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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
20 factor was attenuated and endogenous GATA-1, EKLF and betamaj-globin gene expression was activated.
22 ht and electron microscopic analyses of E9.5 EKLF(-/-)KLF2(-/-) yolk sacs, and cytospins, indicate th
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
33 between two of their target genes, Fli-1 and EKLF, with victory for GATA-1 and EKLF leading to erythr
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
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
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
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
55 atients show higher level expression of both EKLF and PlGF mRNA in circulating blood cells, and marke
57 t assays, the AHSP promoter CACCC site bound EKLF in a manner comparable to the beta-globin promoter
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
65 conclude that the cell cycle as regulated by EKLF during late stages of differentiation is inherently
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
80 egulatory pathways, whereas in erythroblasts EKLF is associated with repression of these pathways.
82 d intrinsic contributions to erythropoiesis, EKLF thus plays a coordinating role between two differen
84 uires expression of the transcription factor EKLF, which is not present in K562 cells but is required
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
104 iption factor erythroid Kruppel-like factor (EKLF) is an important activator of beta-globin gene expr
107 embers of the erythroid Kruppel-like factor (EKLF) multigene family contain three C-terminal zinc fin
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
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
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
132 ed pathology, indicating that one functional EKLF allele is sufficient to sustain human erythropoiesi
138 scription of inactivating mutations in human EKLF and the first demonstration of a blood group phenot
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
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
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
152 ) of several zinc finger proteins, including EKLF, interact directly with SWI/SNF to generate DNase I
155 nd die before E11.5, whereas single-knockout EKLF(-/-) or KLF2(-/-) embryos are grossly normal at E10
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
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
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
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
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
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
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
186 on of EKLF, we demonstrate the importance of EKLF acetylation at lysine 288 in the recruitment of CBP
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
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.
196 s is that post-translational modification of EKLF differs within erythroid cell populations and regul
199 ing a crucial pathway to direct the onset of EKLF and GATA1 expression during hematopoietic different
201 Wild-type chromatin demonstrated a peak of EKLF binding over a promoter region CACCC box that diffe
204 hroid leukemia cells, whereas recruitment of EKLF to 5'HS2 occurred in both gamma-globin-expressing K
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
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
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,
226 NA was consistently induced by overexpressed EKLF in resting RAW264.7 cells, whereas EKLF suppressed
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
235 exhibits stage specificity, with reversible EKLF-Sin3A interactions playing a key role in this proce
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
240 that two nuclear localization signals target EKLF to the nucleus and suggest this transport relies pr
254 These results support the hypothesis that EKLF acts as a transcription factor and a chromatin modu
256 AHSP and beta-globin genes and indicate that EKLF may play similar roles for other erythroid genes.
259 sed the in vivo PIN*POINT assay to show that EKLF is recruited to the beta-globin promoter but not to
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
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
274 n essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF level
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
281 cent protein or pyruvate kinase was fused to EKLF domains, and localization was monitored and quantit
285 markably, even when mutant Nan and wild-type EKLF alleles are expressed at equivalent levels, the mut
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
296 reduced in EKLF(-/-)KLF2(-/-), compared with EKLF(-/-) or KLF2(-/-) embryos, consistent with the obse
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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