ライフサイエンスコーパス: CTCF

1 cription and DNA-bound CCCTC-binding factor (CTCF).

2 undaries, enriched for CCCTC-binding factor (CTCF).

3 e CTCF on only one side, and 32% are without CTCF.

4 nested within constitutive loops anchored by CTCF.

5 Tol2 also correlated with Cohesin and CTCF.

6 ive histone modifications) were enriched for CTCF.

7 s in structuring the genome independently of CTCF.

8 er analogous to DNA interactions mediated by CTCF.

9 Mice with cardiac-specific deletion of CTCF (a ubiquitous chromatin structural protein) were ge

10 ft ventricular assist devices show increased CTCF abundance.

11 TCF target sites (1xCTSes) that are bound by CTCF alone (CTCF-only) or double CTCF target sites (2xCT

12 The CTCF anchor regions we identified are conserved across s

13 rget sites (2xCTSes) simultaneously bound by CTCF and BORIS (CTCF&BORIS) or BORIS alone (BORIS-only)

14 Our data suggest that CTCF and BORIS cooperate with additional TSTRs to regula

15 s, binding sites of the transcription factor CTCF and brain eQTLs.

16 ad from one gene to another, suggesting that CTCF and BRD2 form a transcriptional boundary.

17 depletion weakens boundaries co-occupied by CTCF and BRD2, but not those that lack BRD2.

18 Since CTCF and cohesin are required for loop domain formation,

19 omic and biochemical approaches we show that CTCF and cohesin co-occupy the same sites and physically

20 mong diverse cell types and are dependent on CTCF and cohesin complex.

21 The insulator protein CTCF and cohesin control domain location by folding doma

22 Thus, CTCF and cohesin form a rapidly exchanging 'dynamic comp

23 ring between two loci-almost always bound by CTCF and cohesin-lying on the same chromosome.

24 le defined by maximal boundary enrichment in CTCF and maximal cell-type conservation.

25 n important, unanticipated interplay between CTCF and nuclear lamina to control the transcription of

26 ent in the nucleus where it colocalizes with CTCF and represses a megakaryocytic transcriptional prog

27 cies comparisons to macaques, indicated that CTCF and TF binding likelihood predicts the strength and

28 gulated by this phenomenon; and variation in CTCF and TF binding sites is an underlying mechanism, an

29 2 is associated with the chromatin insulator CTCF and the cohesin complex to support cis-regulatory e

30 ely separated sites on DNA, occupied by both CTCF and the cohesin complex, make physical contacts tha

31 Polymorphic CTCF and transcription factor (TF) binding sites were ov

32 loop anchors bound by CCCTC-binding factor (CTCF) and cohesin are vulnerable to DNA double strand br

33 in vitro and in vivo, CCCTC-binding factor (CTCF) and its paralog brother of the regulator of imprin

34 ng proteins, including CCCTC-binding factor (CTCF) and pluripotency factors.

35 Sequence variants in CCCTC-binding factor (CTCF) and transcription factor binding sites have been m

36 e pair resolution ChIP-exo mapping of TOP2B, CTCF, and cohesin sites revealed a striking structural o

37 y gene-enhancer interactions are anchored by CTCF, and its occupancy is lost in parallel with loop de

38 RNA (TERRA), but the role of transcription, CTCF, and TERRA in telomere replication is not known.

39 1 locus on chromosome 11p15.5 is mediated by CTCF, and this regulation is lost in BWS, leading to abe

40 a are available, is validated to be RNAPII-, CTCF-, and RAD21-mediated.

41 Both MED1 and CTCF are validated conserved miR-122 targets.

42 Once there, the portion of CTCF associated with the nuclear lamina interacts with e

43 CTCF-associated interactions are most strongly enriched

44 stimulate splicing, but efficiently promote CTCF association.

45 We specifically demonstrate that loss of CTCF at a domain boundary permits a constitutive enhance

46 and three-dimensional (3D) genome organizer CTCF at cryptic binding sites, in conjunction with DNA c

47 reater enrichment of chromatin marks such as CTCF at their boundaries.

48 oteins, shields neuronal genomes from excess CTCF binding and is critically required for structural m

49 and a positive correlation is found between CTCF binding and the activity of the associated enhancer

50 epigenetic modifications in combination with CTCF binding at regulatory elements account for the tran

51 uced changes to epigenetic modifications and CTCF binding at select regulatory elements, which corres

52 nogenesis, we show that iAs probably targets CTCF binding at the promoter of DNA methyltransferases,

53 (D)J recombination, we introduced an ectopic CTCF binding element (CBE) immediately downstream of Ede

54 ere we show that mice devoid of an inducible CTCF binding element, located in the alpha constant gene

55 which was exploited to detect footprints of CTCF binding events and to estimate the average nucleoso

56 NA methylation in the first exon can prevent CTCF binding in most cancers, but the molecular mechanis

57 to have decreased IRF3 binding and increased CTCF binding in promoter-binding assays, and risk allele

58 Reduced CTCF binding is associated with loss of insulation betwe

59 Recent reports have suggested that CTCF binding is more dynamic during development than pre

60 hing, but also afforded discovery of a novel CTCF binding motif.

61 These findings reveal how CTCF binding regulates DNA methyltransferase to reprogra

62 that knocking down of CTCF or deletion of a CTCF binding site results in increased cell-to-cell vari

63 onnected by DNA loops, which are proximal to CTCF binding sites and expressed at elevated levels comp

64 We show that CTCF binding sites are interwoven with enhancers within

65 We have identified two CTCF binding sites flanking the locus and two associated

66 Conversely, CTCF binding sites in NPCs are largely preexisting in pl

67 ral and regulatory interactions supported by CTCF binding sites, DNase accessibility, and/or active h

68 fied by ClusterTAD have a high enrichment of CTCF binding sites, promoter-related marks, and enhancer

69 found at promoters and transcription factor CTCF binding sites.

70 trumental for splicing and inhibits Tet1 and CTCF binding thereby negatively impacting DNA methylatio

71 The continuity of Ctcf binding through the murine germline may permit rapi

72 CTCF binding to enhancer regions results in modulation o

73 Here, we report that CTCF binding to enhancer RNAs is enriched when breast ca

74 forced transcription of TERRA independent of CTCF binding.

75 ylation at cohesin and CCCTC-binding factor (CTCF)-binding sites, compromising binding of this methyl

76 Removal of an upstream CTCF-binding insulator alters the interaction profile, b

77 e first exon of hTERT and located within the CTCF-binding region can form two secondary structures, a

78 on was mapped to a DNA methylation-sensitive CTCF-binding site (CTCF-BS3) within the third intron of

79 ory elements upstream of the disrupted ZPBP2 CTCF-binding site interacted with the ORMDL3 promoter re

80 In this study, we created a mouse model with CTCF-binding site mutations at the Igf2-H19 imprint cont

81 Deletion of the distal CTCF-binding site results in loss of Ramp3 expression in

82 F DNA-binding domain in complex with a known CTCF-binding site.

83 have used CRISPR/Cas9 gene editing to mutate CTCF-binding sites at the putative start site of TERRA t

84 otemporal lobar degeneration are enriched in CTCF-binding sites found in brain-relevant tissues, impl

85 k variants rs4065275 and rs12936231 switched CTCF-binding sites in the 17q21 locus, and 4C-Seq assays

86 rboxylcytosine are enriched at an intragenic CTCF-binding sites in the CD45 model gene and are associ

87 lcytosine and 5-methylcytosine at downstream CTCF-binding sites is a general feature of alternative s

88 elomere repeats can initiate at subtelomeric CTCF-binding sites to generate telomere repeat-encoding

89 hanisms governing dynamic DNA methylation at CTCF-binding sites were unclear.

90 , using single-molecule imaging we find that CTCF binds chromatin much more dynamically than cohesin

91 d by CTCF self-dimerisation in normal cells (CTCF binds to both unmethylated CTCF-BS3 and CTCF-BS2).

92 l characterized, little is known on how long CTCF binds to chromatin and how binding evolves during t

93 We show that subsets of CTCF&BORIS and BORIS-only sites are occupied by several

94 BORIS-bound regions (CTCF&BORIS and BORIS-only sites) are, on average, enrich

95 Ses) simultaneously bound by CTCF and BORIS (CTCF&BORIS) or BORIS alone (BORIS-only) in germ cells an

96 y, ChIP-seq analysis revealed two classes of CTCF/BORIS-bound regions: single CTCF target sites (1xCT

97 ymoD transcription promoted demethylation at CTCF bound sites and activated cohesin-dependent looping

98 mong IFITM3-neighboring genes, indicative of CTCF boundary activity.

99 Disruption of a CTCF/BRD2-occupied element positioned between two unrela

100 CTCF binds to both unmethylated CTCF-BS3 and CTCF-BS2).

101 ormal cells (CTCF binds to both unmethylated CTCF-BS3 and CTCF-BS2).

102 DNA methylation-sensitive CTCF-binding site (CTCF-BS3) within the third intron of GAD1.

103 xtruding chromatin loops until it encounters CTCF, but direct evidence for this hypothesis is missing

104 equently affect binding of multiple TFs, and CTCF can recruit all five TFs to its binding sites.

105 Together, our results indicate that CSB and CTCF can regulate each other's chromatin association, th

106 We conclude that CTCF can regulate V(D)J recombination by segregating RSS

107 bourhoods, formed by the zinc-finger protein CTCF, can sequester enhancers and their target genes, th

108 Mutations in CTCF cause intellectual disability and autistic features

109 Human mutations in CTCF cause intellectual disability and autistic features

110 roles of two chromatin structural proteins, Ctcf (CCCTC-binding factor) and Hmgb2 (high mobility gro

111 Here, we show that deletion of CTCF (CCCTC-binding factor)-binding sites at TAD and sub

112 We monitored CTCF-chromatin interactions by live cell single molecule

113 CTCF-DNA interactions in vitro and regulates CTCF-chromatin interactions in oxidatively stressed cell

114 g crosstalk between neurons and microglia in Ctcf CKO hippocampus.

115 Ctcf CKO mice also had reduced dendritic spine density i

116 We demonstrate that Ctcf CKO mice overexpress inflammation-related genes in

117 e lacking Ctcf in Camk2a-expressing neurons (Ctcf CKO mice) have spatial learning/memory deficits, im

118 analysis of mRNA isolated specifically from Ctcf CKO mouse hippocampal neurons by ribosomal affinity

119 Finally, we found that microglia in Ctcf CKO mouse hippocampus had abnormal morphology by Sh

120 Microarray analysis of mRNA from Ctcf CKO mouse hippocampus identified increased transcri

121 Ctcf(loxP/loxP);Camk2a-Cre(+) (Ctcf CKO) mice of both sexes were viable and exhibited p

122 SS), and the number of CCCTC-binding factor (CTCF)-cohesin complexes between the interacting DNA segm

123 that most high-intensity interactions have a CTCF-cohesin complex in at least one of the interacting

124 These ordered TOP2B-CTCF-cohesin sites flank the boundaries of topologically

125 is a highly ordered and prevalent feature of CTCF/cohesin binding sites that flank TADs.

126 e mechanisms.CFTR occupies a TAD bordered by CTCF/cohesin binding sites within which are cell-type-se

127 olymorphisms in the genome that redistribute CTCF/cohesin occupancy rewire DNA cleavage sites to nove

128 Approximately half of all CTCF/cohesion-bound regions coincided with TOP2B binding

129 The multidomain CCCTC-binding factor (CTCF), containing a tandem array of 11 zinc fingers (ZFs

130 enes and their regulatory elements depend on CTCF-CTCF interactions, but most enhancer-promoter inter

131 hem within the context of cohesin-associated CTCF-CTCF loops using cohesin ChIA-PET data.

132 The CTCF-CTCF loops we identified form a chromosomal framewo

133 on with native ChIP-seq and applied to human CTCF, CUT&RUN mapped directional long range contact site

134 Here we report that CTCF decreases cell-to-cell variation of expression by s

135 CTCF deficiency in embryonic neurons is lethal in mice,

136 s lethal by neonatal age, but the effects of CTCF deficiency in postnatal neurons are less well studi

137 interactions are factors in the pathology of CTCF deficiency.

138 Moreover, CTCF-deficient cells are hypersensitive to genotoxic str

139 nts but is required for TADs and loops, that CTCF defines their boundaries, and that the cohesin unlo

140 genes, there is limited in vivo evidence for CTCF demarcating super-enhancers and preventing cross ta

141 Moreover, our data suggest that CTCF-dependent boundary function can be modulated by com

142 Therefore, we propose that loss of CTCF-dependent imprinting of tumor-promoting genes, such

143 s is lethal in mice, but mice with postnatal CTCF depletion are less well studied.

144 type in mice and provide novel evidence that CTCF depletion leads to overexpression of inflammation-r

145 In addition, pressure overload or CTCF depletion remodeled long-range interactions of card

146 Pressure overload or CTCF depletion selectively altered boundary strength bet

147 compartments remain properly segregated upon CTCF depletion, revealing that compartmentalization of m

148 The CTCF dimer then interacted with suppressor of zeste 12 h

149 tion (FISH) reveals that, upon site-specific CTCF disruption or BRD2 depletion, expression of the two

150 We crystallized the human CTCF DNA-binding domain in complex with a known CTCF-bin

151 rocally, we demonstrate that CSB facilitates CTCF-DNA interactions in vitro and regulates CTCF-chroma

152 Under replication stress, telomeres lacking CTCF-driven TERRA exhibit sister-telomere loss and upon

153 Our findings also demonstrate that CTCF-driven TERRA transcription acts in cis to facilitat

154 DNA structuring proteins such as CTCF facilitate DNA loop formation and are presumed to b

155 Our findings indicate that subtelomeric CTCF facilitates telomeric DNA replication by promoting

156 or genes to nuclear lamina that mediates the CTCF function.

157 vide directionality to these movements, that CTCF functions as a boundary element for moving cohesin,

158 CTCF genetic deletion occurs predominantly in poor progn

159 ural/insulator protein CCCTC-binding factor (CTCF) genome-wide.

160 In addition, we have shown that CTCF haploinsufficiency also occurs in poor prognosis en

161 However the mechanism by which CTCF haploinsufficiency contributes to cancer developmen

162 at most CTCF mutations effectively result in CTCF haploinsufficiency through nonsense-mediated decay

163 Using shRNA targeting CTCF to recapitulate CTCF haploinsufficiency, we have identified a novel role

164 The zinc finger protein CTCF has been invoked in establishing boundaries between

165 se by loop extrusion, until it is delayed by CTCF in a manner dependent on PDS5 proteins, or until it

166 We find that mice lacking Ctcf in Camk2a-expressing neurons (Ctcf CKO mice) have s

167 rchestration of oncogenic gene expression by CTCF in cancer cells.

168 dicating a powerful instructive function for CTCF in chromatin folding.

169 Beyond defining the functions of CTCF in chromosome folding, these results provide new fu

170 a reciprocal relationship between Hmgb2 and Ctcf in controlling aspects of chromatin structure and g

171 However, the role of CTCF in DNA damage response remains elusive.

172 ng cell polarity) for genetic alterations of CTCF in endometrial cancer.

173 ant, rs1990620, that differentially recruits CTCF in lymphoblastoid cell lines and human brain to inf

174 Furthermore, depletion of Ahr, Med1, or Ctcf in Mir122(-/-) hepatocytes reduced Cyp1a2 expressio

175 Knocking out Ctcf in mouse embryonic neurons is lethal by neonatal ag

176 The role of the zinc finger protein CTCF in organizing the genome within the nucleus is now

177 iciency, we have identified a novel role for CTCF in the regulation of cellular polarity of endometri

178 ing the consensus binding motifs of IRF4 and CTCF in the XL9 regulatory complex modified the transcri

179 We show that CSB directly interacts with CTCF in vitro and that oxidative stress enhances the CSB

180 results suggest that genomic factors such as CTCF inhibit mutagenesis.

181 ch, we found that nucleosomes flanking human CTCF insulation sites are similarly disrupted.

182 f2-H19 imprint control region that abolishes CTCF insulator activity, resulting in biallelic Igf2 exp

183 insertion of a GL promoter downstream of the CTCF insulator led to premature activation of the ectopi

184 Convergent CTCF insulator sites flanking the HLA-A gene promoter an

185 ctivity is delayed, at least in part, by the CTCF insulator, which borders a transcriptionally active

186 o and that oxidative stress enhances the CSB-CTCF interaction in cells.

187 Whereas sites of CTCF interactions are well characterized, little is know

188 t and evolutionarily most conserved of these CTCF interactions have specific rules for the orientatio

189 Here, we report that CTCF interacts extensively with the HSV-1 DNA during lyt

190 The transcription factor CTCF is a candidate regulator of chromosomal structure.

191 CTCF is a haploinsufficient tumour suppressor gene with

192 in mouse embryonic stem cells, we show that CTCF is absolutely and dose-dependently required for loo

193 CTCF is an architectural protein with a critical role in

194 CTCF is an essential chromatin regulator implicated in i

195 CTCF is frequently mutated in endometrial cancer.

196 an ultrasensitive response of Jpx signal on CTCF is important in this mechanism.

197 CTCF is known to bind several sites in the HSV-1 genome

198 Here, we show that CTCF is quickly recruited to the sites of DNA damage.

199 CTCF is sensitive to cytosine methylation at position 2,

200 SIGNIFICANCE STATEMENT CCCTC-binding factor (CTCF) is a DNA-binding protein that organizes nuclear ch

201 CCCTC-binding factor (CTCF) is an 11 zinc finger DNA-binding domain protein th

202 at chromatin insulator CCCTC-binding factor (CTCF) is TGF-beta inducible and facilitates TGF-beta-med

203 CTCF knockdown led to increased H3K9me3 and H3K27me3, an

204 Consistent with this, CTCF knockdown reduced the Ser2P but increased Ser5P mod

205 Our findings confirm that Ctcf KO in postnatal neurons causes a neurobehavioral ph

206 II pausing, whereas 5-methylcytosine evicts CTCF, leading to exon exclusion.

207 mmals, compartmental domains exist alongside CTCF loop domains to form topological domains.

208 Topologically associating domains (TADs), CTCF loop domains, and A/B compartments have been identi

209 tween neighboring regions in Drosophila, but CTCF loops do not play a distinct role in this organism.

210 Ctcf(loxP/loxP);Camk2a-Cre(+) (Ctcf CKO) mice of both se

211 Intragenic 5-methylcytosine and CTCF mediate opposing effects on pre-mRNA splicing: CTCF

212 enases TET1 and TET2 as active regulators of CTCF-mediated alternative splicing through conversion of

213 our assembly along with the current model of CTCF-mediated chromatin looping to predict regions of th

214 found in brain-relevant tissues, implicating CTCF-mediated gene regulation in risk of neurodegenerati

215 opological framework created by constitutive CTCF-mediated interactions.

216 toid cell lines and human brain to influence CTCF-mediated long-range chromatin-looping interactions

217 In this study, to assess mechanisms by which CTCF-mediated looping can impact V(D)J recombination, we

218 CTCF-mediated looping can influence recombination signal

219 CTCF-mediated looping has also been shown to limit direc

220 However, in all prior instances in which CTCF-mediated looping was shown to influence V(D)J recom

221 long range to predominantly short range, and CTCF-mediated loops and contact domains double in number

222 Furthermore, our data support that CTCF mediates transcriptional insulator function through

223 In G1-, S-, and G2-phases, a majority of CTCF molecules was bound transiently ( approximately 0.2

224 onversely, CRISPR-mediated disruption of the CTCF motif in IDH wild-type gliomaspheres upregulates PD

225 cers and promoters is similarly dependent on ctcf motif orientation.

226 strongly dependent on the orientation of the ctcf motif, and, moreover, we find that the interaction

227 se proteins along the genome relative to the CTCF motif.

228 Further incorporation of CTCF-motif orientation and high-resolution looping patte

229 specificity for long-range contacts between CTCF motifs in Drosophila, highlighting its conserved pr

230 Conversely, we identified a recurrent CTCF mutation K365T, which alters a DNA binding residue,

231 Here we show that most CTCF mutations effectively result in CTCF haploinsuffici

232 ibed in childhood T-ALL (for example, CCND3, CTCF, MYB, SMARCA4, ZFP36L2 and MYCN).

233 both proteins share gene targets, Hmgb2 and Ctcf, neither binds these genes simultaneously nor do th

234 nd the extent to which shifts in genome-wide CTCF occupancy contribute to the 3D reconfiguration of f

235 Unexpectedly, we observe a sharp decrease in CTCF occupancy during the transition from naive/primed p

236 poorly reprogrammed interactions, reinstate CTCF occupancy, and restore expression levels.

237 splay only partially recovered, ESC-specific CTCF occupancy.

238 -bound sites whereas BRD2 is dispensable for CTCF occupancy.

239 ption-primed promoters and enhancers, and to CTCF occupied, untranscribed chromatin.

240 cription-primed promoters and enhancers, and CTCF-occupied, non-transcribed chromatin.

241 However, 46% have CTCF on only one side, and 32% are without CTCF.

242 retention in mature spermatozoa relative to CTCF-only sites, but little else is known about them.

243 ites (1xCTSes) that are bound by CTCF alone (CTCF-only) or double CTCF target sites (2xCTSes) simulta

244 assays, we demonstrate that knocking down of CTCF or deletion of a CTCF binding site results in incre

245 of HNRNPU peaks coincide with the binding of CTCF or RAD21.

246 nvert, delete, or inactivate one of a mating CTCF pair result in major changes in patterns of organiz

247 Taken together, these results suggest that CTCF participate in DNA damage response via poly(ADP-rib

248 level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the viral genom

249 for domain structure in all eukaryotes, with CTCF playing an important role in domain formation in ma

250 the long-range chromatin-structure regulator CTCF plays a pivotal role in regulating sites of genomic

251 ge promoter-enhancer interaction mediated by CTCF plays important roles in controlling the cell-to-ce

252 CCCTC-binding factor (CTCF) plays an essential role in regulating the structur

253 We knocked out Ctcf postnatally in glutamatergic forebrain neurons unde

254 These results suggest that CTCF promotes HSV-1 lytic transcription by facilitating

255 diate opposing effects on pre-mRNA splicing: CTCF promotes inclusion of weak upstream exons through R

256 he interaction of two DNA sites bound by the CTCF protein and occupied by the cohesin complex.

257 nding that the quadruplex formation disrupts CTCF protein binding, which results in an increase in hT

258 boundaries or "anchors" are associated with CTCF protein in mammals, loop anchors in Drosophila were

259 Moreover, after unbinding, CTCF quickly rebinds another cognate site unlike cohesin

260 CTCF recruits BRD2 to co-bound sites whereas BRD2 is dis

261 ooping mediated by the CCCTC binding factor (CTCF) regulates V(D)J recombination at Ag receptor loci.

262 Restoring CTCF reinstates proper architecture on altered chromosom

263 CTCF remains essential for TAD organization in non-divid

264 ed disease etiology in that host genes (e.g. CTCF, RHOA, and CDKN1B) identified were frequently essen

265 To assess the nature and function of this CTCF-rich DNA region in embryos, we compared chromatin i

266 Our data suggest that CTCF scans DNA in search for two different subsets of sp

267 that an intrachromosomal loop was formed by CTCF self-dimerisation in normal cells (CTCF binds to bo

268 ata collectively support a mechanism wherein CTCF serves to translate alphaKG-sensitive metabolic cha

269 Loss of this CTCF site led to de novo interactions between the Sult1d

270 However, deletion of the border CTCF site separating the Csn1s1 mammary enhancer from ne

271 Many CTCF sites are also involved in other functions such as

272 This suggests that CTCF sites are porous borders, allowing a super-enhancer

273 Only a small number of CTCF sites arise de novo in NPCs.

274 e needed to determine the biological role of CTCF sites associated with enhancers.

275 Deletion of CTCF sites compromises enhancer-promoter interactions.

276 mammary-specific super-enhancer separated by CTCF sites from widely expressed genes.

277 IL-2- and alphaKG-sensitive CTCF sites in T cells were also associated with genes fr

278 y demonstrates that only one out of the four CTCF sites in the casein locus had a measurable in vivo

279 Likewise, CTCF sites shield a widely expressed gene from suppressi

280 Notably, CTCF sites were correlated with PB but not with MLV, sug

281 alphaKG-sensitive CTCF sites were often associated with loci containing IL

282 forms extended loops, presumably by passing CTCF sites, accumulates in axial chromosomal positions (

283 ific rules for the orientation of the paired CTCF sites, implying the existence of a nonequilibrium m

284 n in stabilizing long-range contacts between CTCF sites.

285 cer controls Ramp3, despite three separating CTCF sites.

286 classes of CTCF/BORIS-bound regions: single CTCF target sites (1xCTSes) that are bound by CTCF alone

287 re bound by CTCF alone (CTCF-only) or double CTCF target sites (2xCTSes) simultaneously bound by CTCF

288 ose-dependently required for looping between CTCF target sites and insulation of topologically associ

289 architectural protein CCCTC-binding factor (CTCF) that binds to the boundaries of topologically asso

290 ations from the consensus sequence, allowing CTCF to adapt to sequence variations.

291 Using shRNA targeting CTCF to recapitulate CTCF haploinsufficiency, we have id

292 Binding of CCCTC-binding factor (CTCF) to the first exon of the hTERT gene can down-regul

293 nscriptional repressor CCCTC-binding factor (CTCF) to the MSMP enhancer region was decreased by histo

294 During mitosis, CTCF was mostly excluded from chromatin.

295 Depletion of CTCF was sufficient to induce heart failure in mice, and

296 andidate enhancer-bound regulatory proteins, Ctcf, was associated with chromatin domain boundaries in

297 DNA insulator protein CCCTC-binding factor (CTCF), which is associated with suppression of splicing

298 e methylation-sensitive transcription factor CTCF, whose binding is known to play a role in enhancer

299 ntified association of CCCTC-binding factor (CTCF) with Ahr promoter in mouse livers.

300 ted the association of CCCTC-binding factor (CTCF) with select genomic sites.