ライフサイエンスコーパス: FOXM1

1 rative transcription factor Forkhead box M1 (FoxM1).

2 (FAK) signaling and Forkhead box protein M1 (FoxM1).

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

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

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

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

7 seq with wild-type and DNA binding deficient FOXM1.

8 the phosphorylated, likely active, forms of FoxM1.

9 NBS1 is indispensable for the HR function of FOXM1.

10 otifs yielded a SUMOylation-deficient mutant FOXM1.

11 activity reverses OGT-mediated regulation of FOXM1.

12 ture expression via induction and binding of FOXM1.

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

14 hereby deubiquitination and stabilization of FoxM1.

15 et genes, including the transcription factor FOXM1.

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

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

18 BBC, a feature that is largely dependent on FoxM1, a master mitotic transcription factor that is als

19 vation of the PI3K pathway and expression of FoxM1, a positive regulator of cell cycle progression ge

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

21 Loss of FOXM1 abolished TGF-beta-induced SMAD3/SMAD4 formation.

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

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

24 FoxM1 accumulation in the nucleus promotes recruitment o

25 shows that FDI-6 specifically downregulates FOXM1-activated genes with FOXM1 occupancy confirmed by

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

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

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

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

30 findings suggest that SUMOylation attenuates FOXM1 activity and causes mitotic delay in cytotoxic dru

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

35 d mutants revealed that SUMOylation inhibits FOXM1 activity, promotes translocation to the cytoplasm

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

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

38 f FOXM1 decreases tumor size in vivo, making FOXM1 an attractive therapeutic target for the treatment

39 vB core complex in association with BMYB and FOXM1 and activate gene expression during the G2 and M p

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

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

42 correlation between the expression levels of FOXM1 and AURKA.

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

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

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

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

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

48 1 expression, and simultaneous inhibition of FOXM1 and HSP70 increases the sensitivity of human cance

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

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

51 l role for the forkhead transcription factor FOXM1 and its targets, and for heparin-binding epidermal

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

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

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

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

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

57 Analysis of wild-type FOXM1 and mutants revealed that SUMOylation inhibits FOX

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

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

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

61 uction of 14-3-3zeta collaborate to regulate FoxM1 and promote invasion of breast cancer cells and fu

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

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

64 study highlights the critical interaction of FOXM1 and SMAD3 for controlling TGF-beta signaling durin

65 Moreover, the interaction of FOXM1 and SMAD3 promoted TGF-beta/SMAD3-mediated transcr

66 tion of SMAD3 and identify crosstalk between FOXM1 and TGF-beta/SMAD3 pathways.

67 and significant correlation between nuclear FOXM1 and total NBS1 expression in breast cancer patient

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

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

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

71 of the forkhead family transcription factor, FoxM1, and its transcriptional targets, including matrix

72 cycle regulators including E2F1, E2F2, EXO1, FOXM1, and MCM2.

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

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

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

76 Here we identify FOXM1 as a candidate responsible for an aggressive clini

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

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

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

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

81 Taken together, our data identify FOXM1 as a novel therapeutic target, and demonstrate fea

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

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

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

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

86 Consistently, overexpression of FOXM1 augmented and FOXM1 depletion reduced NBS1 express

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

88 1-AS disrupted GSC tumorigenesis through the FOXM1 axis.

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

90 The transcription factor FOXM1 binds to sequence-specific motifs on DNA (C/TAAACA

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

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

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

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

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

96 Inhibition of FoxM1 by RNA interference prevented induction of invasio

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

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

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

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

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

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

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

104 ll molecule-mediated effect is selective for FOXM1-controlled genes with no effect on genes regulated

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

106 Finally, pharmacologic inhibition of FOXM1 decreases tumor size in vivo, making FOXM1 an attr

107 epair-defective and senescence phenotypes in FOXM1-deficent cells can be effectively rescued by overe

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

109 reversed the loss of quiescence observed in Foxm1-deficient cells in vivo.

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

111 Foxm1-deficient islets indeed displayed reduced insulin

112 Conversely, reconstitution of FOXM1 in FOXM1-deficient MEFs alleviates the accumulation of sene

113 peptide-recapitulate the findings of genetic FOXM1 deletion.

114 Cells expressing activated FoxM1 demonstrated enhanced glucose-stimulated Ca2+ infl

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

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

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

118 ently, overexpression of FOXM1 augmented and FOXM1 depletion reduced NBS1 expression and epirubicin-i

119 We show here that FOXM1-depletion can sensitize breast cancer cells and mo

120 FOXM1 directly bound to promoter regions of Ikbkb, Nfkb2

121 Mechanistically, Foxm1 directly bound to the promoter region of the gene

122 Notably, FOXM1 directly interacts with the YAP transcriptional co

123 This shows that interaction of the FOXM1 DNA binding domain with target DNA is essential fo

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

125 o and in vitro demonstrates that the loss of FoxM1 elicits diploid cell deficiency with enhanced arre

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

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

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

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

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

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

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

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

134 FOXM1 expression reduced upon OTUB1 depletion by siRNA a

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

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

137 lls, arguing that OTUB1 positively regulates FOXM1 expression.

138 XM1 nascent transcripts, leading to enhanced FOXM1 expression.

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

140 Crucially, overexpression of FOXM1 failed to augment HR activity in the background of

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

142 ciates from p107/p130 and recruits B-Myb and FoxM1 for up-regulating mitotic gene expression.

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

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

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

146 bind directly to FOXM1 protein, to displace FOXM1 from genomic targets in MCF-7 breast cancer cells,

147 Conditional deletion of Foxm1 from Kras(G12D)-expressing respiratory epithelium

148 Conditional deletion of the Foxm1 gene from either airway epithelium or myeloid infl

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

150 Conversely, fusion of the E2 ligase Ubc9 to FOXM1 generated an auto-SUMOylating mutant (FOXM1-Ubc9).

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

152 FOXM1 has been implicated in taxane resistance, but the

153 vity of the transcription factors NF-kappaB, FoxM1, Hif1alpha, the translation regulator HuR, and the

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

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

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

157 size-matched islets from young mice lacking FoxM1 in beta-cells.

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

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

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

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

162 Conversely, reconstitution of FOXM1 in FOXM1-deficient MEFs alleviates the accumulatio

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

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

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

166 , at 2 months of age, induction of activated FoxM1 in male mice improved glucose homeostasis with unc

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

168 ion of invasion by IR, and overexpression of FoxM1 in MCF10A cells was sufficient to promote IR-induc

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

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

171 Importantly, the function of FOXM1 in TGF-beta-induced invasion was not dependent on

172 as previously demonstrated that mice lacking FoxM1 in the pancreas display glucose intolerance or dia

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

174 Together these findings suggest that FOXM1 increases NBS1 expression and ATM phosphorylation,

175 Knockdown of SMAD3 diminished FOXM1-induced metastasis.

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

177 The loss of Foxm1 inhibited expression of K-Ras target genes critica

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

179 eutic target, and demonstrate feasibility of FOXM1 inhibition in ALL.

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

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

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

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

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

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

186 nes, we found that oncogene forkhead box M1 (FOXM1) interacts with SMAD3 to sustain activation of the

187 Aberrant overexpression of FOXM1 is a key feature in oncogenesis and progression of

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

189 FOXM1 is a transcription factor of the Forkhead family t

190 The forkhead box transcription factor FOXM1 is an essential effector of G2/M-phase transition,

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

192 beta-cell mass, suggesting that the loss of FoxM1 is detrimental to beta-cell function.

193 Here we report that FOXM1 is dynamically modified by SUMO1 but not by SUMO2/

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

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

196 ance of the regulation of NBS1 expression by FOXM1 is further underscored by the strong and significa

197 FOXM1 is implicated in genotoxic drug resistance but its

198 Foxm1 is known as a typical proliferation-associated tra

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

200 FOXM1 is negatively regulated by FOXO3A, supports cell s

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

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

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

204 FOXM1 is required for K-Ras-mediated lung tumorigenesis

205 ese results strongly support a model whereby FOXM1 is specifically recruited to chromatin through co-

206 sitive breast cancer cells and together with FoxM1 is sufficient for invasion in ErbB2-negative breas

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

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

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

210 Similar to FOXM1, KIF20A expression is downregulated by paclitaxel

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

212 Compared with normal B-cell populations, FOXM1 levels are 2- to 60-fold higher in ALL cells and a

213 Furthermore, FOXM1 levels correlated with activated TGF-beta signalin

214 We show that FOXM1 levels peak at the pre-B-cell receptor checkpoint

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

216 and early development loci--including ETV4, FOXM1, LSR, CD9, RAB11FIP4, and FGFRL1.

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

218 nvolves EGFR signaling, mTOR activation, and FOXM1-mediated cell proliferation.

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

220 Transgenic overexpression of activated FOXM1 mutant was sufficient to induce expression of thes

221 Even in FOXM1 mutants with almost complete loss of binding, the

222 such genes are controlled by DREAM, MMB and FOXM1-MuvB and that these protein complexes can contact

223 hanism: sequential binding of DREAM, MMB and FOXM1-MuvB complexes to late cell cycle genes requires C

224 late cell cycle genes binding DREAM, MMB, or FOXM1-MuvB.

225 n of late cell cycle genes by DREAM, MMB and FOXM1-MuvB.

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

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

228 Resembling FOXM1, NBS1 depletion also rendered MCF-7 and MCF-7Epi(R

229 Like FOXM1, NBS1 is overexpressed in the epirubicin-resistant

230 lly downregulates FOXM1-activated genes with FOXM1 occupancy confirmed by ChIP-PCR.

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

232 ation and may account for the high levels of FOXM1 often observed in poor-risk cervical cancers.

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

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

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

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

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

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

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

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

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

242 FOXM1 prevented the E3 ubiquitin-protein ligase transcri

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

244 Together, our data indicate that FOXM1 promotes breast cancer metastasis by increasing nu

245 n K-Ras oncogene and increased expression of FOXM1 protein are associated with poor prognosis in pati

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

247 ed in depth and is shown to bind directly to FOXM1 protein, to displace FOXM1 from genomic targets in

248 ole of direct versus indirect DNA binding in FOXM1 recruitment by performing ChIP-seq with wild-type

249 We also demonstrate that FOXM1 regulates NBS1 at the transcriptional level throug

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

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

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

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

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

255 Re-expression of FoxM1 restored the invasive potential of IGF-1R knockdow

256 F-beta-induced invasion was not dependent on FOXM1's transcriptional activity.

257 me of wild-type versus DNA binding deficient FOXM1 shows that the reduced recruitment is not due to i

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

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

260 AG1478 or rapamycin blocked the increase in FOXM1 signaling, beta-cell proliferation, and beta-cell

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

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

263 FOXM1, similar to other FKH factors, binds to a canonica

264 Moreover, overexpression of NBS1 and FOXM1 similarly enhanced and their depletion downregulat

265 We found that FOXM1/SMAD3 interaction was required for TGF-beta-induce

266 We show that FOXM1 SUMOylation is enhanced in MCF-7 breast cancer cel

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

268 mples, further suggesting that NBS1 as a key FOXM1 target gene involved in DNA damage response, genot

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

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

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

272 kn2a, indicating that these genes are direct FOXM1 targets.

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

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

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

276 identify novel small molecule inhibitors of FOXM1 that block DNA binding.

277 point mutations in the DNA binding domain of FOXM1 that inhibit binding to a FKH consensus sequence.

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

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

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

281 Foxm1 transcription factor, a downstream target of K-Ras

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

283 Inhibition of FOXM1 transcriptional autoregulation by HSP70 leads to t

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

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

286 ctopic VprBP expression strongly activates a FoxM1 transcriptional reporter.

287 n compared with wild-type FOXM1, whereas the FOXM1-Ubc9 fusion protein resulted in persistent cyclin

288 FOXM1 generated an auto-SUMOylating mutant (FOXM1-Ubc9).

289 1 is critical for OGT-mediated regulation of FOXM1 ubiquitination and reducing SIRT1 activity reverse

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

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

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

293 Here we found that Foxm1 was essential for maintenance of the quiescence an

294 ontrol of Sftpc promoter to demonstrate that Foxm1 was induced in type II epithelial cells before the

295 Induction of an activated form of FoxM1 was sufficient to increase beta-cell mass and prol

296 In this study we found that FoxM1 was up-regulated by heat shock factor 1 (HSF1) und

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

298 d cell proliferation compared with wild-type FOXM1, whereas the FOXM1-Ubc9 fusion protein resulted in

299 ression of the forkhead transcription factor FoxM1, which binds to the majority of cell division prom

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