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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 expression of the beta-globin gene
8                                              EKLF is essential for the expression of the beta-globin
9                                              EKLF residues acetylated by CREB binding protein (CBP) i
10                                              EKLF serves mostly as an activator of expression of thes
11                                              EKLF(-/-) embryos display a marked deficit in beta-globi
12                                              EKLF(-/-)KLF2(-/-) erythroid cells are markedly irregula
13                                              EKLF(-/-)KLF2(-/-) mice appear anemic at embryonic day 1
14                                              EKLF-deficient (Eklf(-/-)) mice die at day 14.5 of gesta
15                                              EKLF-specific binding to the CACCC element (-224 to -220
16                                              EKLF/KLF-1 containing histidine to alanine mutations tha
17                                              EKLF/KLF-1 is a 358-amino acid nuclear protein with an a
18                                              EKLF/KLF-1 is an erythroid-restricted transcription fact
19 acts with multiple proteins including FOG-1, EKLF, SP1, CBP/p300 and PU.1.
20 factor was attenuated and endogenous GATA-1, EKLF and betamaj-globin gene expression was activated.
21 pistatic reintroduction of either of these 2 EKLF target cell cycle inhibitors.
22 ht and electron microscopic analyses of E9.5 EKLF(-/-)KLF2(-/-) yolk sacs, and cytospins, indicate th
23                          Finally, acetylated EKLF has a higher affinity for the SWI-SNF chromatin rem
24                                          All EKLF mutants were expressed at wild-type levels, localiz
25                                     Although EKLF interacts equally well with H3.1 and H3.3, we find
26                                     Although EKLF's function during early erythropoiesis is well stud
27 ol region gamma/Luc-beta/Cat reporter and an EKLF expression vector.
28                           By establishing an EKLF-null erythroid line whose closed beta-locus chromat
29 es over the human beta-globin promoter in an EKLF-dependent manner.
30 vates p21 not only by directly binding to an EKLF site within a previously characterized GC-rich regi
31 plexes co-immunoprecipitates with GATA-1 and EKLF in murine fetal liver cells in vivo and is recruite
32  Fli-1 and EKLF, with victory for GATA-1 and EKLF leading to erythroid lineage specification.
33 between two of their target genes, Fli-1 and EKLF, with victory for GATA-1 and EKLF leading to erythr
34 ng phospho-CREB, JUN/FOS, GATA-1, Pit-1, and EKLF, failed to stimulate HAT activity.
35 r transcription factors, including NF-E2 and EKLF.
36 -specific nuclear factors GATA-1, NF-E2, and EKLF were identified within the first 300bp region of th
37 ved in early hematopoiesis (TAL1, GATA1, and EKLF) and overexpression of proteins involved in signali
38 fer from those seen in EKLF-heterozygous and EKLF-null red blood cells and presents a unique and unex
39 tigated the functional link between PIT1 and EKLF.
40                  Significant loss of Sp- and EKLF-mediated activation was observed with some internal
41 ediated acetylation is implicated in SP1 and EKLF, and may be a mechanism through which SCFAs induce
42  512 amino acids revealed that, like Sp1 and EKLF, FKLF has three contiguous zinc fingers at the near
43 Kruppel-like factor (BKLF) inhibited Sp1-and EKLF-mediated promoter activation.
44                                SP1, SP3, and EKLF further increased expression from HS2 epsilony prom
45 ggest that strategies designed to antagonize EKLF function in adults with hemoglobinopathy, in an att
46 olled by transcriptional regulators, such as EKLF and GATA1, that themselves exhibit tissue-restricte
47 ter-associated transcription factors such as EKLF.
48                                In this assay EKLF mediates a 500-fold induction of beta/CAT expressio
49 bin transcription, which surprisingly became EKLF dependent.
50        We demonstrate an interaction between EKLF and PIAS proteins confirmed by in vivo coimmunoprec
51 ults demonstrate that an interaction between EKLF and PIAS3 provides a novel mode of regulation of EK
52 We now find that a novel interaction between EKLF and the histone cell cycle regulation defective hom
53 sic or erythroid Kruppel-like factors (BKLF, EKLF) at the epsilony-CACCC site.
54                                         Both EKLF and KLF2 play roles in primitive erythroid cell dev
55 atients show higher level expression of both EKLF and PlGF mRNA in circulating blood cells, and marke
56                           Surprisingly, both EKLF NLSs, but principally the zinc finger domain, bind
57 t assays, the AHSP promoter CACCC site bound EKLF in a manner comparable to the beta-globin promoter
58 remodeling and transcriptional activation by EKLF in vitro.
59        Although site-specific DNA binding by EKLF is unaffected by the acetylation status of either o
60 the selective activation of the beta gene by EKLF, the CACCC boxes of beta and gamma genes were swapp
61  IL-12 p40 NFkappaB half-site was induced by EKLF for down-regulation of IL-12 p40 transcription in a
62 us, modification of histone H3, occupancy by EKLF, opening of the chromatin structure, and transcript
63     The bifunctional control of IL-12 p40 by EKLF and its modulation of NFkappaB support a potential
64 inhibition is achieved, at least in part, by EKLF repression of Fli-1 message levels.
65 conclude that the cell cycle as regulated by EKLF during late stages of differentiation is inherently
66      The AHSP promoter was transactivated by EKLF in K562 cells, which lack EKLF.
67                         In progenitor cells, EKLF is found predominantly at the periphery of the nucl
68                         In progenitor cells, EKLF modulates general cell growth and cell cycle regula
69                                 In contrast, EKLF increased the activity of the reporter plasmid by 3
70    We find that stimulation by cotransfected EKLF is retained with the mutant promoter, whereas repre
71 erted in the beta-globin promoter, decreases EKLF recruitment to and activity of the beta-globin prom
72 in immunoprecipitation analysis demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo.
73  ubiquitin-related modifier (SUMO)-dependent EKLF interaction with the Mi-2beta component of the NuRD
74 box in the beta or gamma promoter determined EKLF specificity, the proximal beta CACCC box sequence w
75 ythroid transcription factors GATA-1, NF-E2, EKLF, and tal-1/SCL.
76 oter configuration is important for enabling EKLF to exhibit any repressive activity.
77 an erythroblast cell line lacking endogenous EKLF expression (J2eDeltaeklf).
78 ansgene expression mimics that of endogenous EKLF as it begins by day 7.5 (d7.5) to d8.0.
79          In this case, TAF9 does not enhance EKLF activity and depletion of TAF9 has no effect on AHS
80 egulatory pathways, whereas in erythroblasts EKLF is associated with repression of these pathways.
81                            In erythroblasts, EKLF is distributed throughout the nucleus, and erythrob
82 d intrinsic contributions to erythropoiesis, EKLF thus plays a coordinating role between two differen
83                      These results establish EKLF as a tissue-specific transcription factor that unde
84 uires expression of the transcription factor EKLF, which is not present in K562 cells but is required
85               Erythroid Kruppel-like factor (EKLF [KLF1]) is a transcriptional regulator that plays a
86               Erythroid Kruppel-like factor (EKLF or KLF1) is a transcription factor crucial for red
87               Erythroid Kruppel-like factor (EKLF or KLF1) is a transcriptional regulator that plays
88               Erythroid Kruppel-like factor (EKLF or KLF1) positively regulates the beta-globin gene
89               Erythroid Kruppel-like factor (EKLF or KLF1) regulates adult beta-globin gene expressio
90  true for the erythroid Kruppel-like factor (EKLF) and the beta-globin promoter CACCC, a protein(s) b
91 itation, that erythroid-Krupple-like factor (EKLF) binds to embryonic/fetal globin gene promoters in
92  in the human erythroid Kruppel-like factor (EKLF) can lead to either anemia or the benign InLu pheno
93 eling complex erythroid Kruppel-like factor (EKLF) coactivator-remodeling complex 1 (E-RC1) disrupts
94 e lacking the erythroid Kruppel-like factor (EKLF) die in utero at embryonic day 15 (E15) from severe
95  of the human erythroid Kruppel-like factor (EKLF) in human primary macrophages and identify the role
96               Erythroid Kruppel-like factor (EKLF) is a hematopoietic-specific transcription factor t
97           The erythroid Kruppel-like factor (EKLF) is a key regulatory protein in globin gene express
98               Erythroid Kruppel-like factor (EKLF) is a Kruppel-like transcription factor identified
99               Erythroid Kruppel-like factor (EKLF) is a red cell-specific transcriptional activator t
100               Erythroid Kruppel-like factor (EKLF) is a zinc finger transcription factor required for
101               Erythroid Kruppel-like factor (EKLF) is an erythroid cell-specific transcription factor
102               Erythroid Kruppel-like factor (EKLF) is an erythroid zinc finger protein identified by
103               Erythroid Kruppel-like Factor (EKLF) is an erythroid-specific transcription factor that
104 iption factor erythroid Kruppel-like factor (EKLF) is an important activator of beta-globin gene expr
105  this regard, erythroid Kruppel-like factor (EKLF) is critical.
106               Erythroid Kruppel-like factor (EKLF) is essential for beta-globin gene transcription.
107 embers of the erythroid Kruppel-like factor (EKLF) multigene family contain three C-terminal zinc fin
108               Erythroid Kruppel-like factor (EKLF) plays an essential role in enabling beta-globin ex
109 expression of erythroid Kruppel-like factor (EKLF) precedes PlGF, and its enforced expression in huma
110 , Sp3, Sp4 or erythroid Kruppel-like factor (EKLF) specifically activates the hmGPD promoter B up to
111  site for the erythroid kruppel-like factor (EKLF) was placed in the epsilon-globin promoter at a pos
112 finger of the erythroid Kruppel-like factor (EKLF), a critical erythroid regulatory transcription fac
113  studies that erythroid Kruppel-like factor (EKLF), a transcription factor whose role in erythroid ge
114               Erythroid Kruppel-like factor (EKLF), which binds to the CACCC box in the beta-globin p
115 , GATA-1, and erythroid kruppel-like factor (EKLF), which function through cis elements of the beta-g
116 ctors such as erythroid Kruppel-like factor (EKLF), which is also known as Kruppel-like factor 1 (KLF
117 iption factor erythroid Kruppel-like factor (EKLF), which, like Sp1, binds to CACCC boxes.
118       Because Erythroid Kruppel-like Factor (EKLF)-knockout mice showed similar maturation defects, w
119 ion activator erythroid Kruppel-like factor (EKLF).
120 roid-specific erythroid Kruppel-like factor (EKLF).
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 nd die before E11.5, whereas single-knockout EKLF(-/-) or KLF2(-/-) embryos are grossly normal at E10
156 sactivated by EKLF in K562 cells, which lack EKLF.
157 ed to a GAL4 DNA binding domain, full-length EKLF or its zinc finger domain alone can repress transcr
158 required for establishment of both lineages, EKLF is uniquely down-regulated in megakaryocytes after
159 de by describing recent studies of mammalian EKLF/KLF1 mutations that lead to altered red cell phenot
160  not express the committed erythroid markers EKLF and GATA1, nor the terminally differentiated beta-l
161                Similar to its family member, EKLF, Neptune can bind CACCC-box and GC-rich DNA element
162 enable us to propose a model of how modified EKLF integrates coactivators, chromatin remodelers, and
163 th the role of EKLF as a chromatin modifier, EKLF binding sites in the E2f2 promoter were located in
164 r phosphorylation plays a role in modulating EKLF action.
165 t in the distal promoter region of the mouse EKLF gene that is critical for the expression of this tr
166  recombinant forms of wild-type and 5 mutant EKLF proteins and quantitated their binding affinity to
167                      In all cases the mutant EKLF allele occurred in the presence of a normal EKLF al
168                                  When mutant EKLF proteins were tested for beta/CAT activation, a nov
169                                      Mutated EKLF is attenuated in its ability to repress megakaryocy
170 en when expressed as a heterozygote, the Nan-EKLF protein accomplishes this by direct binding and abe
171    We concluded that deficiency of nonglobin EKLF target genes is a major contributor to the definiti
172  allele occurred in the presence of a normal EKLF allele.
173 r, we describe the identification of a novel EKLF interactor, Ppm1b, a serine-threonine protein phosp
174 8 (but not Lys-302) decreases the ability of EKLF to transactivate the beta-globin promoter in vivo a
175 f these genes in the presence and absence of EKLF.
176  We have investigated how the acetylation of EKLF plays a role in its ability to alter the beta-like
177 ells; therefore, the differential binding of EKLF to these promoters does not appear to result from c
178 fy PIAS3 as a transcriptional corepressor of EKLF for at least a subset of its target genes during er
179                          Third, depletion of EKLF prevents recruitment of TAF9 to the beta-globin pro
180 ese results with the nuclear distribution of EKLF, RNA-Seq analysis of the transcriptome, and the occ
181 G1 interacted with an even smaller domain of EKLF, suggesting that additional protein interactions ar
182 dult beta-globin gene, functional domains of EKLF were examined in the context of chromatin remodelin
183 n activated RAW264.7 cells, but no effect of EKLF on NFkappaB activity was observed in resting RAW264
184 rm selectively interferes with expression of EKLF target genes whose promoter elements it no longer b
185 lls but rescued by conditional expression of EKLF.
186 on of EKLF, we demonstrate the importance of EKLF acetylation at lysine 288 in the recruitment of CBP
187  all expressed in the EBs, BMP4 induction of EKLF and GATA1 transcription is not immediate.
188 ibitory Smad6 protein prevented induction of EKLF or GATA1 even in the presence of serum.
189 ay plays a critical role in the induction of EKLF, and transient transfection analyses demonstrate th
190 us can be rescued by retroviral infection of EKLF, we demonstrate the importance of EKLF acetylation
191 We used ChIP-Seq to study the interactome of EKLF in mouse erythroid progenitor cells and more differ
192                  Interestingly, the level of EKLF in definitive cells is 3-fold higher than the level
193 -hgamma(2) hemoglobin in the fetal livers of EKLF(-/-) animals, hemolysis was not corrected and survi
194 R319Efs) EKLF mutations, monoallelic loss of EKLF does not result in haploinsufficiency at all loci.
195          However, a TAF9-independent mode of EKLF transcriptional activation is exhibited by the alph
196 s is that post-translational modification of EKLF differs within erythroid cell populations and regul
197 2)-terminal and internal deletion mutants of EKLF were constructed.
198     The nuclear localization signal (NLS) of EKLF/KLF-1 has not been empirically determined.
199 ing a crucial pathway to direct the onset of EKLF and GATA1 expression during hematopoietic different
200 on, which coincides with the normal onset of EKLF expression.
201   Wild-type chromatin demonstrated a peak of EKLF binding over a promoter region CACCC box that diffe
202 titated their binding affinity to a range of EKLF-regulated genes.
203 e role of the promoter on the recruitment of EKLF to 5'HS2 and 5'HS3 of the LCR.
204 hroid leukemia cells, whereas recruitment of EKLF to 5'HS2 occurred in both gamma-globin-expressing K
205                  We find that recruitment of EKLF to 5'HS2 requires the TATA box, but recruitment to
206        We have found that the recruitment of EKLF to 5'HS3 depends on the presence of 5'HS2 in cis, b
207                  Furthermore, recruitment of EKLF to 5'HS3 only occurred in beta-globin-expressing mu
208                      Although recruitment of EKLF to a promoter is required to show repression, its z
209 ined how one 5'HS affects the recruitment of EKLF to another 5'HS.
210 he E2f2 promoter were located in a region of EKLF-dependent DNase I sensitivity in early erythroid pr
211 PIAS3 provides a novel mode of regulation of EKLF activity in the absence of sumolylation and further
212  this issue by focusing on the regulation of EKLF/KLF1, a zinc finger transcription factor that plays
213                  Consistent with the role of EKLF as a chromatin modifier, EKLF binding sites in the
214 primary macrophages and identify the role of EKLF in IL-12 p40 expression.
215 ng flow cytometry to investigate the role of EKLF in vivo and have performed functional studies using
216 ations in the promoter or coding sequence of EKLF in 21 of 24 persons with the In(Lu) phenotype.
217 tation alters the DNA-binding specificity of EKLF so that it no longer binds promoters of a subset of
218 throid cell alters the acetylation status of EKLF and plays a critical role in directing its coactiva
219 s demonstrate that the acetylation status of EKLF is critical for its optimal activity and suggest a
220 ssion of p18 and p27, a new direct target of EKLF.
221 KLF promoter and exerts a positive effect on EKLF levels.
222   Mutation of this site has little effect on EKLF's ability to function as a transcriptional activato
223 rythroid NIH/3T3 cells of SP1, SP3, BKLF, or EKLF and HS2 epsilony promoter-luciferase constructs, wi
224 hat shRNA-driven depletion of either PIT1 or EKLF impairs erythroid maturation of G1E cells in vitro,
225                  We sought to identify other EKLF target genes and determine the chromatin status of
226 NA was consistently induced by overexpressed EKLF in resting RAW264.7 cells, whereas EKLF suppressed
227                        To discover potential EKLF target genes responsible for the failure of erythro
228  by the binding of a repressor that prevents EKLF from activating the epsilon-globin gene.
229 tained only when it is fused to the proximal EKLF promoter, which contains an important GATA site.
230  K292X) and frameshift (P190Lfs and R319Efs) EKLF mutations, monoallelic loss of EKLF does not result
231 BMP4 was necessary and sufficient to recover EKLF and GATA1 expression and could be further stimulate
232 omoters by studying their ability to recruit EKLF.
233 1b likely has an indirect role in regulating EKLF turnover via its zinc finger domain.
234  activation of the erythropoietic regulators EKLF and GATA binding protein 1 (GATA1).
235  exhibits stage specificity, with reversible EKLF-Sin3A interactions playing a key role in this proce
236  critical role of residues within the second EKLF zinc finger domain.
237 ghout the nucleus, and erythroblast-specific EKLF occupancy is predominantly in intragenic regions.
238 cell line, we show that Ppm1b superactivates EKLF at the beta-globin and BKLF promoters, dependent on
239            First, TAF9 functionally supports EKLF activity by enhancing its ability to activate the b
240 that two nuclear localization signals target EKLF to the nucleus and suggest this transport relies pr
241 ain transcription factors (TFIIEbeta, TFIIF, EKLF and p53).
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

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