ライフサイエンスコーパス: EKLF

1 EKLF activates p21 not only by directly binding to an EK

2 EKLF and KLF2 may have coordinate roles in a common prog

3 EKLF binds strongly to adult globin gene promoters and t

4 EKLF inhibits the formation of megakaryocytes while at t

5 EKLF is a key transcription factor that is necessary for

6 EKLF is a red cell-specific activator whose presence is

7 EKLF is essential for the expression of the beta-globin

8 EKLF residues acetylated by CREB binding protein (CBP) i

9 EKLF serves mostly as an activator of expression of thes

10 EKLF(-/-) embryos display a marked deficit in beta-globi

11 EKLF(-/-)KLF2(-/-) erythroid cells are markedly irregula

12 EKLF(-/-)KLF2(-/-) mice appear anemic at embryonic day 1

13 EKLF-deficient (Eklf(-/-)) mice die at day 14.5 of gesta

14 EKLF-specific binding to the CACCC element (-224 to -220

15 EKLF/KLF-1 containing histidine to alanine mutations tha

16 EKLF/KLF-1 is a 358-amino acid nuclear protein with an a

17 EKLF/KLF-1 is an erythroid-restricted transcription fact

18 acts with multiple proteins including FOG-1, EKLF, SP1, CBP/p300 and PU.1.

19 factor was attenuated and endogenous GATA-1, EKLF and betamaj-globin gene expression was activated.

20 pistatic reintroduction of either of these 2 EKLF target cell cycle inhibitors.

21 ht and electron microscopic analyses of E9.5 EKLF(-/-)KLF2(-/-) yolk sacs, and cytospins, indicate th

22 Finally, acetylated EKLF has a higher affinity for the SWI-SNF chromatin rem

23 All EKLF mutants were expressed at wild-type levels, localiz

24 Although EKLF interacts equally well with H3.1 and H3.3, we find

25 Although EKLF's function during early erythropoiesis is well stud

26 ol region gamma/Luc-beta/Cat reporter and an EKLF expression vector.

27 By establishing an EKLF-null erythroid line whose closed beta-locus chromat

28 es over the human beta-globin promoter in an EKLF-dependent manner.

29 vates p21 not only by directly binding to an EKLF site within a previously characterized GC-rich regi

30 plexes co-immunoprecipitates with GATA-1 and EKLF in murine fetal liver cells in vivo and is recruite

31 Fli-1 and EKLF, with victory for GATA-1 and EKLF leading to erythroid lineage specification.

32 between two of their target genes, Fli-1 and EKLF, with victory for GATA-1 and EKLF leading to erythr

33 ng phospho-CREB, JUN/FOS, GATA-1, Pit-1, and EKLF, failed to stimulate HAT activity.

34 r transcription factors, including NF-E2 and EKLF.

35 -specific nuclear factors GATA-1, NF-E2, and EKLF were identified within the first 300bp region of th

36 ved in early hematopoiesis (TAL1, GATA1, and EKLF) and overexpression of proteins involved in signali

37 fer from those seen in EKLF-heterozygous and EKLF-null red blood cells and presents a unique and unex

38 tigated the functional link between PIT1 and EKLF.

39 Significant loss of Sp- and EKLF-mediated activation was observed with some internal

40 ediated acetylation is implicated in SP1 and EKLF, and may be a mechanism through which SCFAs induce

41 512 amino acids revealed that, like Sp1 and EKLF, FKLF has three contiguous zinc fingers at the near

42 Kruppel-like factor (BKLF) inhibited Sp1-and EKLF-mediated promoter activation.

43 SP1, SP3, and EKLF further increased expression from HS2 epsilony prom

44 ggest that strategies designed to antagonize EKLF function in adults with hemoglobinopathy, in an att

45 olled by transcriptional regulators, such as EKLF and GATA1, that themselves exhibit tissue-restricte

46 ter-associated transcription factors such as EKLF.

47 In this assay EKLF mediates a 500-fold induction of beta/CAT expressio

48 bin transcription, which surprisingly became EKLF dependent.

49 We demonstrate an interaction between EKLF and PIAS proteins confirmed by in vivo coimmunoprec

50 ults demonstrate that an interaction between EKLF and PIAS3 provides a novel mode of regulation of EK

51 We now find that a novel interaction between EKLF and the histone cell cycle regulation defective hom

52 sic or erythroid Kruppel-like factors (BKLF, EKLF) at the epsilony-CACCC site.

53 Both EKLF and KLF2 play roles in primitive erythroid cell dev

54 atients show higher level expression of both EKLF and PlGF mRNA in circulating blood cells, and marke

55 Surprisingly, both EKLF NLSs, but principally the zinc finger domain, bind

56 t assays, the AHSP promoter CACCC site bound EKLF in a manner comparable to the beta-globin promoter

57 remodeling and transcriptional activation by EKLF in vitro.

58 Although site-specific DNA binding by EKLF is unaffected by the acetylation status of either o

59 the selective activation of the beta gene by EKLF, the CACCC boxes of beta and gamma genes were swapp

60 IL-12 p40 NFkappaB half-site was induced by EKLF for down-regulation of IL-12 p40 transcription in a

61 us, modification of histone H3, occupancy by EKLF, opening of the chromatin structure, and transcript

62 The bifunctional control of IL-12 p40 by EKLF and its modulation of NFkappaB support a potential

63 inhibition is achieved, at least in part, by EKLF repression of Fli-1 message levels.

64 conclude that the cell cycle as regulated by EKLF during late stages of differentiation is inherently

65 The AHSP promoter was transactivated by EKLF in K562 cells, which lack EKLF.

66 In progenitor cells, EKLF is found predominantly at the periphery of the nucl

67 In progenitor cells, EKLF modulates general cell growth and cell cycle regula

68 In contrast, EKLF increased the activity of the reporter plasmid by 3

69 We find that stimulation by cotransfected EKLF is retained with the mutant promoter, whereas repre

70 erted in the beta-globin promoter, decreases EKLF recruitment to and activity of the beta-globin prom

71 in immunoprecipitation analysis demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo.

72 ubiquitin-related modifier (SUMO)-dependent EKLF interaction with the Mi-2beta component of the NuRD

73 box in the beta or gamma promoter determined EKLF specificity, the proximal beta CACCC box sequence w

74 ythroid transcription factors GATA-1, NF-E2, EKLF, and tal-1/SCL.

75 oter configuration is important for enabling EKLF to exhibit any repressive activity.

76 an erythroblast cell line lacking endogenous EKLF expression (J2eDeltaeklf).

77 ansgene expression mimics that of endogenous EKLF as it begins by day 7.5 (d7.5) to d8.0.

78 In this case, TAF9 does not enhance EKLF activity and depletion of TAF9 has no effect on AHS

79 egulatory pathways, whereas in erythroblasts EKLF is associated with repression of these pathways.

80 In erythroblasts, EKLF is distributed throughout the nucleus, and erythrob

81 d intrinsic contributions to erythropoiesis, EKLF thus plays a coordinating role between two differen

82 These results establish EKLF as a tissue-specific transcription factor that unde

83 uires expression of the transcription factor EKLF, which is not present in K562 cells but is required

84 Erythroid Kruppel-like factor (EKLF [KLF1]) is a transcriptional regulator that plays a

85 Erythroid Kruppel-like factor (EKLF or KLF1) is a transcription factor crucial for red

86 Erythroid Kruppel-like factor (EKLF or KLF1) is a transcriptional regulator that plays

87 Erythroid Kruppel-like factor (EKLF or KLF1) positively regulates the beta-globin gene

88 Erythroid Kruppel-like factor (EKLF or KLF1) regulates adult beta-globin gene expressio

89 true for the erythroid Kruppel-like factor (EKLF) and the beta-globin promoter CACCC, a protein(s) b

90 itation, that erythroid-Krupple-like factor (EKLF) binds to embryonic/fetal globin gene promoters in

91 in the human erythroid Kruppel-like factor (EKLF) can lead to either anemia or the benign InLu pheno

92 eling complex erythroid Kruppel-like factor (EKLF) coactivator-remodeling complex 1 (E-RC1) disrupts

93 e lacking the erythroid Kruppel-like factor (EKLF) die in utero at embryonic day 15 (E15) from severe

94 of the human erythroid Kruppel-like factor (EKLF) in human primary macrophages and identify the role

95 Erythroid Kruppel-like factor (EKLF) is a hematopoietic-specific transcription factor t

96 The erythroid Kruppel-like factor (EKLF) is a key regulatory protein in globin gene express

97 Erythroid Kruppel-like factor (EKLF) is a Kruppel-like transcription factor identified

98 Erythroid Kruppel-like factor (EKLF) is a red cell-specific transcriptional activator t

99 Erythroid Kruppel-like factor (EKLF) is a zinc finger transcription factor required for

100 Erythroid Kruppel-like factor (EKLF) is an erythroid cell-specific transcription factor

101 Erythroid Kruppel-like factor (EKLF) is an erythroid zinc finger protein identified by

102 Erythroid Kruppel-like Factor (EKLF) is an erythroid-specific transcription factor that

103 iption factor erythroid Kruppel-like factor (EKLF) is an important activator of beta-globin gene expr

104 this regard, erythroid Kruppel-like factor (EKLF) is critical.

105 Erythroid Kruppel-like factor (EKLF) is essential for beta-globin gene transcription.

106 embers of the erythroid Kruppel-like factor (EKLF) multigene family contain three C-terminal zinc fin

107 Erythroid Kruppel-like factor (EKLF) plays an essential role in enabling beta-globin ex

108 expression of erythroid Kruppel-like factor (EKLF) precedes PlGF, and its enforced expression in huma

109 , Sp3, Sp4 or erythroid Kruppel-like factor (EKLF) specifically activates the hmGPD promoter B up to

110 site for the erythroid kruppel-like factor (EKLF) was placed in the epsilon-globin promoter at a pos

111 finger of the erythroid Kruppel-like factor (EKLF), a critical erythroid regulatory transcription fac

112 studies that erythroid Kruppel-like factor (EKLF), a transcription factor whose role in erythroid ge

113 Erythroid Kruppel-like factor (EKLF), which binds to the CACCC box in the beta-globin p

114 , GATA-1, and erythroid kruppel-like factor (EKLF), which function through cis elements of the beta-g

115 ctors such as erythroid Kruppel-like factor (EKLF), which is also known as Kruppel-like factor 1 (KLF

116 iption factor erythroid Kruppel-like factor (EKLF), which, like Sp1, binds to CACCC boxes.

117 Because Erythroid Kruppel-like Factor (EKLF)-knockout mice showed similar maturation defects, w

118 ion activator erythroid Kruppel-like factor (EKLF).

119 roid-specific erythroid Kruppel-like factor (EKLF).

120 ter regulator erythroid Kruppel-like factor (EKLF, also known as KLF1).

121 Erythroid Kruppel-like Factor (EKLF/KLF-1) is an erythroid-specific transcription facto

122 Erythroid Kruppel-like Factor (EKLF/KLF1) is a master transcriptional regulator of eryt

123 Erythroid Kruppel-like factor (EKLF/KLF1) is one of a very small number of intrinsic tr

124 n (Tal1), and Erythroid Kruppel-like factor (EKLF; henceforth referred to as Klf1)].

125 Erythroid Kruppel-like factor (EKLF; KLF1) is an erythroid-specific transcription facto

126 Erythroid Kruppel-like factor (EKLF; KLF1), a crucial zinc finger transcription factor,

127 -1 (including erythroid Kruppel-like factor [EKLF] and the erythropoietin [Epo] receptor).

128 Each site is essential for EKLF expression indicating that the three binding sites

129 To identify essential domains required for EKLF transactivation function, we cotransfected a human

130 CACCC element revealed a dependent role for EKLF binding in activating IL-12 p40 transcription in re

131 Chromatin at the AHSP promoter from EKLF-deficient cells lacked a DNase I hypersensitive sit

132 ed pathology, indicating that one functional EKLF allele is sufficient to sustain human erythropoiesi

133 ing the FOG-1-independent GATA-1 target gene EKLF.

134 potential interactions between these genes, EKLF/KLF2 double-mutant embryos were analyzed.

135 lts, we present a model that illustrates how EKLF may be recruited to the beta-globin locus.

136 between these two elements may regulate how EKLF is recruited to the LCR.

137 Human EKLF (hEKLF) sequences, linked to an estrogen-responsive

138 scription of inactivating mutations in human EKLF and the first demonstration of a blood group phenot

139 Taken together, we identify EKLF as a transcription factor in macrophages able to re

140 s megakaryocyte differentiation, implicating EKLF sumoylation status in differentiative decisions ema

141 n-induced expression of PlGF is abolished in EKLF-deficient murine erythroid cells but rescued by con

142 tion in AHSP mRNA and the absence of AHSP in EKLF-deficient cells.

143 ts suggest that temporal-specific changes in EKLF abundance result in differential binding of this es

144 during development and that these changes in EKLF binding specificity mediate the competitive interac

145 ood cell abnormalities and prenatal death in EKLF(-/-) embryos.

146 mented by coactivators and was diminished in EKLF mutants that were unable to undergo histone/factor-

147 , we corrected the globin chain imbalance in EKLF(-/-) embryos by breeding with a strain of mice that

148 ls in vitro, whereas reexpression of PIT1 in EKLF-depleted G1E cells partially restores erythroid mat

149 and betah1-globin mRNA is greatly reduced in EKLF(-/-)KLF2(-/-), compared with EKLF(-/-) or KLF2(-/-)

150 deficiencies that differ from those seen in EKLF-heterozygous and EKLF-null red blood cells and pres

151 ll-specific transcription factors, including EKLF and Tal-1.

152 ) of several zinc finger proteins, including EKLF, interact directly with SWI/SNF to generate DNase I

153 Most intriguingly, EKLF repression exhibits stage specificity, with reversi

154 For example, erythroid KLF (EKLF) regulates beta-globin expression during erythroid

155 Kruppel-like factor 1 (KLF1/EKLF) is a transcription factor that globally activates

156 nd die before E11.5, whereas single-knockout EKLF(-/-) or KLF2(-/-) embryos are grossly normal at E10

157 sactivated by EKLF in K562 cells, which lack EKLF.

158 ed to a GAL4 DNA binding domain, full-length EKLF or its zinc finger domain alone can repress transcr

159 required for establishment of both lineages, EKLF is uniquely down-regulated in megakaryocytes after

160 de by describing recent studies of mammalian EKLF/KLF1 mutations that lead to altered red cell phenot

161 not express the committed erythroid markers EKLF and GATA1, nor the terminally differentiated beta-l

162 Similar to its family member, EKLF, Neptune can bind CACCC-box and GC-rich DNA element

163 enable us to propose a model of how modified EKLF integrates coactivators, chromatin remodelers, and

164 th the role of EKLF as a chromatin modifier, EKLF binding sites in the E2f2 promoter were located in

165 r phosphorylation plays a role in modulating EKLF action.

166 t in the distal promoter region of the mouse EKLF gene that is critical for the expression of this tr

167 recombinant forms of wild-type and 5 mutant EKLF proteins and quantitated their binding affinity to

168 In all cases the mutant EKLF allele occurred in the presence of a normal EKLF al

169 When mutant EKLF proteins were tested for beta/CAT activation, a nov

170 Mutated EKLF is attenuated in its ability to repress megakaryocy

171 en when expressed as a heterozygote, the Nan-EKLF protein accomplishes this by direct binding and abe

172 We concluded that deficiency of nonglobin EKLF target genes is a major contributor to the definiti

173 allele occurred in the presence of a normal EKLF allele.

174 r, we describe the identification of a novel EKLF interactor, Ppm1b, a serine-threonine protein phosp

175 8 (but not Lys-302) decreases the ability of EKLF to transactivate the beta-globin promoter in vivo a

176 f these genes in the presence and absence of EKLF.

177 We have investigated how the acetylation of EKLF plays a role in its ability to alter the beta-like

178 ells; therefore, the differential binding of EKLF to these promoters does not appear to result from c

179 fy PIAS3 as a transcriptional corepressor of EKLF for at least a subset of its target genes during er

180 Third, depletion of EKLF prevents recruitment of TAF9 to the beta-globin pro

181 ese results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occ

182 G1 interacted with an even smaller domain of EKLF, suggesting that additional protein interactions ar

183 dult beta-globin gene, functional domains of EKLF were examined in the context of chromatin remodelin

184 n activated RAW264.7 cells, but no effect of EKLF on NFkappaB activity was observed in resting RAW264

185 rm selectively interferes with expression of EKLF target genes whose promoter elements it no longer b

186 lls but rescued by conditional expression of EKLF.

187 on of EKLF, we demonstrate the importance of EKLF acetylation at lysine 288 in the recruitment of CBP

188 all expressed in the EBs, BMP4 induction of EKLF and GATA1 transcription is not immediate.

189 ibitory Smad6 protein prevented induction of EKLF or GATA1 even in the presence of serum.

190 ay plays a critical role in the induction of EKLF, and transient transfection analyses demonstrate th

191 us can be rescued by retroviral infection of EKLF, we demonstrate the importance of EKLF acetylation

192 We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differ

193 Interestingly, the level of EKLF in definitive cells is 3-fold higher than the level

194 -hgamma(2) hemoglobin in the fetal livers of EKLF(-/-) animals, hemolysis was not corrected and survi

195 R319Efs) EKLF mutations, monoallelic loss of EKLF does not result in haploinsufficiency at all loci.

196 However, a TAF9-independent mode of EKLF transcriptional activation is exhibited by the alph

197 s is that post-translational modification of EKLF differs within erythroid cell populations and regul

198 2)-terminal and internal deletion mutants of EKLF were constructed.

199 The nuclear localization signal (NLS) of EKLF/KLF-1 has not been empirically determined.

200 ing a crucial pathway to direct the onset of EKLF and GATA1 expression during hematopoietic different

201 on, which coincides with the normal onset of EKLF expression.

202 Wild-type chromatin demonstrated a peak of EKLF binding over a promoter region CACCC box that diffe

203 titated their binding affinity to a range of EKLF-regulated genes.

204 e role of the promoter on the recruitment of EKLF to 5'HS2 and 5'HS3 of the LCR.

205 hroid leukemia cells, whereas recruitment of EKLF to 5'HS2 occurred in both gamma-globin-expressing K

206 We find that recruitment of EKLF to 5'HS2 requires the TATA box, but recruitment to

207 We have found that the recruitment of EKLF to 5'HS3 depends on the presence of 5'HS2 in cis, b

208 Furthermore, recruitment of EKLF to 5'HS3 only occurred in beta-globin-expressing mu

209 Although recruitment of EKLF to a promoter is required to show repression, its z

210 ined how one 5'HS affects the recruitment of EKLF to another 5'HS.

211 he E2f2 promoter were located in a region of EKLF-dependent DNase I sensitivity in early erythroid pr

212 PIAS3 provides a novel mode of regulation of EKLF activity in the absence of sumolylation and further

213 this issue by focusing on the regulation of EKLF/KLF1, a zinc finger transcription factor that plays

214 Consistent with the role of EKLF as a chromatin modifier, EKLF binding sites in the

215 primary macrophages and identify the role of EKLF in IL-12 p40 expression.

216 ng flow cytometry to investigate the role of EKLF in vivo and have performed functional studies using

217 ations in the promoter or coding sequence of EKLF in 21 of 24 persons with the In(Lu) phenotype.

218 tation alters the DNA-binding specificity of EKLF so that it no longer binds promoters of a subset of

219 throid cell alters the acetylation status of EKLF and plays a critical role in directing its coactiva

220 s demonstrate that the acetylation status of EKLF is critical for its optimal activity and suggest a

221 ssion of p18 and p27, a new direct target of EKLF.

222 KLF promoter and exerts a positive effect on EKLF levels.

223 Mutation of this site has little effect on EKLF's ability to function as a transcriptional activato

224 rythroid NIH/3T3 cells of SP1, SP3, BKLF, or EKLF and HS2 epsilony promoter-luciferase constructs, wi

225 hat shRNA-driven depletion of either PIT1 or EKLF impairs erythroid maturation of G1E cells in vitro,

226 We sought to identify other EKLF target genes and determine the chromatin status of

227 NA was consistently induced by overexpressed EKLF in resting RAW264.7 cells, whereas EKLF suppressed

228 To discover potential EKLF target genes responsible for the failure of erythro

229 by the binding of a repressor that prevents EKLF from activating the epsilon-globin gene.

230 tained only when it is fused to the proximal EKLF promoter, which contains an important GATA site.

231 K292X) and frameshift (P190Lfs and R319Efs) EKLF mutations, monoallelic loss of EKLF does not result

232 BMP4 was necessary and sufficient to recover EKLF and GATA1 expression and could be further stimulate

233 omoters by studying their ability to recruit EKLF.

234 1b likely has an indirect role in regulating EKLF turnover via its zinc finger domain.

235 activation of the erythropoietic regulators EKLF and GATA binding protein 1 (GATA1).

236 exhibits stage specificity, with reversible EKLF-Sin3A interactions playing a key role in this proce

237 critical role of residues within the second EKLF zinc finger domain.

238 ghout the nucleus, and erythroblast-specific EKLF occupancy is predominantly in intragenic regions.

239 cell line, we show that Ppm1b superactivates EKLF at the beta-globin and BKLF promoters, dependent on

240 First, TAF9 functionally supports EKLF activity by enhancing its ability to activate the b

241 that two nuclear localization signals target EKLF to the nucleus and suggest this transport relies pr

242 e grossly normal at E10.5 and die later than EKLF(-/-)KLF2(-/-) embryos.

243 We conclude that EKLF is a phosphoprotein whose ability to transcriptiona

244 These studies demonstrate that EKLF directs different modes of tissue-specific transcri

245 Our findings demonstrate that EKLF, likely in coordination with other transcription fa

246 We demonstrated that EKLF increases PIT1 expression during RBC maturation by

247 It was recently demonstrated that EKLF is also required for the activity of the beta-globi

248 Here, we present evidence that EKLF interacts with proteins from the PIAS (protein inhi

249 beling-immunoprecipitation experiments, that EKLF is acetylated in the erythroid cell.

250 Here, we find that EKLF also plays a role during the subsequent differentia

251 We also find that EKLF helps to coordinate this process by the specific as

252 We find that EKLF interacts with TATA binding protein-associated fact

253 We find that EKLF is posttranslationally modified by sumoylation at a

254 These results support the hypothesis that EKLF acts as a transcription factor and a chromatin modu

255 The data indicate that EKLF and KLF2 have redundant functions in embryonic beta

256 AHSP and beta-globin genes and indicate that EKLF may play similar roles for other erythroid genes.

257 Chromatin immunoprecipitation reveals that EKLF binds to the PlGF promoter region.

258 Here we show that EKLF can also interact with the corepressors mSin3A and

259 sed the in vivo PIN*POINT assay to show that EKLF is recruited to the beta-globin promoter but not to

260 We had previously shown that EKLF preferentially interacts with histone H3 and that t

261 These results suggest that EKLF may function in vivo as a transcription repressor a

262 The EKLF interactome shows very little overlap with the inte

263 only the BRG1-BAF155 minimal complex and the EKLF zinc finger DBD, whereas transcription requires, in

264 lates, both the locus control region and the EKLF-binding site are important for their recruitment to

265 ating a broader recognition sequence for the EKLF consensus binding site.

266 moter region CACCC box that differs from the EKLF consensus by a nucleotide.

267 sus sequences eliminates expression from the EKLF promoter in transgenic mice.

268 ts with known regulatory DNA elements in the EKLF and Tal-1 gene loci in erythroid cells.

269 tation abolished a GATA1 binding site in the EKLF promoter (-124T>C).

270 proteins that, although not involved in the EKLF-PIAS3 interaction, is required for the transrepress

271 minant neonatal anemia (Nan) mutation in the EKLF/KLF1 transcription factor leads to ectopic expressi

272 ivator element for in vivo expression of the EKLF gene.

273 n, optimal transcriptional activation of the EKLF locus can be established.

274 n essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF level

275 the availability and optimal activity of the EKLF protein in erythroid cells.

276 o verify that 950 bp located adjacent to the EKLF start site of transcription is sufficient to genera

277 status of a specific site located within the EKLF interaction domain, and that serine/threonine kinas

278 However, regions within the EKLF protein that serve as signals for its nuclear local

279 Thus, EKLF possesses at least two potent transactivation domai

280 T) family that convey repressive activity to EKLF in the absence of sumoylation.

281 cent protein or pyruvate kinase was fused to EKLF domains, and localization was monitored and quantit

282 This mutation led to EKLF-independent epsilon-globin transcription during def

283 KLF2 (LKLF) is closely related to EKLF and is expressed in erythroid cells.

284 Co-transfected EKLF was synergistic with either Sp1 or Sp3.

285 markably, even when mutant Nan and wild-type EKLF alleles are expressed at equivalent levels, the mut

286 is required for superactivation of wild-type EKLF.

287 Unlike EKLF, Sp1, which also binds to CACCC boxes, is not recru

288 antly at the periphery of the nucleus, where EKLF primarily occupies the promoter regions of genes an

289 scription in resting RAW264.7 cells, whereas EKLF overexpression in the presence or absence of this e

290 ssed EKLF in resting RAW264.7 cells, whereas EKLF suppressed IL-12 p40 expression in activated RAW264

291 al activity and suggest a mechanism by which EKLF acts as an integrator of remodeling and transcripti

292 acetylation and suggest a mechanism by which EKLF is able to alter chromatin structure and induce bet

293 GATA2, or TAL1, leading to a model in which EKLF directs programs that are independent of those regu

294 s 3 major aspects of erythropoiesis in which EKLF plays crucial functions: (1) at the megakaryocyte-e

295 We propose a model in which EKLF-dependent activation and modification of the E2f2 l

296 reduced in EKLF(-/-)KLF2(-/-), compared with EKLF(-/-) or KLF2(-/-) embryos, consistent with the obse

297 We show that Ppm1b interacts with EKLF via its PEST1 sequence.

298 f the beta-globin gene, which interacts with EKLF, and the basic transcription element (BTE) of the C

299 rotein may therefore actively interfere with EKLF-dependent processes by destabilizing transcription

300 omatin over the beta-globin promoter without EKLF in vitro, it has been proposed that SWI/SNF1-like c