ライフサイエンスコーパス: KLF6

1 scriptional activator Kruppel-like factor-6 (Klf6).

2 a direct interaction of transfected SV1 with KLF6.

3 ona fide transcriptional target repressed by KLF6.

4 t is upregulated in ES cells over-expressing Klf6.

5 egulators of cell proliferation, p21Cip1 and KLF6.

6 ng the SP/KLF transcription factors, SP2 and KLF6.

7 genous Dlk1 promoter where it interacts with KLF6.

8 of increased H3K9me3 may be mediated through KLF6.

9 nsactivation of a p21 promoter luciferase by KLF6.

10 onsistent with transcriptional repression by KLF6.

11 owth suppression, which was abrogated by the KLF6-4A phosphomutant.

12 andidate phosphorylation sites to alanines ('KLF6-4A' phosphomutant) eliminated a higher molecular we

13 e transactivation by wild-type KLF6, but not KLF6-4A, towards the p21 promoter, and increased p21 pro

14 transcription factor Kruppel-like factor 6 (KLF6), a putative tumor suppressor in prostate cancer.

15 We have identified Kruppel-like factor-6 (KLF6), a recently described tumor suppressor gene, as a

16 Here, we identified Kruppel-like factor 6 (KLF6), a zinc finger domain transcription factor, as an

17 Kruppel-like factor 6 (KLF6), a zinc finger transcription factor and tumor supp

18 KLF6, a ubiquitously expressed Kruppel-like transcriptio

19 Klf6 acts as a gp130-sensitive transactivator of the nuc

20 contrast, mice with targeted deletion of one KLF6 allele (KLF6+/-) display increased liver mass with

21 KLF6 alternative splicing is not coupled to its transcri

22 etween activated Ras signaling and increased KLF6 alternative splicing.

23 from prostate cancer reduces acetylation of KLF6 and abrogates its capacity to up-regulate endogenou

24 Moreover, SV1 binds directly to KLF6 and accelerates its degradation.

25 istry studies confirm falling levels of both KLF6 and GCK in fat-laden hepatocytes.

26 uantified messenger RNA (mRNA) expression of KLF6 and glucokinase (GCK), as an important mediator of

27 t-derived epithelial ovarian tumors with low KLF6 and high KLF6-SV1 expression ratios had significant

28 ivation of gp130 signaling display defective Klf6 and Impalpha5 expression, OLP maturation arrest and

29 o understanding possible mechanisms by which KLF6 and its antagonistic splice form, KLF6-SV1, regulat

30 nally important mediator by which changes in KLF6 and KLF6-SV1 can directly alter ovarian tumor invas

31 a synergistic cooperative mechanism between KLF6 and specificity protein 1, and in vascular smooth m

32 r study reveals a novel relationship between Klf6 and the Shh pathway.

33 the tumor suppressors Kruppel-like factor 6 (KLF6) and forkhead box O1 (FOXO1) that negatively regula

34 ed include a global heterozygous KLF6 mouse (Klf6+/-), and transgenic mice expressing either hKLF6(WT

35 KLF6-SV1 (SV1), the major splice variant of KLF6, antagonizes the KLF6 tumor suppressor by an unknow

36 uman adipogenesis, and highlight the role of KLF6 as a multifunctional transcriptional regulator capa

37 Collectively, these observations identify KLF6 as a novel transcriptional regulator of macrophage

38 s identify the interaction between HDAC3 and KLF6 as a potential mechanism underlying human adipogene

39 rofiling of murine HCC cell lines identified KLF6 as a potential regulator of HCC cell migration.

40 We previously identified KLF6 as mediator of hepatocyte glucose and lipid homeost

41 study, we identified Kruppel-like factor 6 (KLF6) as a critical transcription factor essential for i

42 ify the Kruppel-like transcription factor 6 (KLF6) as a molecular toggle controlling macrophage speci

43 protein 4 (PDCD4) and Kruppel-like factor 6 (KLF6) as critical regulators and surrogate markers of pr

44 ional and chromatin occupancy analyses place Klf6 at the nexus of a novel gp130-Klf-importin axis, wh

45 Reconstitution of KLF6 attenuates their malignant phenotype and induces ne

46 ify the Kruppel-like transcription factor 6 (KLF6)-B cell leukemia/lymphoma 6 (BCL6) signaling axis a

47 r molecular weight phosphorylated isoform of KLF6 based on western blot.

48 Kruppel-like factor 6 (Klf6) belongs to a family of zinc finger transcription f

49 association in MESA Hispanics-rs12253976 in KLF6 (beta = 5.792 kg/m(2) per-allele, 95 % confidence i

50 noprecipitation assays indicate that SP2 and KLF6 bind to the matrix metalloproteinase-9 promoter and

51 In multiple cancer cells, LCoR and KLF6 bind together on the promoters of the genes encodin

52 KLF6 binds directly to and activates the ATF3 promoter.

53 KLF6 binds to the liver-specific Gck promoter and activa

54 to 0.97) peripheral blood three-gene assay (KLF6, BNC2, CYP1B1) to detect the state of operational t

55 a augmented the transactivation by wild-type KLF6, but not KLF6-4A, towards the p21 promoter, and inc

56 Wild-type KLF6, but not patient-derived mutants, suppresses cell g

57 and induced apoptosis, whereas knockdown of KLF6 by small interference RNA blocked the increase of A

58 n and transcriptional activity, reduction in KLF6 by small interfering RNA led to increased MDM2 and

59 a, Gata4, Sox17, and CxCr4 is not induced in Klf6(-/-) cells but is upregulated in ES cells over-expr

60 aled an increase in Mdm2 mRNA in tumors from KLF6+/- compared with KLF6+/+ mice, which was validated

61 st that decreased availability of functional KLF6 contributes to clinical PC progression.

62 Kruppel-like factor 6 (Klf6; copeb in zebrafish) is a zinc-finger transcription

63 Functionally, wild-type KLF6 decreased cellular proliferation of HepG2 cells, wh

64 However, blockade of KLF6 decreased cisplatin-induced up-regulation of Noxa i

65 Our findings indicate that KLF6 deficiency contributes significantly to the carcino

66 Klf6-deficiency leads to elevated levels of hedgehog pat

67 macological or genetic inhibition of BCL6 in KLF6-deficient macrophages completely abrogated the atte

68 We have generated a prostate-specific Klf6-deficient mouse model and report here a novel role

69 Accelerated KLF6 degradation in the presence of SV1 was abrogated by

70 cy is a clinically relevant means of evading KLF6-dependent regulation of NF-kappaB.

71 Together, these findings indicate that KLF6-dependent regulation of the cytochrome c oxidase as

72 more histologically advanced tumors, whereas Klf6-depleted mice developed bigger tumors compared to t

73 c animals and those with hepatocyte-specific Klf6 depletion displayed increased DNA synthesis, with a

74 e months after DEN, SV1 transgenic mice with Klf6 depletion had the greatest tumor burden.

75 m of the study was to evaluate the impact of KLF6 depletion on human HCC and experimental hepatocarci

76 ocytes harboring both SV1 overexpression and Klf6 depletion.

77 GCK promoter-reporter, identifying GCK as a KLF6 direct transcriptional target.

78 These changes resulted from KLF6 directly transactivating the E-cadherin promoter as

79 e with targeted deletion of one KLF6 allele (KLF6+/-) display increased liver mass with reduced p21 e

80 ctivation of FXR, SHP interacts with SP2 and KLF6, disrupting the SP2/KLF6 repressor complex.

81 Mechanistically, KLF6 downregulates expression and secretion of GM-CSF.

82 -related pathways, we analysed the effect of KLF6 dysregulation on a recognized suppressor of cellula

83 mesoderm induction were also observed in the Klf6-/- EBs, associated with delayed expression of Brach

84 further analyze this phenotype, we generated Klf6-/- embryonic stem (ES) cells by homologous recombin

85 ietic lineage with that of either Klf6+/- or Klf6+/+ ES cells.

86 tent with the phenotype in the early embryo, Klf6-/- ES cells displayed significant hematopoietic def

87 estigated the prevalence and significance of KLF6 exon 2 mutations and splice variants (SVs) in diffe

88 Decreased KLF6 expression in human hepatocellular carcinoma (HCC)

89 Podocyte-specific deletion of Klf6 expression in mice leads to mitochondrial dysfuncti

90 development was investigated by manipulating Klf6 expression in mouse ES cells driven to differentiat

91 Here we show, that KLF6 expression is induced in ALF and in the regeneratin

92 the JCI, Mallipattu and coworkers show that KLF6 expression is reduced in mouse and human glomerular

93 e cancer tumors and cell lines and decreased KLF6 expression levels in recurrent prostate cancer samp

94 pal neurons, and siRNA-mediated knockdown of KLF6 expression promotes neuronal cell death and also an

95 KLF6 expression was induced early in response to ADR in

96 Additionally, KLF6 expression was reduced in podocytes from HIV-1 tran

97 KLF6 expression was robustly induced by pro-inflammatory

98 nzymes, thereby abolishing the activation of KLF6 expression.

99 ted in studies using TCGA data (e.g., SYNE1, KLF6, FGFR4, and EPHB4).

100 lotinib resistance through modulation of the KLF6/FOXO1 signaling cascade in both cell culture and xe

101 KLF6 function is abrogated in human cancers owing to inc

102 data indicate that acetylation may regulate KLF6 function, and its loss in some tumor-derived mutant

103 ed the role of GSK3beta in the regulation of KLF6 function.

104 e possibility that haploinsufficiency of the KLF6 gene alone contributes to cellular growth dysregula

105 Indeed, mutations of the KLF6 gene have recently been reported in this tumor type

106 bitor p21 as a transcriptional target of the KLF6 gene in cultured cells, but not in vivo.

107 data suggest that haploinsufficiency of the KLF6 gene may regulate cellular proliferation in vivo th

108 KLF6 gene silencing in human lung epithelial cells resul

109 ms that are homologous to those of the human KLF6 gene.

110 The Kruppel-like factor 6 (KLF6) gene is a zinc finger transcription factor that in

111 Most recently, we identified a common KLF6 germ line single nucleotide polymorphism that is as

112 on factors acting at the SP1-like motif, but KLF6 had some features of such a candidate.

113 ctor/tumor suppressor Kruppel-like factor 6 (KLF6) has been described in prostate cancer (PC).

114 T3 cells in vivo, whereas down-regulation of KLF6 in 3T3-L1 cells by small interfering RNA prevents a

115 Concordantly, single-copy deletion of Klf6 in a HCC mouse model results in increased tumor for

116 Here we explore the role of KLF6 in acute liver injury models in mice, and in patien

117 r, our data demonstrate a novel function for KLF6 in constraining HCC dissemination through the regul

118 A cell autonomous role for Klf6 in endoderm and hepatic development was investigate

119 Collectively, these findings implicate Klf6 in ES-cell differentiation and hematopoiesis.

120 uncover a novel tumor suppressor activity of KLF6 in HCC by linking its transcriptional repression of

121 identified novel transcriptional targets of KLF6 in HCC cells including VAV3, a known activator of t

122 tial induction, sustained down-regulation of KLF6 in liver injury may allow de-repression of fibrogen

123 To explore the potential role of Klf6 in mouse development, we analyzed Klf6-/- mice and

124 c mouse models to define the in vivo role of KLF6 in regulating cell proliferation and p21 expression

125 To explore a potential role for KLF6 in the development of insulin resistance, central t

126 Transgenic overexpression of KLF6 in the liver resulted in a runted phenotype with de

127 mouse model and report here a novel role for Klf6 in the regulation of prostate branching morphogenes

128 Conversely, in mice with lineage-selective Klf6 inactivation, OLP undergo maturation arrest followe

129 observed that podocyte-specific deletion of Klf6 increased the susceptibility of a resistant mouse s

130 Thus, ATF3 is a key mediator of KLF6-induced apoptosis in prostate cancer cells.

131 wn of ATF3 by small interference RNA blocked KLF6-induced apoptosis.

132 Here we show that KLF6 induces apoptosis in prostate cancer cells by ATF3

133 Furthermore, KLF6 inhibits anti-inflammatory gene expression by negat

134 del of LCoR function in which promoter-bound KLF6 inhibits transcription of the CDKN1A gene and other

135 romatin immunoprecipitation assays show that KLF6 interacts with ALK1 promoter in ECs, and this inter

136 Multiple lines of evidence now suggest that KLF6 is a key prostate cancer tumor suppressor gene incl

137 The tumor suppressor KLF6 is a member of the Kruppel-like family of transcrip

138 We first showed that KLF6 is a tumor suppressor somatically inactivated in pr

139 Inactivation of KLF6 is common in hepatocellular carcinoma (HCC) associa

140 d loss-of-function studies, we observed that KLF6 is essential for macrophage motility under ex vivo

141 ectively, these findings indicate that copeb/Klf6 is essential for the development of endoderm-derive

142 We have previously established that Klf6 is expressed in neuronal tissue, hindgut, heart, lu

143 KLF6 is heterozygously deleted in 74.5% of the analyzed

144 Although Klf6 is highly mutated in prostate cancer, its function

145 The loss or reduction of KLF6 is linked to the progression of hepatocellular carc

146 Klf6 is rapidly induced in oligodendrocyte progenitors (

147 n- and loss-of-function studies suggest that KLF6 is required for optimal LPS-induced pro-inflammator

148 mechanism of growth inhibition by wild-type KLF6 is through p53-independent up-regulation of p21(WAF

149 We demonstrate that KLF6 is transactivating ALK1 gene, and this transactivat

150 Kruppel-like factor 6 (KLF6) is a member of a growing family of transcription f

151 Kruppel-like factor 6 (KLF6) is a transcription factor and tumor suppressor.

152 Kruppel-like factor 6 (KLF6) is a tumor suppressor gene that is functionally in

153 Kruppel-like factor 6 (KLF6) is a ubiquitous zinc finger tumor suppressor that

154 Kruppel-like factor 6 (KLF6) is a zinc finger transcription factor and tumor su

155 isoform of the Kruppel-like tumor suppressor KLF6, is a critical prosurvival/antiapoptotic protein.

156 Following a transient increase, all rat Klf6 isoforms decreased in response to acute carbon tetr

157 ree alternatively spliced, dominant-negative KLF6 isoforms.

158 transcription of three alternatively spliced KLF6 isoforms.

159 central to NAFLD pathogenesis, we genotyped KLF6-IVS1-27 in healthy subjects and assayed fasting pla

160 The KLF6-IVS1-27A polymorphism, which generates more KLF6-SV

161 The polymorphism, KLF6-IVS1-27A, in the Kruppel-like factor 6 (KLF6) trans

162 KLF6-IVS1-27Gwt (i.e., less KLF6 splicing) was associate

163 on led us to explore the biology of wildtype KLF6 (KLF6(WT) ) and its antagonistic, alternatively spl

164 confer favorable prognosis in human cancers (Klf6, Klf9, Nid2, Ntn4, Per1, and Txnip) and underexpres

165 KLF6 knock down in human umbilical vein ECs promotes ALK

166 many proapoptotic genes, and shRNA-mediated KLF6 knockdown abrogated the ability of ERMAs to induce

167 KLF6 knockdown increases cell migration, consistent with

168 s and in liver tissues derived from a murine Klf6 knockdown model (DeltaKlf6).

169 Indeed, RAC1 activity is increased in KLF6-knockdown cells in a VAV3-dependent manner, and kno

170 In mice with hepatocyte-specific Klf6 knockout (DeltaKlf6), cell proliferation following

171 KLF6 (Kruppel-like factor 6) is a zinc finger transcript

172 onal repression, siRNA-mediated knockdown of KLF6, LCoR, or CtBP1 in PC-3 cells induced expression of

173 ssion was reduced and stable transfection of Klf6 led to up-regulation of Gck.

174 Additionally, loss of the KLF6 locus in the absence of somatic mutation in the rem

175 nism is circumvented in glioblastoma through KLF6 loss.

176 KLF6-mediated changes in E-cadherin levels were accompan

177 A key mechanism of KLF6-mediated growth suppression is through p53-independ

178 Functionally, GSK3beta enhanced KLF6-mediated growth suppression, which was abrogated by

179 riant 1 (SV1), which antagonizes full-length KLF6-mediated growth suppression.

180 LCoR contributes to KLF6-mediated transcriptional repression in a promoter-

181 Moreover, Klf6(+/-) mice have lower levels of Alk1 in their vascul

182 Klf6(-)(/)(-) mice have defects in hematopoiesis and ang

183 However, the vascular abnormalities in Klf6(-/-) mice obfuscate its role in liver development s

184 m2 mRNA in tumors from KLF6+/- compared with KLF6+/+ mice, which was validated by way of quantitative

185 res in both surrounding tissue and tumors of KLF6+/- mice closely recapitulated those associated with

186 After acute CCl(4), Klf6+/- mice developed significantly increased fibrosis

187 sistent with its role as a tumor suppressor, KLF6+/- mice developed significantly more tumors in resp

188 le of Klf6 in mouse development, we analyzed Klf6-/- mice and found that the homozygous mutation is e

189 dels generated include a global heterozygous KLF6 mouse (Klf6+/-), and transgenic mice expressing eit

190 stent with the correlation between decreased KLF6 mRNA levels and the presence of vascular invasion i

191 GCK and KLF6 mRNAs correlate directly in human NAFLD tissues and

192 KLF6 mutants derived from clinical prostate cancers fail

193 Several cancer-derived KLF6 mutants lead to the loss of p21-mediated growth sup

194 e growth-promoting effects of cancer-derived KLF6 mutants that lack tumor suppressor activity.

195 e growth-promoting effects of cancer-derived KLF6 mutants that lack tumor suppressor activity.Oncogen

196 cancer and hepatocellular carcinoma-derived KLF6 mutations affect a glycogen synthase kinase 3beta (

197 Transcription factor Kruppel-like factor 6 (KLF6)-myeloid-specific conditional deficient mice exhibi

198 on that transactivation of p21(WAF1/cip1) by KLF6 occurs through its direct recruitment to the p21(WA

199 he hematopoietic lineage with that of either Klf6+/- or Klf6+/+ ES cells.

200 nerated either by increasing SV1, decreasing KLF6, or both, accelerates hepatic carcinogenesis.

201 Whereas KLF6 overexpression in HCC cell lines and primary hepato

202 KLF6 overexpression partially phenocopied chaetocin trea

203 Klf6 overexpression studies in a mouse hepatocyte line w

204 Direct lysine acetylation of KLF6 peptides can be shown by mass spectrometry.

205 KLF6 phosphorylation is augmented in the presence of GSK

206 ealed that p73 and Sp1-like factors, Sp1 and KLF6, played key roles in the transcriptional control of

207 tumor suppressor gene Kruppel-like factor 6 (KLF6) plays a role in ERMA-induced apoptosis in LNCaP pr

208 tic splicing sites and encoded nonfunctional KLF6 proteins.

209 An increased SV1/KLF6 ratio correlates with more aggressive HCC.

210 In mice, an increased SV1/KLF6 ratio, generated either by increasing SV1, decreasi

211 KLF6 reduces fibrogenic activity of HSCs by way of two d

212 Targeted KLF6 reduction in an ovarian cancer cell line, SKOV-3, r

213 ur study identifies a new mechanism by which KLF6 regulates NF-kappaB signaling, and how this mechani

214 KLF6 regulates the expression of many proapoptotic genes

215 KLF6 regulation of GCK contributes to the development of

216 Collectively, our observations reveal that KLF6 repress BCL6 to enhance macrophage inflammatory gen

217 eracts with SP2 and KLF6, disrupting the SP2/KLF6 repressor complex.

218 observations, myeloid-specific deficiency of KLF6 significantly attenuates macrophage pro-inflammator

219 ction in flu-mediated apoptosis was noted in KLF6-silenced cells, cells treated with iNOS inhibitor,

220 Here we show that a germline KLF6 single nucleotide polymorphism, confirmed in a tri-

221 ing that yields a dominant-negative isoform, KLF6 splice variant 1 (SV1), which antagonizes full-leng

222 In contrast to full-length KLF6, splice variant KLF6-SV1 increases in NAFLD hepatoc

223 The molecular basis for stimulation of KLF6 splicing is unknown.

224 KLF6-IVS1-27Gwt (i.e., less KLF6 splicing) was associated with stepwise increases in

225 Forced expression of KLF6 strongly inhibits Dlk1 expression in preadipocytes

226 At the molecular level, KLF6 suppresses BCL6 mRNA and protein expression by elev

227 ungs and decreased survival, indicating that KLF6 suppresses both HCC development and metastasis.

228 KLF6 suppresses tumor growth and induces apoptosis in ca

229 r a farnesyl-transferase inhibitor decreases KLF6 SV1 and suppresses growth.

230 gonism between wtKLF6 and its splice variant KLF6 SV1 in tumor growth and dissemination.

231 mice >2-fold, short interfering RNA-mediated KLF6 SV1 inhibition reduces growth by approximately 50%

232 the splice factor ASF/SF2 by siRNA increases KLF6 SV1 messenger RNA levels.

233 otide polymorphism-increased splice isoform, KLF6 SV1, displays a markedly opposite effect on cell pr

234 s, Ras signaling increases the expression of KLF6 SV1, relative to full-length KLF6, thereby enhancin

235 l lines is overcome by ectopic expression of KLF6 SV1.

236 c transgenic mice overexpressing KLF6(WT) or KLF6(SV1) developed significantly diminished fibrosis wi

237 antagonistic, alternatively spliced isoform KLF6(SV1) in cultured HSCs and animal models.

238 late cells overexpressing either KLF6(WT) or KLF6(SV1) were more susceptible to apoptotic stress base

239 KLF6-SV1 (SV1), the major splice variant of KLF6, antago

240 The KLF6 variant proteins KLF6-SV1 and KLF6-SV2 are mislocalized to the cytoplasm,

241 KLF6-SV1 binds the proapoptotic BH3-only protein NOXA, w

242 ortant mediator by which changes in KLF6 and KLF6-SV1 can directly alter ovarian tumor invasion and m

243 Together, these findings demonstrate that KLF6-SV1 expression levels in PCa tumors at the time of

244 helial ovarian tumors with low KLF6 and high KLF6-SV1 expression ratios had significantly decreased E

245 these findings highlight a critical role for KLF6-SV1 in lung cancer, and show a potential novel ther

246 contrast to full-length KLF6, splice variant KLF6-SV1 increases in NAFLD hepatocytes and inversely co

247 ally delivered small interfering RNA against KLF6-SV1 induces spontaneous apoptosis of tumor cells, d

248 KLF6-SV1 inhibition using RNAi induced spontaneous apopt

249 In addition, KLF6-SV1 is a novel antiapoptotic protein in lung cancer

250 Here we show that increased expression of KLF6-SV1 is associated with decreased survival in patien

251 Analysis of tumor samples revealed that KLF6-SV1 levels were specifically upregulated in hormone

252 Interestingly, while KLF6-SV1 overexpression increased metastasis, it did not

253 Thus, KLF6-SV1 represents a novel regulator of protein interac

254 cadherin expression (P<0.01) and conversely, KLF6-SV1 silencing upregulated E-cadherin approximately

255 cancer cell lines, and targeted reduction of KLF6-SV1 using siRNA induces apoptosis both alone and in

256 -IVS1-27A polymorphism, which generates more KLF6-SV1, combats this, lowering hepatic insulin resista

257 tor 6 (KLF6) tumor suppressor gene, known as KLF6-SV1, in tumors from men after prostatectomy predict

258 which KLF6 and its antagonistic splice form, KLF6-SV1, regulate this development.

259 Here, we show that KLF6-SV1, whose overexpression is associated with poor s

260 omplementary mouse models of metastatic PCa, KLF6-SV1-overexpressing PCa cells were shown by in vivo

261 e splicing into an oncogenic splice variant, KLF6-SV1.

262 t generates a dominant-negative splice form, KLF6-SV1.

263 The KLF6 variant proteins KLF6-SV1 and KLF6-SV2 are mislocalized to the cytoplasm, antagonize w

264 eriments revealed LCoR regulation of several KLF6 target genes notably p21(WAF1/CIP1) (CDKN1A) and to

265 expression of CDKN1A and CDH1 and additional KLF6 target genes.

266 ression of KLF6 SV1, relative to full-length KLF6, thereby enhancing proliferation.

267 d by viral SV1 transduction and depletion of Klf6 through adenovirus-Cre infection of primary Klf6fl(

268 gnaling to increased alternative splicing of KLF6 through signaling by phosphatidylinositol-3 kinase

269 We show that KLF6 transactivates multiple genes negatively controllin

270 The rat Klf6 transcript has multiple splice forms that are homol

271 iption (RT)-PCR was performed to measure the KLF6 transcript level in eyes enucleated at embryonic st

272 uted to the action of a miR-122a target, the Klf6 transcript.

273 KLF6-IVS1-27A, in the Kruppel-like factor 6 (KLF6) transcription factor gene enhances its splicing in

274 noprecipitation analysis indicates that this KLF6 transcriptional activation was associated with incr

275 precipitation studies revealed that putative KLF6 transcriptional binding sites are present in the pr

276 in tissue remodeling, Kruppel-like factor 6 (KLF6) translocates to the cell nucleus during wound heal

277 ajor splice variant of KLF6, antagonizes the KLF6 tumor suppressor by an unknown mechanism.

278 ion in glioblastoma through depletion of the KLF6 tumor suppressor.

279 splice variant of the Kruppel-like factor 6 (KLF6) tumor suppressor gene, known as KLF6-SV1, in tumor

280 Forced expression of KLF6 using a tet-inducible system enhanced the hematopoi

281 tion of hemagglutinin (HA)-GSK3beta and Flag-KLF6 validated the interaction between these two protein

282 The KLF6 variant proteins KLF6-SV1 and KLF6-SV2 are mislocal

283 ly resected HCC, reduced tumor expression of KLF6 was associated with decreased survival.

284 Using luciferase assay and ChIP, KLF6 was established as a direct transcriptional activat

285 KLF6 was induced in hepatocytes in ALF, and in both acet

286 , whereas a candidate tumor suppressor gene (KLF6) was decreased.

287 Kruppel-like factor 6 (KLF6) was identified as a key transcriptional target of

288 Among these, Kruppel-like factor 6 (KLF6) was reduced in DDLPS, with increased H3K9me3 at as

289 ablish that GSK3beta directly phosphorylates KLF6, which augments its induction of p21 and resultant

290 e line were utilized to mechanistically link KLF6 with Gck promoter activity.

291 ation assay revealed a direct interaction of KLF6 with iNOS promoter during in vitro and in vivo flu

292 (HCV)-related HCC, an increased ratio of SV1/KLF6 within the tumor was associated with features of mo

293 us to explore the biology of wildtype KLF6 (KLF6(WT) ) and its antagonistic, alternatively spliced i

294 se HSCs overexpressing KLF6(WT) demonstrated KLF6(WT) binding to GC boxes in promoters of Colalpha1 (

295 chain reaction in mouse HSCs overexpressing KLF6(WT) demonstrated KLF6(WT) binding to GC boxes in pr

296 HSC-specific transgenic mice overexpressing KLF6(WT) or KLF6(SV1) developed significantly diminished

297 Stellate cells overexpressing either KLF6(WT) or KLF6(SV1) were more susceptible to apoptotic

298 Here we show that although wild-type KLF6 (wtKLF6) acts as a classic tumor suppressor, the si

299 Wild-type KLF6 (wtKLF6) expression is decreased in many human mali

300 d Gata1 were reduced by approximately 80% in Klf6-/- yolk sacs.