ライフサイエンスコーパス: CTCF

1 ed DNAm changes: ABLIM3, APCDD1L, MTMR6, and CTCF.

2 HNF4A, histone H3-lysine-27-acetylation, and CTCF.

3 tion) and cardiomyocyte-specific knockout of Ctcf.

4 ll activation by stem cell regulatory factor CTCF.

5 oops are formed by cohesin and positioned by CTCF.

6 gulation of chromatin folding by cohesin and CTCF.

7 f the genome into loops that are anchored by CTCF(1).

8 graded the cohesin component RAD21(10-12) or CTCF(12,13) in these G1-arrested lines.

9 e demonstrate that the CCCTC-binding factor (CTCF), a crucial chromatin organizer, is essential for S

10 NC00346 interacts with CCCTC-binding factor (CTCF), a known transcriptional repressor of c-Myc.

11 , both lncRNAs demonstrate robust binding to CTCF, a protein that is central to Jpx's role in X chrom

12 Furthermore, we show that cohesin and CTCF also exert effects on the host cell that promote an

13 disrupted gene expression near the on-target CTCF anchor.

14 his interaction is specifically required for CTCF-anchored loops and contributes to the positioning o

15 matin contact patterns that are dependent on CTCF anchors and enhancer activity.

16 d long-range interactions are independent of CTCF and can bridge sites at a megabase scale.

17 CTCF and cohesin also bind to herpesvirus genomes at spe

18 e analyzed the interdependence of binding of CTCF and cohesin and demonstrate that while CTCF is requ

19 or oocyte-specific interactions mediated by CTCF and cohesin are only present in the paternal or mat

20 NUP153 depletion results in altered CTCF and cohesin binding and differential gene expressio

21 We find that NUP153 controls CTCF and cohesin binding at the cis-regulatory elements

22 is study, we examined the interdependence of CTCF and cohesin binding to the KSHV genome.

23 dulated by binding of the host cell proteins CTCF and cohesin complex to the KSHV genome.

24 represent the concomitant depletion of both CTCF and cohesin components.

25 Thus, CTCF and cohesin have both positive and negative effects

26 k co-expressed loci, often in the absence of CTCF and cohesin occupancy.

27 CTCF and cohesin play a key role in organizing chromatin

28 Many studies have shown that CTCF and cohesin protein-mediated chromosome looping hav

29 s with the chromatin architectural proteins, CTCF and cohesin, and mediates their binding across cis-

30 ically associated domain (TAD) demarcated by CTCF and cohesin, but shows cell-type specific control m

31 Here, we report the quantification of CTCF and cohesin, two causal regulators of topologically

32 We show that CTCF and cohesin, which are master regulators of chromat

33 esvirus (KSHV) transcription is regulated by CTCF and cohesin, with both proteins previously reported

34 ), consisting of chromatin loops anchored by CTCF and cohesin.

35 By analyzing CTCF and CTCFL binding in tandem, we identify phenotypic

36 t shared and unique zinc finger sequences in CTCF and CTCFL enable CTCFL to bind competitively to a s

37 fy the relative and combined contribution of CTCF and CTCFL to chromosome organization and transcript

38 fies the unique and combined contribution of CTCF and CTCFL to chromosome organization and transcript

39 Therefore, selected TFs such as CTCF and Esrrb act as resilient TFs governing the inheri

40 ween chromatin accessibility and TF binding (CTCF and KLF4) at methylated sites.

41 ome regions, and chromatin regulators (e.g., CTCF and SATBs) establish looping configurations.

42 CTCF and the cohesin complex modify chromatin by binding

43 , but disruptive SNPs in specific classes of CTCF and transcription factor binding motifs are similar

44 hared mechanism involving disruptive SNPs in CTCF and transcription factor binding sites in both norm

45 CCCTC-binding factor (CTCF) and cohesin play critical roles in organizing mamm

46 llelic partitioning of CCCTC-binding factor (CTCF) and show that tethering DCP1A to one Tsix allele i

47 rated that a chromosomal networking protein (CTCF) and tumor protein p53 (TP53) bind to TP73 promoter

48 ogen receptor (AR) and CCCTC-binding factor (CTCF), and modulates AR-dependent gene expression.

49 other DNA binding factors, including FOXA1, CTCF, and OCT1.

50 affects binding by the transcription factor, CTCF, and that the high-affinity allele usually occurs o

51 The multiple functions of CTCF are accomplished by co-association with other prote

52 R-DeeP identified the transcription factor CTCF as completely RNA dependent, and we uncovered that

53 using ENCODE ChIP-sequencing data identified CTCF as the common transcription factor at the site of t

54 CTCF-associated domain boundaries were dispensable for R

55 BRD9 causes the loss of non-canonical BAF at CTCF-associated loci and promotes melanomagenesis.

56 enhancer-RNAs (eRNA), bivalent-lncRNAs, and CTCF-associated, among others.

57 report two independent features that disrupt CTCF association with chromatin: inhibition of transcrip

58 rystal structure of SA2-SCC1 in complex with CTCF at a resolution of 2.7 angstrom, which reveals the

59 Our results substantiate CTCF binding alteration as a functional epigenomic signa

60 There was a strong anticorrelation between CTCF binding and DNA methylation.

61 specifically in nociceptors, likely permits CTCF binding and expression of Ca(V)2.2 channel isoforms

62 ootprint in prometaphase, suggesting loss of CTCF binding and rearrangement of the nucleosomal array

63 show that removal of DNA methylation enables CTCF binding and recruitment of the cohesin complex, whi

64 nd DNA sequence that determines differential CTCF binding and regulates gene expression.

65 show that oncogenic NOTCH1 induces specific CTCF binding and they cooperatively activate expression

66 ghly enriched at promoters, strongly overlap CTCF binding and topological associating domain boundari

67 ockdown of CTCF in K562 cells caused loss of CTCF binding and transcriptional repression of genes wit

68 In cancer cells, the disruption of CTCF binding at specific loci by somatic mutation(3,4) o

69 To gain clues about the role of CTCF binding at the murine immunoglobulin heavy chain (I

70 F binding site, and we found that it reduces CTCF binding by approximately 40-fold.

71 We studied CTCF binding by chromatin immunoprecipitation sequencing

72 Cancer-specific CTCF binding can be induced by other transcription facto

73 CTCF binding contributes to the establishment of a highe

74 We demonstrate that TE-derived CTCF binding divergence may explain a large fraction of

75 SHV genome is highly CTCF dependent, whereas CTCF binding does not require cohesin.

76 We show that cancer-specific lost and gained CTCF binding events are associated with altered chromati

77 arily occur near gene promoters, most gained CTCF binding events exhibit enhancer activities and are

78 Specific CTCF binding events occur in human cancers.

79 usters is an apparently important feature of CTCF binding evolution that is critical to the functiona

80 scriptional repression of genes with changed CTCF binding in AML, as well as loss of RUNX1 binding at

81 ve insulators where DNA methylation replaced CTCF binding in SDH-deficient GISTs.

82 rtance and conservation of TADs, the role of CTCF binding in their evolution and stability remains el

83 Our analyses reveal that CTCF binding is maintained at TAD boundaries by a balanc

84 Still, it is unclear how CTCF binding is perturbed in leukemia or in cancer in ge

85 tion is disrupted, possibly due to decreased CTCF binding on the Xi.

86 re is no comprehensive survey of genome-wide CTCF binding patterns across different human cancers.

87 ues and cancers and identify cancer-specific CTCF binding patterns in six cancer types.

88 s five closely related species to assess how CTCF binding patterns stably fixed by evolution in each

89 Here, we show that -31-Kb CTCF binding site (-31CBS) serves as chromatin boundary

90 e mechanism of the Ealpha and its downstream CTCF binding site (here named EACBE) in dynamic chromati

91 port the relative contributions of TE-driven CTCF binding site expansions to conserved and divergent

92 Disruption of a single CTCF binding site is sufficient to change chromosomal in

93 ely DNA loop-extruding cohesin complexes and CTCF binding site occupancy.

94 demethylated context, either deletion of the CTCF binding site or depletion of RAD21 cohesin complex

95 conserved loops across both species through CTCF binding site turnover.

96 which generates E344Q is within a predicted CTCF binding site, and we found that it reduces CTCF bin

97 in polycomb repressive complex occupancy and CTCF binding sites are associated with cancer-specific g

98 e CTCFL to bind competitively to a subset of CTCF binding sites as well as its own unique locations,

99 rdless of their conservation across species, CTCF binding sites at TAD boundaries are subject to stro

100 tudy provides a new insight into the role of CTCF binding sites at TAD boundaries in gene regulation.

101 While many CTCF binding sites fall within transposable elements (TE

102 hich explains the requirement for convergent CTCF binding sites in loop formation.

103 romoter, leading to DNA demethylation of the CTCF binding sites proximal to each promoter.

104 flanking regions, transcription factors and CTCF binding sites that are linked to doxorubicin resist

105 observations explain how the orientation of CTCF binding sites translates into genome folding patter

106 verted this sub-TAD boundary, eliminated the CTCF binding sites, or inverted the entire T-DOM to exch

107 tance of an orientation-specific grammar for CTCF binding sites.

108 DR/DQ-SE also interacted with neighboring CTCF binding sites.

109 ssociating domains, and interactions between CTCF binding sites.

110 f key loops such as those between convergent CTCF binding sites.

111 contributes to the positioning of cohesin at CTCF binding sites.

112 Combined, our results demonstrate loss of CTCF binding to CTCF sites during prometaphase and rearr

113 ts 11 zinc fingers that are not required for CTCF binding to its cognate DNA site: zinc finger 1 (ZF1

114 king assays and ChIP-chip analysis confirmed CTCF binding to these sites both in vitro and in vivo.

115 Aberrant CTCF binding was enriched for motifs for key myeloid tra

116 CTCF binding was increased in AML compared with NBM.

117 ver, was diminished by combining the loss of CTCF binding with a hypomorphic ZRS allele, resulting in

118 c, H3K36me3; repressive: H3K27me3, H3K9me3), CTCF binding, and gene expression in samples from 5 indi

119 aracterized by a particularly strong gain of CTCF binding, highly enriched for gain in promoter regio

120 nd exon-specific DNA hypomethylation permits CTCF binding, the master regulator of mammalian chromati

121 To dissect functions of CTCF binding, we systematically analyze over 700 CTCF Ch

122 start sites (TSSs) and CCCTC-binding factor (CTCF) binding sites, and uncovered an increase in DSBs a

123 d transcription factor CCCTC-binding factor (CTCF) binding.

124 integrity in concurrence with a reduction in CTCF-binding affinity, while showing no perturbation to

125 In mouse progenitor B cells, the CTCF-binding element (CBE)-anchored chromatin loop domai

126 in AML patient cells, partly by restoring a CTCF-binding pattern similar to NBM.

127 OPRM1 upstream region revealed a functional CTCF-binding region that evolved from tandem insertions

128 issue-invariant domain boundary-containing a CTCF-binding site (CBS) and a transcription start site (

129 al analysis indicated that the prevalence of CTCF-binding sites at the IgH locus is evolutionarily co

130 tional approach that identified 144 putative CTCF-binding sites within this locus.

131 L, as well as loss of RUNX1 binding at RUNX1/CTCF-binding sites.

132 We previously discovered that CTCF binds to large numbers of endogenous RNAs, promotin

133 or resistance-associated genetic variants at CTCF-bound anchors.

134 CTCF knockdown and in silico deletion of CTCF-bound core nodes disrupts core-periphery structure,

135 tes, and shifts in nuclease accessibility of CTCF-bound elements.

136 Thus, downmodulation of CTCF-bound scanning-impediment activity promotes cohesin

137 Manipulation of CTCF boundary can alter TAL1 TAD and oncogenic transcrip

138 ation within the TAL1 locus, suggesting that CTCF boundary plays a pathogenic role in T-ALL.

139 Ds, transcription, and leukemogenesis in the CTCF-boundary-attenuated AML cells.

140 Cohesin and CTCF (CCCTC-binding factor) are key regulators; perturbi

141 gration of matched in situ Hi-C, RNA-seq and CTCF ChIP-seq datasets revealed widespread differences i

142 We perform CTCF ChIP-seq in multiple mouse species to create genome

143 binding, we systematically analyze over 700 CTCF ChIP-seq profiles across human tissues and cancers

144 nd we uncovered that RNA is required for the CTCF-chromatin association.

145 nternal RNA-binding region (RBR(i)) mediates CTCF clustering and RNA interaction in vivo.

146 sing effects of cohesin and transcription on CTCF clustering, and highlights the power of quantitativ

147 Investigating the molecular determinants of CTCF clustering, we found that CTCF self-association in

148 iptional inhibition (TI) result in increased CTCF clustering.

149 dy provides quantitative characterization of CTCF clusters in living cells, uncovers the opposing eff

150 Furthermore, the effect of TI on CTCF clusters is alleviated by the acute loss of the coh

151 han nonclustered CTCF sites, suggesting that CTCF clusters particularly contribute to cohesin stabili

152 A fraction of CTCF clusters, enriched for those with >=3 molecules, ar

153 The formation of CTCF/cohesin co-anchored structural loops follows the ki

154 form rapidly, with rates exceeding those of CTCF/cohesin-anchored contacts.

155 e also introduce remaining questions for how CTCF/cohesin-dependent and -independent genome architect

156 CTCF/cohesin-dependent loops have also been shown to dir

157 pMILO, to predict the effects of variants on CTCF/cohesin-mediated insulator loops.

158 By cytokinesis, cohesin-mediated CTCF-CTCF loops and the positions of TADs emerge.

159 e analyze the impact of expressing CTCFL and CTCF-CTCFL chimeric proteins in the presence or absence

160 , is propagated over a CCCTC-binding factor (CTCF)-demarcated region through a distinct mechanism tha

161 cohesin binding to the KSHV genome is highly CTCF dependent, whereas CTCF binding does not require co

162 Together, our findings reveal a dual role of CTCF-dependent chromatin organization in promoting myeli

163 revious studies that examined the effects of CTCF depletion actually represent the concomitant deplet

164 in-treated versus untreated experiments, and CTCF depletion experiments, multiHiCcompare was able to

165 In contrast, WAPL or CTCF depletion increases inter-domain contacts in a cohe

166 bryonic Stem (ES) cells, we show that the TF CTCF displaces nucleosomes from its binding site and loc

167 Mechanically, acute depletion of CTCF disrupted the direct interaction between the MYC pr

168 -resolution chromatin interactions, MYOD and CTCF DNA-binding profile, and gene expression, revealed

169 iated transcript (LAT) enhancer was bound by CTCF during latency and underwent CTCF eviction at early

170 Our data suggest that CTCF enables the formation of chromatin loops by protect

171 g data implies that some genomic cohesin and CTCF enrichment sites are unoccupied in single cells at

172 We find that CTCF establishes chromatin interaction loops between enh

173 s bound by CTCF during latency and underwent CTCF eviction at early times postreactivation in mice la

174 y greatly reduced accessibility and lose the CTCF footprint in prometaphase, suggesting loss of CTCF

175 oscopy, we demonstrate that in living cells, CTCF forms clusters typically containing 2-8 molecules.

176 st that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the ob

177 3A, dCas9-DNMT3A3L) can selectively displace CTCF from specific insulators, but only when precisely t

178 on through its trans-acting ability to evict CTCF from Xist promoter.

179 n comprehensively analyzed in the context of CTCF function.

180 Stripe-shaped contact patterns-anchored by CTCF-grow in length, which is consistent with a loop-ext

181 f genome organization, CCCTC-binding factor (CTCF) has been characterized as a DNA-binding protein wi

182 -genotype correlations for seven risk genes (CTCF, HNRNPU, KCNQ3, ZBTB18, TCF12, SPEN, and LEO1) base

183 d findings regarding the role of cohesin and CTCF in 3D genome organization, as well as discovering n

184 st in prometaphase, histone acetylation, and CTCF in anaphase/telophase, transcription in cytokinesis

185 Knockdown of CTCF in K562 cells caused loss of CTCF binding and trans

186 with BEAF-32 present in embryonic cells and CTCF in neuronal cells.

187 of this study was to identify novel roles of CTCF in the developing mouse brain.

188 also gain H3K27ac and CCCTC-binding factor (CTCF) in anaphase/telophase.

189 neurological disorders previously linked to CTCF, including schizophrenia, autism, and intellectual

190 activated by a focal deletion that removes a CTCF-insulated neighborhood boundary.

191 editing strategies for perturbing individual CTCF insulators and evaluating consequent effects on gen

192 s systematically, we mapped DNA methylation, CTCF insulators, enhancers, and chromosome topology in K

193 One HSF1 partner, CTCF, interacted with HSF1 in a stress-inducible manner

194 y expands the current knowledge of the human CTCF interactome and represents an important resource to

195 We demonstrate that the N terminus of CTCF interacts with cohesin which explains the requireme

196 In addition, CTCF interacts with SUZ12, a component of polycomb-repre

197 at the nucleosome-depleted region (NDR) near CTCF is asymmetrically located >40 nucleotides 5'-upstre

198 CTCF is essential to define topologically associated dom

199 Ubiquitously expressed CTCF is involved in numerous cellular functions, such as

200 d mitotic nucleosome positioning activity of CTCF is not unique: Esrrb binding regions are also chara

201 CTCF and cohesin and demonstrate that while CTCF is required for cohesin binding to KSHV, they have

202 We provide evidence that CTCF is required for the expression of the LIM homeodoma

203 The CCCTC-binding factor (CTCF) is a central regulator of chromatin topology recen

204 CCTC-binding factor (CTCF) is a key regulator of gene expression through orga

205 CTCF knockdown and in silico deletion of CTCF-bound core

206 In addition, CTCF knockdown caused increased differentiation.

207 Furthermore, depletion of CTCF leads to the almost complete dissociation of cohesi

208 miniAID-mClover3 cassette to the endogenous CTCF locus in a human pediatric B-ALL cell line, SEM, an

209 ffects in genome-scale screens for essential CTCF loop anchors in K562 cells were not single guide RN

210 ribution of several transcription factors to CTCF loop stability in human cells.

211 CTCF looping factor-bound elements (CBEs) within IGCR1 u

212 First, using 5C, we confirmed that TADs and CTCF loops are readily detected in interphase, but absen

213 contribute to the observed loss of TADs and CTCF loops during mitosis and reveals that CTCF sites, k

214 current methods often miss visually evident CTCF loops in Hi-C data sets from mammals, and they comp

215 CTCF loss from such sites, for example, at promoters, bo

216 In SEM cells, CTCF loss notably disrupted intra-TAD loops and TAD inte

217 sites of transcriptional repressors (such as CTCF, MECOM, SMAD4, and SNAI3) and depleted of the bindi

218 omic subcompartment, rather than by cohesion/CTCF-mediated extrusion.

219 up to 60% of T-ALL cases and is involved in CTCF-mediated genome organization within the TAL1 locus,

220 AD 'fusion' event associated with absence of CTCF-mediated insulation, enabling direct interactions b

221 We also demonstrate that CTCF-mediated interactions are well conserved across pop

222 tin accessibility, histone modifications and CTCF-mediated TAD leading to inhibition of TAL1 expressi

223 based on assumptions of how many cohesin and CTCF molecules organise the genome.

224 0 nucleotides 5'-upstream from the centre of CTCF motif.

225 aling effects of nucleotides beyond the core CTCF motif.

226 While the orientation of CTCF motifs determines which pairs of CTCF sites prefere

227 RISPR-mediated excision of the corresponding CTCF motifs in an SDH-intact GIST model disrupted the bo

228 Given the orientation of CTCF motifs presents the N-terminus towards cohesin as i

229 or evolutionarily conserved bases, eQTLs and CTCF motifs, supporting their biological significance.

230 rrangement of the chromatin landscape around CTCF motifs.

231 Although previous studies sought to explain CTCF multivalency based on sequence composition of bindi

232 ducible complementation system, we find that CTCF mutants lacking the N-terminus cannot insulate TADs

233 Here we show that a segment within the CTCF N terminus interacts with the SA2-SCC1 subunits of

234 t the transcription factor binding sites for CTCF, NFATc1 and NR3C1.

235 solute copy numbers and dynamics of cohesin, CTCF, NIPBL, WAPL and sororin by mass spectrometry, fluo

236 Likewise, Ctcf-null MGE cells transplanted into the cortex of wild

237 s of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.

238 s in the genome, several events with altered CTCF occupancy have been reported as associated with eff

239 Azacitidine exposure caused major changes in CTCF occupancy in AML patient cells, partly by restoring

240 de that AML displays an aberrant increase in CTCF occupancy that targets key genes for AML developmen

241 Gain of CTCF occupancy was associated with increased gene expres

242 Furthermore, CTCF or cohesin depletion was found to have regulatory e

243 odomains, which persist in cells depleted of CTCF or cohesin, whereas disruption of nucleosome contac

244 Inhibition of CTCF or its deletion blocks Schwann cell differentiation

245 The CCCTC-binding factor (CTCF) organises the genome in 3D through DNA loops and i

246 romatin binding of the architectural protein CTCF play an important role for establishing cell-type-s

247 Yin Yang 1 (YY1), and CCCTC-binding factor (CTCF) play a role in regulating the accessibility of the

248 CCCTC-binding factor (CTCF) plays a key role in the formation of topologically

249 t uncovering molecular mechanisms modulating CTCF pleiotropic functions throughout the genome.

250 single molecule live imaging we report that CTCF positions cohesin, but does not control its overall

251 mposition of binding sites, few examined how CTCF post-translational modification (PTM) could contrib

252 monstrated that genome architectural protein CTCF prevents excessive clustering of accessible chromat

253 s chromatin contacts and intermingling while CTCF prevents inter-TAD contacts.

254 single and combined depletion indicates that CTCF primarily activates KSHV lytic transcription, where

255 myelinating stage, whereas overexpression of CTCF promotes the myelination program.

256 tween methylation within the IRX2 gene body, CTCF protein binding, three-dimensional (3D) chromatin i

257 ne, HUDEP-2, to allow for acute depletion of CTCF protein by the auxin-inducible degron system.

258 In mammals, the CTCF protein defines the boundaries of most chromatin lo

259 CTCF protein depletion weakened most TAD boundaries but

260 domains (TADs) arise from the ability of the CTCF protein to stop extrusion of chromatin loops by coh

261 f Top2 activity in humans: tightly localised CTCF-proximal, and broadly distributed transcription-pro

262 ng sites for architectural proteins, such as CTCF, RAD21, and SMC3, that are involved in tethering ch

263 conserved zinc finger CCCTC-binding factor (CTCF) regulates genomic imprinting and gene expression b

264 is divided into two sub-TADs separated by a CTCF-rich boundary, which defines two regulatory submodu

265 ng RNAs (lncRNAs), and CCCTC-binding factor (CTCF)-RNA interactions, but systematic approaches are ne

266 nhibition of transcription and disruption of CTCF-RNA interactions through mutations of 2 of its 11 z

267 To understand CTCF's direct role in global transcriptional regulation,

268 Strikingly, the overall effect of CTCF's loss on transcription was minimal.

269 terminants of CTCF clustering, we found that CTCF self-association in vitro is RNase sensitive and th

270 CTCF Ser(224)-P is chromatin-associated, mapping to at l

271 hylation (H3K4me3) and CCCTC-binding factor (CTCF) signals.

272 Dynamic conservation of CTCF site clusters is an apparently important feature of

273 The deletion and inversion of a CTCF site located near these regulatory sequences did no

274 ription units, with or without a neighboring CTCF site.

275 A number of CTCF sites also displayed direct correlations with the C

276 regulatory SVs, particularly those altering CTCF sites and provides a simple approach for functional

277 containing both evolutionarily old and young CTCF sites as a result of the repeated acquisition of ne

278 The overwhelming majority of clustered CTCF sites colocalize with cohesin and are significantly

279 Second, ATAC-seq analysis showed that CTCF sites display greatly reduced accessibility and los

280 results demonstrate loss of CTCF binding to CTCF sites during prometaphase and rearrangement of the

281 Cohesin remains at CTCF sites in this mutant, albeit with reduced enrichmen

282 fferentiation, a subset of preserved, common CTCF sites maintains asymmetric nucleosome pattern and s

283 facilitates the contacts of AEs with distant CTCF sites near promoter of other cell-cycle genes, whic

284 ion of CTCF motifs determines which pairs of CTCF sites preferentially stabilize loops, the molecular

285 Repeat Length (NRL) for ~20 nucleosomes near CTCF sites, affecting up to 10% of the genome.

286 d CTCF loops during mitosis and reveals that CTCF sites, key architectural cis-elements, display cell

287 transcription start sites than nonclustered CTCF sites, suggesting that CTCF clusters particularly c

288 TAD border and an unfavorable orientation of CTCF sites.

289 and functional constraints compared to other CTCF sites.

290 iated, mapping to at least a subset of known CTCF sites.

291 The molecular mechanism of how cohesin and CTCF structure the 3D genome has remained unclear.

292 Remarkably, while degradation of CTCF suppressed most CBE-based chromatin interactions, i

293 l extrusion until unidirectional blockage by CTCF that is presumed to occur in mammals.

294 ons within TADs are regulated by cohesin and CTCF through distinct mechanisms: cohesin generates chro

295 ins in the presence or absence of endogenous CTCF to clarify the relative and combined contribution o

296 2D revealed enrichment for SMAD3, HNF4A, and CTCF transcription factor binding sites.

297 orrelations with the CpG modification state: CTCF was preferentially lost from sites that were marked

298 The CCCTC-binding factor (CTCF), which anchors DNA loops that organize the genome

299 ering and chromatin binding of RBR(i) mutant CTCF, which in turn results in a failure to halt cohesin

300 tion is linked to alterations in H3K27ac and CTCF within H3K36me2 enriched chromatin.