ライフサイエンスコーパス: KLF6

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

2 onsistent with transcriptional repression by KLF6.

3 a direct interaction of transfected SV1 with KLF6.

4 ona fide transcriptional target repressed by KLF6.

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

6 egulators of cell proliferation, p21Cip1 and KLF6.

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

8 of increased H3K9me3 may be mediated through KLF6.

9 nsactivation of a p21 promoter luciferase by KLF6.

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

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

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

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

14 Here we report that Kruppel like factor 6 (KLF6), a transcription factor of the zinc finger family,

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

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

17 KLF6, a ubiquitously expressed Kruppel-like transcriptio

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

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

20 KLF6 alternative splicing is not coupled to its transcri

21 etween activated Ras signaling and increased KLF6 alternative splicing.

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

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

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

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

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

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

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

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

30 anti-inflammatory agents oppositely regulate KLF6 and miR-223 expression in macrophages.

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 ed, ZZEF1 physically interacts with KLF9 and KLF6, and regulates a common set of target genes of thes

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

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

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

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

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

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

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

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

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

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

46 studies, we observed that overexpression of KLF6 attenuates and deficiency of KLF6 elevates miR-223

47 Reconstitution of KLF6 attenuates their malignant phenotype and induces ne

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

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

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

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

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

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

54 KLF6 binds directly to and activates the ATF3 promoter.

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

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

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

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

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

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

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

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

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

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

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

66 bserved that KLF6 overexpression elevate and KLF6 deficiency attenuate inducible HIF1alpha expression

67 t enrichment analysis studies uncovered that KLF6 deficiency attenuates broad inflammatory and glycol

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

69 Concordantly, myeloid-Klf6 deficiency significantly curbs diet-induced adipose

70 Klf6-deficiency leads to elevated levels of hedgehog pat

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

72 rtantly, genetic inhibition of miR-223-3P in KLF6-deficient macrophages completely reversed attenuate

73 urthermore, heightened miR-223 expression in KLF6-deficient macrophages significantly attenuates indu

74 flammatory and glycolytic gene expression in KLF6-deficient macrophages.

75 Our in vivo studies revealed that myeloid-KLF6-deficient mice were highly resistant to endotoxin-i

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

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

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

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

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

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

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

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

84 ocytes harboring both SV1 overexpression and Klf6 depletion.

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

86 At the molecular level, KLF6 directly represses miR-223 expression by occupying

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

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

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

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

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

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

93 ression of KLF6 attenuates and deficiency of KLF6 elevates miR-223 expression in macrophages.

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

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

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

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

98 Decreased KLF6 expression in human hepatocellular carcinoma (HCC)

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

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

101 KLF6 expression is driven by a robust super enhancer tha

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

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

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

105 KLF6 expression was induced early in response to ADR in

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

107 KLF6 expression was robustly induced by pro-inflammatory

108 nzymes, thereby abolishing the activation of KLF6 expression.

109 d-healing response, and transcription factor Klf6 expression.

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

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

112 KLF6 function is abrogated in human cancers owing to inc

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

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

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

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

117 KLF6 gene silencing in human lung epithelial cells resul

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

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

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

121 Collectively, our studies uncovered that KLF6 govern inflammatory and hypoxic response by regulat

122 e, we discovered that Kruppel-like factor 6 (KLF6) governs macrophage functions by promoting inflamma

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

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

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

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

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

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

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

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

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

132 ranscription factors HES1 in fibroblasts and KLF6 in keratinocytes not only compromised cell prolifer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 KLF6 is heterozygously deleted in 74.5% of the analyzed

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

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

154 Klf6 is rapidly induced in oligodendrocyte progenitors (

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

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

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

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

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

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

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

162 ree alternatively spliced, dominant-negative KLF6 isoforms.

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

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

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

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

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

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

169 KLF6 knock down in human umbilical vein ECs promotes ALK

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

171 KLF6 knockdown increases cell migration, consistent with

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

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

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

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

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

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

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

179 nism is circumvented in glioblastoma through KLF6 loss.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 KLF6 mutants derived from clinical prostate cancers fail

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

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

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

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

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

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

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

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

204 d loss-of-function studies, we observed that KLF6 overexpression elevate and KLF6 deficiency attenuat

205 Whereas KLF6 overexpression in HCC cell lines and primary hepato

206 KLF6 overexpression partially phenocopied chaetocin trea

207 Klf6 overexpression studies in a mouse hepatocyte line w

208 KLF6 phosphorylation is augmented in the presence of GSK

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

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

211 ike transcription factors (KLF), i.e., KLF4, KLF6, PLZF (promyelocytic leukemia zinc finger), and KLF

212 y less efficiently than GR and KL4: however, KLF6, PLZF, and GR had little effect on the bICP0 E prom

213 Collectively, our studies reveal that KLF6 promotes proinflammatory gene expression and functi

214 tic splicing sites and encoded nonfunctional KLF6 proteins.

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

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

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

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

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

220 KLF6 regulates the expression of many proapoptotic genes

221 KLF6 regulation of GCK contributes to the development of

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

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

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

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

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

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

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

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

230 We show that KLF6 supports the expression of lipid metabolism genes a

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

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

233 KLF6 suppresses tumor growth and induces apoptosis in ca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 KLF6-SV1 inhibition using RNAi induced spontaneous apopt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 We show that KLF6 transactivates multiple genes negatively controllin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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