ライフサイエンスコーパス: chromatin

1 pears to negatively modulate Chd1 binding to chromatin.

2 iated protein (ORCA/LRWD1) stabilizes ORC on chromatin.

3 interact with target loci in the context of chromatin.

4 s are located within regions of inaccessible chromatin.

5 endently of ATRX and H3.3 incorporation into chromatin.

6 one acetyltransferases of the MYST family to chromatin.

7 anscriptional repression via condensation of chromatin.

8 by extensive ZMYND8 domains on the flanking chromatin.

9 , Arp2/Arp3, CPF, CF 1A and Lsm complexes in chromatin.

10 HIRA-mediated incorporation of H3.3/H4 into chromatin.

11 ntirely lost upon RNaseA digestion of native chromatin.

12 We further associated chromatin aberrations with gene expression changes from

13 identity and function of ILC1s by promoting chromatin accessibility and deposition of STAT5 at the p

14 eatures of fibroblasts being visible both in chromatin accessibility and gene expression.

15 nfarction, which was associated with loss of chromatin accessibility around cell cycle genes during p

16 noncoding regions exhibit dynamic changes in chromatin accessibility between developmental stages and

17 Single-cell chromatin accessibility can guide prospective characteri

18 as cell type-specific features derived from chromatin accessibility data.

19 n On (GRO-seq) data, and characterization of chromatin accessibility from ATAC-seq datasets.

20 developing computational methods to identify chromatin accessibility from MAPit-BGS and NOMe-seq.

21 Analysis of chromatin accessibility in F3 and F4 sperm reveals signi

22 Integrating chromatin accessibility information with sequence inform

23 lated CD8(+) T cells, we define a pattern of chromatin accessibility specific for T-cell exhaustion,

24 n leukemia and define its role in regulating chromatin accessibility to lineage-specific transcriptio

25 int demonstrated that changes in genome-wide chromatin accessibility were similar across hiPSC and hE

26 (miR-9/9( *)-124) trigger reconfiguration of chromatin accessibility, DNA methylation, and mRNA expre

27 tein binds these GA repeat motifs, increases chromatin accessibility, enhances histone gene transcrip

28 by inducing enhancer components and enhancer chromatin accessibility.

29 brown fat gene enhancers, thereby regulating chromatin accessibility.

30 alling within immune pathways and regions of chromatin accessible in immune cells that was also repre

31 These findings identify perturbed chromatin acetylation in irinotecan resistance and estab

32 Here, we use ChAP-MS (chromatin affinity purification with mass spectrometry),

33 Chromatin analysis and shRNA-mediated gene suppression e

34 SUMOylated beta-catenin accumulates at the chromatin and activates multiple oncogenes.

35 ferences in the dependency of TF activity on chromatin and classify TFs by their differential capacit

36 ship between the physical nanoenvironment of chromatin and gene transcription in vitro.

37 oteins from membranes, protein complexes, or chromatin and has an essential role in autophagy and the

38 or understanding the differential effects of chromatin and lamin A/C in cell nuclear mechanics and th

39 TFs by their differential capacity to alter chromatin and promote expression.

40 RNA polymerase II (Pol2) movement through chromatin and the co-transcriptional processing and fate

41 omplex for oxidized bases in non-replicating chromatin, and allow repair when oxidized bases are indu

42 Many chromatin- and DNA-modifying enzymes make use of substra

43 Notably, the effects of HBBP1 removal on chromatin architecture and gene expression closely mimic

44 t chromatin remodeling complexes control the chromatin architecture and have important roles in gene

45 n chromosome 6, potentially representing the chromatin architecture at the histone locus body.

46 This hampers the investigation of chromatin architecture in rare cell populations.

47 These findings provide a high-resolution chromatin architecture resource for cardiac epigenomic i

48 cm7 ubiquitylation and CRL2(Lrr1) binding to chromatin are temporally linked and occur only during re

49 the paper "Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leuka

50 one chaperone function and play key roles in chromatin assembly and disassembly pathways.

51 Chromatin assembly factor 1 (CAF-1) is the histone chape

52 at Hat1 is transiently recruited to sites of chromatin assembly, dissociating prior to the maturation

53 te-restricted lncRNAs, including a conserved chromatin-associated lncOL1.

54 The gist of this technology is to ligate chromatin-associated RNAs (caRNAs) with their target gen

55 We found that deficient pS38 abated AID chromatin association and CSR but not mutation at Myc.

56 ubnuclear localization, gene expression, and chromatin association did not provide evidence for an in

57 that ChlR1 is an important regulator of the chromatin association of E2 and of the establishment and

58 and NPC segregation via the mitotic specific chromatin association of Nup2.

59 he absence of DNA damage, on the other hand, chromatin association of XRCC5 requires DDB2.

60 ors requires the establishment of accessible chromatin at lineage-specific transcriptional enhancers

61 these data define METTL3 as a regulator of a chromatin-based pathway that is necessary for maintenanc

62 hese novel mutations are predicted to affect chromatin (BCOR, KDM6A, SMARCB1, TRRAP), immune surveill

63 Strikingly, we find a median value of 5 TBP-chromatin binding events associated with the synthesis o

64 h proteins to greatly reduce or ablate XRCC1 chromatin binding following H2O2 treatment.

65 ed to ablate both ADP-ribosylation and XRCC1 chromatin binding following H2O2 treatment.

66 rotein 1 (HP1) family proteins are conserved chromatin binding proteins involved in gene silencing, c

67 inking data to extract kinetic parameters of chromatin binding.

68 Thus, our work identifies a critical chromatin-binding DNA damage response factor, ZMYM3, whi

69 rement of the fraction of histones remaining chromatin-bound in the individual nuclei using histone t

70 itosis, Repo-Man/PP1 remains associated with chromatin but its function in interphase is not known.

71 tion of transcription requires alteration of chromatin by complexes that increase the accessibility o

72 PRDM13 does this via recruitment to chromatin by multiple neural bHLH factors to restrict ge

73 is achieved by assisted loading of STAT3 on chromatin by NF-kappaB.

74 tethers to the nuclear envelope and internal chromatin-chromatin tethers, together with microtubule d

75 or oligomerized condensin in driving gradual chromatin compaction by step-like and slow "creeping" dy

76 Finally, we show that chromatin compaction in preimplantation embryos can part

77 unsuspected function for the Pf1-associated chromatin complex in the ribosomal biogenesis and senesc

78 The COMPASS chromatin complex, which trimethylates lysine 4 on histo

79 nteraction of the Fpr4 FKBP with recombinant chromatin complexes condenses nucleosome arrays independ

80 re and block the binding of the regulator of chromatin condensation 1 (RCC1) acidic patch-binding pro

81 echanical properties of the nucleus and also chromatin condensation.

82 mbined with assay for transposase-accessible chromatin coupled to high-throughput sequencing (ATAC-se

83 e nucleus is altered intrinsically, inducing chromatin decondensation or cell differentiation.

84 usual behaviours of heterochromatin, and how chromatin domains in general regulate essential nuclear

85 Ac) recruits repair proteins and reorganizes chromatin during DNA repair is unclear.

86 We uncover a dual regulatory role for chromatin during DNA replication: promoting origin depen

87 that often have pivotal roles in regulating chromatin dynamics and in the accessibility of the under

88 nique transcription factor that may regulate chromatin dynamics during development.

89 raises an interesting question regarding how chromatin dysregulation contributes to different disease

90 hyltransferase Ezh2 to Suz12 and reduce PRC2 chromatin engagement.

91 anti-O-GlcNAc antibody revealed significant chromatin enrichment of O-GlcNAc-modified proteins at th

92 Chromatin entry sites (CES) are 100- to 1,500-bp element

93 study revealed a dynamic hTERT regulation by chromatin environment and promoter-bound TFs during ESC

94 hylation machinery to establish a repressive chromatin environment at a subset of origins, which prim

95 BRD2 therefore creates a restricted chromatin environment surrounding DSBs which facilitates

96 get regions, PKL may be required to create a chromatin environment that influences non-coding RNA pro

97 Actively transcribed genes adopt a unique chromatin environment with characteristic patterns of en

98 fication of histones, serves to modulate the chromatin environment.

99 nal response between subclasses is the local chromatin environment.

100 gene was dictated by distal elements and its chromatin environment.

101 gs uncover an essential role for PRDM15 as a chromatin factor that modulates the transcription of ups

102 comparative analysis of transcriptional and chromatin features of inactive X-linked genes in WT and

103 ersonal regulome" analysis framework reveals chromatin features that may be predictive of clinical re

104 th and location of the DNA region within the chromatin fiber.

105 In vitro, the compounds induce misfolding of chromatin fibre and block the binding of the regulator o

106 nclude many genes involved in nucleosome and chromatin formation, and are extensively and significant

107 A-PET that includes cell fixation and lysis, chromatin fragmentation by sonication, ChIP, proximity l

108 Through immunoprecipitation of YY1-bound chromatin from affected individuals' cells with antibodi

109 PSR prevents the paternal chromatin from forming chromosomes during the first embr

110 are transcribed and are enriched for active chromatin hallmarks on the inactive-X, including RNA Pol

111 al interactions, this approach uncovered the chromatin helicase DNA-binding factor CHD1 as a putative

112 NA binding protein MeCP2 and with the active chromatin histone modification H3K4me2 in mouse neurons.

113 Thus, chromatin histone modification state is a major determin

114 The validation with the chromatin immunoprecipitation (ChIP) sequencing (ChIP-Se

115 To determine direct targets, we performed a chromatin immunoprecipitation against Lmx1b in mouse lim

116 Chromatin immunoprecipitation analyses demonstrated that

117 EBF1 promoter was demonstrated by EMSAs and chromatin immunoprecipitation analysis, suggesting trans

118 o two locations in the tru1 gene as shown by chromatin immunoprecipitation and gel shifts.

119 Chromatin immunoprecipitation and NNMT promoter lucifera

120 Chromatin immunoprecipitation assays indicated that PAF-

121 ernative splicing and performed quantitative chromatin immunoprecipitation at downstream targets in N

122 Chromatin immunoprecipitation experiments reveal increas

123 We performed co-immunoprecipitation and chromatin immunoprecipitation experiments.

124 he more common scenario of ERG upregulation, chromatin immunoprecipitation followed by sequencing ind

125 Using chromatin immunoprecipitation sequencing (ChIP-seq) comb

126 ole for CLOCK in human neurons by performing chromatin immunoprecipitation sequencing for endogenous

127 forward and reverse genetic approaches with chromatin immunoprecipitation to identify centromeres of

128 Here, by combining studies using chromatin immunoprecipitation with sequencing and RNA se

129 qRT-PCR, Western blotting, ELISA, and ChIP (chromatin immunoprecipitation) to characterize Pb-induce

130 c analyses such as RNA sequencing (RNA-Seq), chromatin immunoprecipitation, and ribosome profiling.

131 Analysis by the chromatin immunoprecipitation-exonuclease (ChIP-exo) met

132 Chromatin immunoprecipitation-PCR detected increased ETS

133 chromatin immunoprecipitation-seq analyses of NRSF targe

134 Genome-wide chromatin immunoprecipitation-sequencing analysis reveal

135 Chromatin-immunoprecipitation experiments showed that HE

136 ption factors remain associated with mitotic chromatin in ESCs and during iPSC reprogramming, demonst

137 xpression, and epigenetic features of closed chromatin in male germ cells, which suggests that CNVs m

138 Multiple lines of evidence implicate chromatin in the regulation of premessenger RNA (pre-mRN

139 molecular type (RNA, methylated DNA or open chromatin) in a single cell, furthermore, provides insig

140 n by modulating DAXX-H3.3 association on the chromatin, independently of PTEN enzymatic activity.

141 CTCF-rich DNA region in embryos, we compared chromatin interaction profiles between proximal and dist

142 genome-wide function in mediating long-range chromatin interactions and support the hypothesis that c

143 Besides cell lines, we could observe chromatin interactions by a Chromosome Conformation Capt

144 Furthermore, we demonstrate that chromatin interactions detected by Capture-C do not depe

145 Spatial chromatin interactions in the nucleus involving gene pro

146 Assuming that most mRNA-chromatin interactions indicate the physical proximity o

147 ated STAT5 binding induces new and augmented chromatin interactions within superenhancer-containing g

148 omains (TADs), defined by preferential local chromatin interactions, and chromosome compartments, def

149 activity is also associated with long-range chromatin interactions, suggesting that enhancers can in

150 phased genotype data to call allele-specific chromatin interactions.

151 present study provides new insights into the chromatin landscape and Blimp1-dependent regulatory netw

152 iated with almost complete remodeling of the chromatin landscape, as well as alteration of the transc

153 itical role in blocking modifications to the chromatin landscape.

154 d HF tumor-initiating cells possess distinct chromatin landscapes and gene regulatory networks associ

155 The repressive status of chromatin largely contributes to HIV latency.

156 c replication is primarily controlled at the chromatin level through histone and DNA modifications.

157 mation in Drosophila In addition, the CLAMP (chromatin-linked adaptor for male-specific lethal [MSL]

158 d that NEDDylation-deficient HBx showed less chromatin localization and less DDB1 binding.

159 asricha et al. demonstrate that the hepcidin-chromatin locus displays HDAC3-mediated reversible epige

160 bound to one or two TSSs and are enriched at chromatin loop anchors.

161 -associated SNPs are associated with reduced chromatin looping between the enhancer and the CUPID1 an

162 modulate the release of paused RNAPII via 3D chromatin looping.

163 network through diverse mechanisms including chromatin looping.

164 ops, whereas PB insertion encompasses larger chromatin loops termed topologically associating domains

165 at cohesin forms TADs and loops by extruding chromatin loops until it encounters CTCF, but direct evi

166 e both size and stability of the intervening chromatin loops, and use it to demonstrate that malignan

167 Trimethylation of histone H3K36 is a chromatin mark associated with active gene expression, w

168 roteins associated with Set1) to ensure that chromatin marks are not established until nutrient/energ

169 gins that also associate with the repressive chromatin marks H3K9me3 and methylated-CpGs, consistent

170 epigenomic approaches can infer function for chromatin marks through correlation, it remains challeng

171 The magnitude of chromatin mobility induced by a single double-strand bre

172 Chromatin modification and higher-order chromosome struc

173 ZIP and PR1) and potential genes involved in chromatin modification.

174 Differences in chromatin modifications and epigenetic markers between s

175 oters, suggesting a cross-talk between these chromatin modifications and transcription through the BR

176 ese findings indicate that ostensibly stable chromatin modifications can be dynamically regulated in

177 rough the nucleosome with co-transcriptional chromatin modifications during transcription, which is a

178 o exhibit partial recapitulation of bivalent chromatin modifications that are lost along with pluripo

179 e-specific transcriptional activators and by chromatin modifications to promote pre-initiation comple

180 Chromatin modifications, such as cytosine methylation of

181 h a transcriptional factor conveys a general chromatin modifier to specific genes, thereby allowing t

182 plication patterns, but the role of specific chromatin modifiers in regulating the replication proces

183 The generated metabolites are utilized by chromatin modifiers to affect epigenetic modification.

184 gest that AMPK regulates the activity of the chromatin modifying COMPASS complex (complex proteins as

185 ires both maternal germline nuclear RNAi and chromatin-modifying activity.

186 The Spt-Ada-Gcn5-acetyltransferase (SAGA) chromatin-modifying complex is a transcriptional coactiv

187 Extensive dysregulation of chromatin-modifying genes in clear cell renal cell carci

188 thin DNA, the arrangements of nucleosomes in chromatin modulate the properties of longer polymers.

189 Mechanistically, chromatin occupancy of serine 2-unphosphorylated RNA pol

190 R, intra-nuclear trafficking, and binding to chromatin of the hVDR-hRXR complex.

191 gation of RNA Pol II and preventing silenced chromatin on the viral genome.

192 Chromatin organization can be probed by Chromosomal Capt

193 r self-renewal and that it acts with HIRA in chromatin organization to link epigenetic organization t

194 either act as E3 ubiquitin ligase or affect chromatin organization, inhibits the transcriptional act

195 altering the expression of genes involved in chromatin organization, signaling, adhesion, motility, d

196 ociating Domains (TADs) that represent a sub-chromatin organization.

197 While these events occur in the context of chromatin, our understanding of how TF-nucleosome interp

198 Chromatin per se can stimulate efficient enhancer-promot

199 Epigenetic regulation of chromatin plays a critical role in controlling embryonic

200 al. now show that skin tumors exhibit merged chromatin profiles from distinct stem cell lineages.

201 Based on their chromatin profiles, candidate sequences can be classifie

202 ecovering signal when applied to low-quality chromatin profiling datasets across individuals, cell ty

203 cellular substrates including ubiquitylated chromatin proteins.

204 Chromatin rearrangements in enhancer regions occurred be

205 noic acid (ATRA) induces the interaction and chromatin recruitment of a novel RARbeta-TET2 complex to

206 Most of the identified open chromatin regions (OCRs) are differentially accessible b

207 onstrate that studying the landscape of open chromatin regions in stem cell-derived neurons helps fun

208 elements is often associated with accessible chromatin regions.

209 Recent literature has described chromatin-regulated alternative splicing, suggesting a n

210 proach to unbiasedly identify locus-specific chromatin-regulating protein complexes and long-range DN

211 These findings provide new insights into how chromatin regulation modulates stochastic gene expressio

212 llow chemical-induced proximity of a desired chromatin regulator.

213 tigation of post-transcriptional processing, chromatin regulators for piRNA biogenesis in mammals rem

214 disorders helps us to understand the role of chromatin regulators in brain development, plasticity, a

215 Despite recent progress made in targeting chromatin regulators in cancer, available therapies for

216 Further investigation of drugs targeting chromatin regulators is warranted in HPV-negative HNSCCs

217 er family, and CSB is the only ATP-dependent chromatin remodeler essential for transcription-coupled

218 (CSB) belongs to the SWI2/SNF2 ATP-dependent chromatin remodeler family, and CSB is the only ATP-depe

219 In this study we show that a SWI/SNF chromatin remodeler subunit, BAF60, represses seedling g

220 ated BRG1- or hBRM-associated factors (PBAF) chromatin remodeler, contains six tandem BDs and is freq

221 n plays different roles based on the type of chromatin remodeler.

222 Chromatin remodelers use a helicase-like ATPase motor to

223 ers SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling and global methylation patterns tha

224 n NUPR1 is a multifunctional IDP involved in chromatin remodeling and in the development and progress

225 ell lineages, loss of proliferative control, chromatin remodeling as well as extensive morphological

226 Here we show that the INO80 chromatin remodeling complex is required for oncogenic t

227 ew set of genes encoding subunits of the BAF chromatin remodeling complex that exhibited Ras-mediated

228 which EBF2 cooperates with a tissue-specific chromatin remodeling complex to activate brown fat ident

229 acts with and recruits a tissue-specific BAF chromatin remodeling complex to brown fat gene enhancers

230 Among them, the ATP-dependent chromatin remodeling complexes control the chromatin arc

231 ranscription factors that recruit activating chromatin remodeling complexes.

232 es renal inflammation by several mechanisms: chromatin remodeling in promoter regions of specific gen

233 While chromatin remodeling mediated by post-translational modi

234 stablish an in vivo function of CHD Type III chromatin remodeling proteins in this process, and revea

235 te that interplay of p300-HDAC2-Sin3A in the chromatin remodeling system is involved in HIF-1alpha de

236 ns were predominantly in genes that regulate chromatin remodeling, chromosome alignment, and stabilit

237 low adaptation to new conditions by delaying chromatin remodeling.

238 ct with CSB and greatly enhance CSB-mediated chromatin remodeling.

239 eterminant is Swi1, a subunit of the SWI/SNF chromatin-remodeling complex.

240 modeling factor (NURF), a member of the ISWI chromatin-remodeling complex.

241 Human ALC1 is an oncogene-encoded chromatin-remodeling enzyme required for DNA repair that

242 a catalytic subunit of the mammalian SWI/SNF chromatin-remodeling enzymes, is required for both myobl

243 nges in the histone modification profile and chromatin-remodeling events leading to Sp7 gene expressi

244 The multi-subunit chromatin-remodeling SWI/SNF complex determines gene exp

245 These chromatin remodellers generally function by translocatin

246 ion of long-range resection, indicating that chromatin remodelling during resection is underlying DSB

247 Here we show that large-scale chromatin remodelling occurs during Drosophila neural de

248 e acidic patch may be generally required for chromatin remodelling.

249 the essential ATPase subunit of the SWI/SNF chromatin-remodelling complex, is required for expressio

250 hese findings reveal essential functions for chromatin-remodelling in the activation of EPDCs during

251 xa2 and Lhx1 is associated with higher order chromatin reorganisation.

252 PRC2 is required for chromatin reprogramming in the germline, and the transcr

253 The modulation of p53 residence times on chromatin requires C-terminal acetylation-a classical ma

254 emia epigenomes in the healthy hematological chromatin sample space gives us insights on the healthy

255 The chromatin scaffolding protein SMCHD1 (structural mainten

256 Strikingly, chromatin shows greatly diminished higher-order structur

257 link between alternative polyadenylation and chromatin signaling.

258 Here, we use a chromatin signature to infer MAE for genes in lymphoblas

259 Female-biased genes already in an active chromatin state in male liver generally showed early cGH

260 This chromatin state in the sporozoite also correlates with t

261 , and this suggests that target sequence and chromatin state modulate cleavage and repair kinetics.

262 ed early cGH responses; genes in an inactive chromatin state often responded late.

263 ntified surface markers associated with each chromatin state that distinguished reprogrammable from n

264 fy histones but it is unclear how changes in chromatin states alter kinetics of transcription.

265 These findings highlight the importance of chromatin states and transcriptional priming in dictatin

266 kov model, diHMM, to systematically annotate chromatin states at multiple length scales.

267 ding of the relationship between TF binding, chromatin status and the regulation of gene expression.

268 Chromatin structural analyses revealed interactions with

269 diac-specific deletion of CTCF (a ubiquitous chromatin structural protein) were generated to explore

270 Chromatin structure affects DNA replication patterns, bu

271 rated to explore the role of this protein in chromatin structure and cardiac phenotype.

272 er communication (EPC); however, the role of chromatin structure and dynamics in this process remains

273 ategy to illuminate the interplay between 3D chromatin structure and epigenetic dynamics.

274 tilization triggers assembly of higher-order chromatin structure from a condensed maternal and a naiv

275 t CNVs may repress recombination by altering chromatin structure in meiosis.

276 lex involved in gene repression and telomere chromatin structure, and a DAXX-SETDB1-KAP1-HDAC1 comple

277 mutational burden is known to be coupled to chromatin structure, we examine how somatic mutations ar

278 tion that necessitates epigenomic changes in chromatin structure.

279 bly, dissociating prior to the maturation of chromatin structure.

280 lication and is facilitated by a decondensed chromatin structure.

281 using Shannon's entropy, associating it with chromatin structure.

282 endent changes in the composition of nascent chromatin structure.

283 uman erythroblasts and found that, globally, chromatin structures and compartments A/B are highly sim

284 -rich regions plays an instrumental role for chromatin targeting and subsequent implementation of H3K

285 e RNA pol II C-terminal domain (CTD) and the chromatin template.

286 L4 promotes the expression of Glut1 and open chromatin through a HP1alpha-dependent mechanism.

287 n and discuss best practices for engineering chromatin to assist scientists in advancing the field of

288 ISWI subunits BAZ1A and BAZ1B might contact chromatin to direct the ATPase SMARCA5.

289 MYM3, which modulates BRCA1 functions within chromatin to ensure the maintenance of genome integrity.

290 bind their target sequences in inaccessible chromatin to establish new transcriptional networks thro

291 omplex to X-linked genes and modification of chromatin to increase expression.

292 , and colocated with AR at specific sites on chromatin to regulate genes relevant to disease progress

293 ferons and TNF is integrated at the level of chromatin to reprogram inflammatory responses, and ident

294 romotes the recruitment of FACT (facilitates chromatin transcription that enhances the engagement of

295 nstrate that global structural remodeling of chromatin underpins heart failure.

296 Each complex associates with chromatin via distinct mechanisms, conferring different

297 To analyze an RNA-dependent interaction with chromatin, we purified native nucleosomes from mouse ES

298 Localizing ESRRA binding sites in cortical chromatin, we show that this nuclear receptor binds both

299 rossovers reside in genomic regions of "open chromatin", which were identified based on hypersensitiv

300 yses show that HOXA1 physically interacts on chromatin with PBX, MEIS, and PREP family members, but n