxm1 expression, via liposomal delivery of Foxm1 plasmi

143 decrease in Erk signaling and inhibition of FOXM1 expression.

144 nistically, AhR transcriptionally suppresses FoxM1 expression.

145 XM1 nascent transcripts, leading to enhanced FOXM1 expression.

146 activity, in turn, leads to de-repression of FOXM1 expression.

147 lls, arguing that OTUB1 positively regulates FOXM1 expression.

148 inhibition of CDK6-regulated phospho-RB and FOXM1 expression.

149 We show that HSP70 binds to FOXM1 following proteotoxic stress and that HSP70 inhibi

150 B 200-222/217 amino acid (aa) region and the FOXM1 Forkhead domain.

151 livery of proangiogenic transcription factor FOXM1 (forkhead box M1) or FOXF1 (forkhead box F1), both

152 ssion of the promitotic transcription factor FOXM1 (Forkhead box protein M1).

153 Once activated, Brg1 and FoxM1 form a protein complex on Ace and Ace2 promoters t

154 thermore, a long non-coding RNA antisense to FOXM1 (FOXM1-AS) promotes the interaction of ALKBH5 with

155 ing pre-mRNA stability and expression of the FOXM1 gene.

156 The forkhead transcription factor FOXM1 has a key role in DNA damage response, and its der

157 FOXM1 has been implicated in taxane resistance, but the

158 We identified key novel regulators (TFs Foxm1, Hif1a, Zbtb16, Myog, Myod1 and Tcf7, and miRNAs m

159 verexpression of FOXO3a or downregulation of FOXM1 impairs both GOF mutant p53-mediated cell invasion

160 This study reveals a significant role of FOXM1 in 5-FU resistance.

161 egradation of oncogenic transcription factor FOXM1 in an MEK/ERK-dependent manner.

162 Constitutive expression of FoxM1 in AREG knockdown cells normalized cell proliferat

163 limits the ubiquitination and degradation of FOXM1 in breast cancer and has a key role in genotoxic a

164 trogen receptor and directly correlated with FOXM1 in breast tumours.

165 itors as the first type of drugs that target FOXM1 in cancer cells.

166 Overexpression and knock-down studies of FOXM1 in colon cancer cells suggest the importance of FO

167 Moreover, inhibition of FOXM1 in diabetic mouse models (STZ-induced and db/db) r

168 Finally, we demonstrate the causality of FOXM1 in driving WEE1i sensitivity.

169 stress activates the expression of Brg1 and FoxM1 in endothelial cells.

170 s that HOTAIR is co-expressed with FOXA1 and FOXM1 in HER2-enriched tumours, and these factors enhanc

171 sion of Met correlated directly with that of FOXM1 in human tumor specimens.

172 We have ectopically expressed FOXM1 in keratinocytes of the skin after overexpression

173 tudy shows a critical role and mechanisms of Foxm1 in MA9-LSCs, and indicates that FOXM1 is a potenti

174 siRNA resulted in an increase in turnover of FOXM1 in MCF-7 cells treated with the protein synthesis

175 n and intra-nuclear protein translocation of FoxM1 in polyploid cells, respectively.

176 oration of expression of either p110gamma or FoxM1 in pulmonary endothelial cells of Pik3cg(-/-) mice

177 emonstrate the cooperation between PRRX1 and FOXM1 in the regulation of FOXM1-dependent transcription

178 dated the regulatory roles of miR-340-5p and Foxm1 in the Wnt-FoxO-Hippo subnetwork, as well as the r

179 colon cancer cells suggest the importance of FOXM1 in TYMS regulation.

180 Our studies reveal that activated FoxM1 increases beta-cell replication while simultaneous

181 The function of FOXM1 independent of nuclear transcription is unknown.

182 We observed that FoxM1 induction in the pulmonary vasculature was inhibit

183 thiazole antibiotic thiostrepton and (ii) an FOXM1 inhibiting ARF-derived peptide-recapitulate the fi

184 complementary approaches of pharmacological FOXM1 inhibition-(i) FOXM1 transcriptional inactivation

185 nstrated that the AURKA inhibitor AKI603 and FOXM1 inhibitor thiostrepton acted synergistically to in

186 uman osteoclastogenesis was inhibited by the FoxM1 inhibitor thiostrepton, constituting a potential t

187 of EGFR (ERBB1) and ERBB2] and thiostrepton (FOXM1 inhibitor) reduced growth and peritoneal spread of

188 Treatment with thiostrepton, a FoxM1 inhibitor, reduced FoxM1 regulated pro-proliferati

189 ng point for development of therapeutic Pin1-FOXM1 inhibitors to target metastatic melanoma.

190 r underscoring the beneficial effect of Pin1-FOXM1 inhibitory peptides as anti-melanoma drugs.

191 c analysis finding that the OTUB1 is a novel FOXM1-interacting protein.

192 The Pin1-FOXM1 interaction was enhanced by BRAF(V600E), the drive

193 Directing FOXM1 into the mitochondria decreased mitochondrial mass

194 The Forkhead (FKH) transcription factor FOXM1 is a key regulator of the cell cycle and is overex

195 sms of Foxm1 in MA9-LSCs, and indicates that FOXM1 is a potential therapeutic target for selectively

196 FOXM1 is a transcription factor of the Forkhead family t

197 n postulated that the oncogenic potential of FOXM1 is determined by its capacity to transactivate tar

198 t the pro-proliferative transcription factor FOXM1 is elevated and activated in malignant melanoma.

199 cal relevance of the regulation of KIF20A by FOXM1 is further highlighted by the strong and significa

200 These results demonstrate that FoxM1 is important for renal tubular regeneration follow

201 oncogenic forkhead box transcription factor, FOXM1 is is regulated by E2F1 which also controls TYMS.

202 nd our data suggest that VprBP activation of FoxM1 is ligase independent.

203 FOXM1 is negatively regulated by FOXO3A, supports cell s

204 The oncogenic transcription factor FOXM1 is overexpressed in the majority of human cancers,

205 However, FOXM1 is repeatedly overexpressed in a variety of human

206 The transcription factor FoxM1 is required for beta-cell replication in various s

207 Here we show that Foxm1 is required for survival, quiescence and self-rene

208 the oncogenic forkhead transcription factor FOXM1 is upregulated by GOF mutant p53s.

209 Forkhead box M1 (FOXM1) is a transcription factor recently proposed to go

210 of the transcription factor forkhead box M1 (FOXM1) is necessary for cell proliferation/tumorigenesis

211 enhance the translation of both ERalpha and FOXM1, it also led to enhanced transcription of FOXM1.

212 Similar to FOXM1, KIF20A expression is downregulated by paclitaxel

213 findings suggest that paclitaxel targets the FOXM1-KIF20A axis to drive abnormal mitotic spindle form

214 Additionally, while total FoxM1 levels remained constant, there was a significant

215 More importantly, inhibition of FOXM1 markedly suppresses leukemogenic potential and ind

216 However, FOXM1 may also play an oncogenic role by interacting wit

217 athogenesis of DFUs, which is facilitated by FOXM1-mediated deregulation of recruitment of neutrophil

218 vate to lactate to detect early response and FOXM1-mediated resistance to PI3K inhibition in estrogen

219 focus on targeting the PLK1-mediated and/or FoxM1-mediated signaling network.

220 ould modulate the translation of ERalpha and FOXM1 mRNA.

221 sing site-directed mutagenesis, we generated FOXM1 mutant proteins that localized to distinct cellula

222 ALKBH5 demethylates FOXM1 nascent transcripts, leading to enhanced FOXM1 exp

223 -AS) promotes the interaction of ALKBH5 with FOXM1 nascent transcripts.

224 more, erastin-induced resistance mediated by FOXM1-Nedd4-VDAC2/3 negative feedback loop provides an i

225 We observe that while both the FoxM1 NRD and TAD are primarily intrinsically disordered

226 Deregulation of FOXM1 occurs in a wide variety of epithelial malignancie

227 GSK3 phosphorylates FoxM1 on serine 474 which induces FoxM1 ubiquitination m

228 d the essential mitotic transcription factor FoxM1 on the cyclin B1 gene promoter.

229 Disruption of endothelial Brg1 or FoxM1 or chemical inhibition of FoxM1 abolishes the stre

230 ning nonintegrating expression plasmids with Foxm1 or Foxf1 cDNAs were injected intravenously.

231 Nanoparticle delivery of either FOXM1 or FOXF1 did not protect endothelial cells from ap

232 lthood.Conclusions: Nanoparticle delivery of FOXM1 or FOXF1 stimulates lung angiogenesis and alveolar

233 iostrepton (an inhibitor of forkhead box M1 [FOXM1]) or verteporfin (inhibitor of the interaction bet

234 In addition, we show that AURKA and FOXM1 participate in a tightly coupled positive feedback

235 obesity-induced activation of the beta-cell FoxM1 pathway and suppresses beta-cell expansion.

236 Wnt signaling activation inhibits FoxM1 phosphorylation by GSK3-Axin complex and leads to

237 Foxm1 expression, via liposomal delivery of Foxm1 plasmid DNA to Hif1a(f/f)/Tie2Cre(+) mice, resulte

238 In summary, this research demonstrated that FOXM1 plays a pivotal role in 5-FU resistance at least p

239 The oncogenic transcription factor FoxM1 plays a vital role in cell cycle progression, is a

240 AURKA activity and disrupt the nuclear AURKA/FOXM1-positive feedback loop, respectively, resulting in

241 dead AURKA can effectively transactivate the FOXM1 promoter through a Forkhead response element, wher

242 ulation by HSP70 leads to the suppression of FOXM1 protein expression.

243 In the present study, we found the FOXM1 protein inside the mitochondria.

244 irect physical interaction between PRRX1 and FOXM1 proteins that requires the PRRX1A/B 200-222/217 am

245 ith thiostrepton, a FoxM1 inhibitor, reduced FoxM1 regulated pro-proliferative factors and cell proli

246 mechanisms that control Aurora B, including FOXM1-regulated expression and proteasomal degradation f

247 We identify a new paradigm that FOXM1 regulates mitochondrial homeostasis in a process i

248 We also demonstrate that FOXM1 regulates the expression of the microtubulin-assoc

249 Our results support a mechanism of FoxM1 regulation in which the TAD undergoes switching be

250 d CSC mitotic progression, through the STAT3-FoxM1 regulatory axis, revealing an iron-regulated CSC p

251 s resource, we identified a forkhead box MI (FOXM1) regulatory network as a major predictor of advers

252 Therefore, Wnt-induced deubiquitination of FoxM1 represents a novel and critical mechanism for cont

253 Ectopic FOXM1 rescues the proliferative capacity of MYC- or p53-

254 ption-independent GOF mutant p53-AMPK-FOXO3a-FOXM1 signaling cascade that plays an important role in

255 A targeted genomic analysis implicated FOXM1 signaling downstream of E6/E7 expression and analy

256 lization and polyploidy development requires FoxM1 signaling downstream of Hoxa10 and cyclin D3.

257 litis-associated tumor model by upregulating FoxM1 signaling.

258 tem cell differentiation, and attenuation of FoxM1 signaling.

259 Dacominitib inhibited PLK1-FOXM1 signalling pathway and its down-stream targets Aur

260 cellular activities mediated by ERalpha and FOXM1 signalling pathways.

261 ade serous ovarian patient tumors, where the FoxM1 signature is amplified.

262 determined the unique and novel mechanism of FOXM1 suppression by proteasome inhibitors.

263 VprBP depletion reduces expression of FoxM1 target genes and impairs mitotic entry, whereas ec

264 s M1 (FOXM1) as a co-factor to transactivate FOXM1 target genes in a kinase-independent manner.

265 ith 4n DNA content and rescued expression of FoxM1 target genes.

266 er-enriched transcriptional regulators p300, FOXM1, TEAD4, FNFIC, CEBP8, and TCF12.

267 This analysis revealed FOXM1, TFDP1, ATF5, HMGA1, and NFYB to be candidate mast

268 discuss the protein-protein interactions of FOXM1 that are critical for cancer development and may r

269 ce of ERalpha, and it was the high levels of FOXM1 that conferred Tamoxifen resistance.

270 treatment of CRC cells with an inhibitor of FOXM1, thiostrepton, in combination with 5-FU.

271 n at cell-cycle gene promoters by recruiting FOXM1 through EZH2 to antagonize EZH2-mediated effects a

272 C tissues, we found that YAP cooperates with FOXM1 to contribute to chromosome instability.

273 FoxM1 construct or the activation domain of FoxM1 to the cyclin B1 gene promoter via clustered regul

274 FoxM1 construct or the activation domain of FoxM1 to the cyclin B1 gene promoter via CRISPR-catalyti

275 ed cell cycle associated genes (E2F1, CCND1, FOXM1, TP53, and RB1), transcription factors (Myc, E2F1,

276 The enhancement of FOXM1 transcription was contingent upon the presence of

277 ERalpha protein expression in turn enhances FOXM1 transcription, which together with its increased t

278 g1) chromatin remodeler and forkhead box M1 (FoxM1) transcription factor cooperate within cardiac (co

279 Inhibition of FOXM1 transcriptional autoregulation by HSP70 leads to t

280 aveled a new interplay between PRRX1 and the FOXM1 transcriptional factors.

281 ches of pharmacological FOXM1 inhibition-(i) FOXM1 transcriptional inactivation using the thiazole an

282 of the PRC2 complex, as well as the E2F2 and FOXM1 transcriptional networks.

283 ctopic VprBP expression strongly activates a FoxM1 transcriptional reporter.

284 Thus, FOXM1 translocates into mitochondria and inhibits mitoch

285 1 is critical for OGT-mediated regulation of FOXM1 ubiquitination and reducing SIRT1 activity reverse

286 phorylates FoxM1 on serine 474 which induces FoxM1 ubiquitination mediated by FBXW7.

287 /DCAF1 (CRL4(VprBP)), which we show regulate FoxM1 ubiquitylation and degradation.

288 Mechanistically, Foxm1 upregulation activates the Wnt/beta-catenin signal

289 syndrome, suggesting that impaired p110gamma-FoxM1 vascular repair signaling pathway is a critical fa

290 Conversely, on stemness genes, FOXM1 was absent and SCIRT antagonized EZH2 and SOX2 act

291 Intriguingly, FOXM1 was found to negatively regulate miR-23c expressio

292 The transcription factor Foxm1 was induced early in injury, was required for epit

293 Conversely, Forkhead box M1 (FOXM1) was required for the induction of integrin beta1,

294 ild-type or DNA binding deficient GFP-tagged FOXM1 were used for genome-wide mapping studies comparin

295 FOXM1, which connected MELK to EZH2 signaling in glioma,

296 rigenic effect of AVIL is partly mediated by FOXM1, which regulates LIN28B, whose expression also cor

297 1 and Cdk kinases cooperate to phosphorylate FoxM1, which releases the TAD into a disordered conforma

298 Finally, we demonstrate that targeting FOXM1 with the small molecule inhibitor FDI6 suppress pa

299 AP and TEAD4 with verteporfin, or inhibiting FOXM1 with thiostrepton, reduced the chromosome instabil

300 acted with EZH2 to increase EZH2 affinity to FOXM1 without binding the latter.