ライフサイエンスコーパス: nuclear body

1 its featured subcellular structure, the PML nuclear body.

2 localizes to promyelocytic leukemia-adjacent nuclear bodies.

3 A in the nucleus and localization of phyA to nuclear bodies.

4 so disorganizes promyelocytic leukemia (PML) nuclear bodies.

5 ounteract RNF4 to inhibit the dissolution of nuclear bodies.

6 distribution of the chromatin into apoptotic nuclear bodies.

7 gh-irradiance white light, phyB formed large nuclear bodies.

8 acts with GATA-1 and can recruit it into PML nuclear bodies.

9 e NIH 3T3 cells led to the appearance of Mx1 nuclear bodies.

10 d chromatin does not localize into apoptotic nuclear bodies.

11 ough to restrain the formation of small phyB nuclear bodies.

12 transporters and/or cargoes to ataxin-1[85Q] nuclear bodies.

13 d their localizations using markers of known nuclear bodies.

14 nsmitted to daughter cells in 53BP1-shielded nuclear bodies.

15 and provide key information for research on nuclear bodies.

16 protein (PML) stability and formation of PML nuclear bodies.

17 s, and the L2/DNA complex accumulates at PML nuclear bodies.

18 required for the accumulation of SMN in sub-nuclear bodies.

19 associate with promyelocytic leukemia (PML) nuclear bodies.

20 assemble, maintain, and regulate particular nuclear bodies.

21 xtaposed with promyelocytic leukemia protein nuclear bodies.

22 nscriptional coregulator Daxx, SUMO, and PML nuclear bodies.

23 n involves two steps that take place at ND10 nuclear bodies.

24 , a phosphoinositide secondary messenger, in nuclear bodies.

25 oplasm to subnuclear foci called phytochrome nuclear bodies.

26 plasmic structures, whereas murine Mx1 forms nuclear bodies.

27 F61p-mediated dispersion of Sp100-containing nuclear bodies.

28 Maf localization into promyelocytic leukemia nuclear bodies.

29 P8 localize in structures that abut the ND10 nuclear bodies.

30 ng PML and Sp100, key components of the ND10 nuclear bodies.

31 and compartments, collectively described as nuclear bodies.

32 arge measure dependent on events in the ND10 nuclear bodies.

33 ic nuclear fission with reduced formation of nuclear bodies.

34 Pol II do not require that it accumulate in nuclear bodies.

35 pends upon prior localization of HIRA to PML nuclear bodies.

36 SUMO-1 is targeted to promyelocytic leukemia nuclear bodies.

37 tion of promyelocytic leukemia (PML) protein nuclear bodies.

38 one, HIRA, into promyelocytic leukemia (PML) nuclear bodies.

39 kt phosphatase PP2a as well as pAkt into Pml nuclear bodies.

40 labeling appeared to colocalize with the PML nuclear bodies.

41 oylation and SF-1 relocalization to discrete nuclear bodies.

42 with Nbs1 or promyelocytic leukemia protein nuclear bodies.

43 it failed to localize efficiently to the PML nuclear bodies.

44 1, was able to target YFP to the nucleus and nuclear bodies.

45 bound to chromatin and were localized to PML nuclear bodies.

46 coiled-coil protein, in the formation of FCA nuclear bodies.

47 of FLL2 increased the size and number of FCA nuclear bodies.

48 ium, protein clusters with the properties of nuclear bodies.

49 chromatin with the surrounding envelope and nuclear bodies.

50 sure an effective mergence of ICP0 with ND10 nuclear bodies.

51 and phytochromes colocalize and interact in nuclear bodies.

52 uding nucleoli (148), promyelocytic leukemia nuclear bodies (38), nuclear speckles (27), paraspeckles

53 paraspeckles (24), Cajal bodies (17), Sam68 nuclear bodies (5), Polycomb bodies (2), and uncharacter

54 5), Polycomb bodies (2), and uncharacterized nuclear bodies (64).

55 breaks, and accumulate high numbers of 53BP1 nuclear bodies, a marker of genomic instability induced

56 se proximity to promyelocytic leukemia (PML) nuclear bodies, a reversible process that recruits the m

57 DAXX's localization in the PML nuclear bodies also plays roles in transcriptional regul

58 Promyelocytic leukemia (PML) nuclear bodies (also known as ND10) are nuclear substruc

59 isintegration of promonocytic leukemia (PML) nuclear bodies, an intracellular event critical to produ

60 teins is critical to form the discrete NAC-1 nuclear bodies and essential for tumor cell proliferatio

61 nuclear speckles, mediates splicing at these nuclear bodies and exports the spliced M2 mRNA from the

62 that associations within and between various nuclear bodies and genomic loci are dynamic and can chan

63 cally induce HIRA/PML co-localization at PML nuclear bodies and HIRA recruitment to IFN target genes,

64 214, although mostly cytoplasmic, also forms nuclear bodies and inhibits nuclear protein but not poly

65 onsive transactivator (CREST) is targeted to nuclear bodies and is required for the normal developmen

66 tly reduces E1B-55K-induced tethering in PML nuclear bodies and p53 nuclear export.

67 ctions, transcription hubs, heterochromatin, nuclear bodies and phase transitions.

68 e first atlas of human proteins in different nuclear bodies and provide key information for research

69 ansformed cells induces the formation of PML nuclear bodies and recruits APC/C to these subnuclear st

70 found that nucleoporins can be released from nuclear bodies and reintegrated into existing NPC.

71 COP1-interacting motifs, still localizes in nuclear bodies and retains weak affinity for COP1.

72 icated oxidative stress in the biogenesis of nuclear bodies and SUMO in their degradation.

73 he first time that MLH1 associates with ND10 nuclear bodies and that like other ND10 proteins, MLH1 i

74 ear movements, resulting in repositioning of nuclear bodies and the associated chromatin within the n

75 enes within chromosomes, the distribution of nuclear bodies and the interplay between these different

76 hat E4 ORF3 regulates activities in both PML nuclear bodies and the MRN complex to stimulate the vira

77 reatly inhibits E1B-55K association with PML nuclear bodies and the p53 nuclear export to cytoplasmic

78 ociated proteins, affect the assembly of PML nuclear bodies and the recruitment of proteins in and ou

79 ctivates p53 by first sequestering it in PML nuclear bodies and then greatly facilitating its nuclear

80 ed with promyelocytic leukemia protein (PML) nuclear bodies and Top3alpha.

81 n the paraspeckles, disassociates from these nuclear bodies and translocates to the cytoplasm to modu

82 The nucleolus is the most prominent nuclear body and serves a fundamentally important biolog

83 5K-induced p53 sumoylation, tethering in PML nuclear bodies, and E1B-55K inhibition of p53 activity.

84 nuclear speckles, mediates splicing at these nuclear bodies, and exports the spliced M2 mRNA from the

85 atial arrangement of lineage-specific genes, nuclear bodies, and heterochromatin.

86 e components of promyelocytic leukemia (PML) nuclear bodies, and IE1 and pp71, acting together, almos

87 ated in promyelocytic leukemia protein (PML) nuclear bodies, and PML induces a striking nuclear accum

88 , we show that HFR1 colocalizes with COP1 in nuclear bodies, and that the HFR1 N-terminal region (ami

89 s associated to promyelocytic leukemia (PML) nuclear bodies, and we show that neither IFN-alpha nor I

90 nds on ALT-associated promyelocytic leukemia nuclear bodies (APBs), whose function is unclear.

91 Nuclear bodies are discrete suborganelle structures that

92 PML nuclear bodies are druggable and could be harnessed in o

93 Nuclear bodies are dynamic structures that form at sites

94 SET-Nup214 nuclear bodies are highly mobile structures, which are i

95 PML nuclear bodies are implicated in transcriptional regulat

96 ND10 nuclear bodies are part of the cell-intrinsic antiviral

97 Nuclear bodies are protein- and RNA-containing structure

98 Nuclear bodies are RNA and protein-rich, membraneless or

99 SUMO-enriched nuclear bodies are stabilized by USP11, which functions

100 Here, we show that in G1 cells, large nuclear bodies arise that contain p53 binding protein 1

101 Our results point to nuclear bodies as a means of preventing the formation of

102 ogether, these results implicate phytochrome nuclear bodies as sites of proteolysis.

103 ND10 nuclear bodies, as part of the intrinsic defenses, impos

104 ein that forms sub-nuclear structures termed nuclear bodies associated with transcriptionally active

105 of the cell nucleus by SUMO modification of nuclear body-associated PML and uptake of the ubiquitin

106 interaction with the promyelocytic leukemia nuclear-body-associated protein Sp100A.

107 and SUMO binding motifs on PML and other PML nuclear-body-associated proteins, affect the assembly of

108 associates with promyelocytic leukemia (PML) nuclear bodies, becomes SUMOylated, and recruits corepre

109 s with MRN in promyelocytic leukemia protein nuclear bodies before MRN is bound by E1B-55K.

110 The nucleolus and other nuclear bodies behave like liquid-phase droplets and app

111 ts, which are defined by several distinctive nuclear bodies believed to be factories of DNA or RNA pr

112 per in this issue highlights key features of nuclear body biogenesis and suggests a unifying model in

113 nst either TopBP1 or Brd4 destroys the E1-E2 nuclear bodies but has no effect on E1-E2-mediated level

114 restingly, the SIM mutant Sizn1 localizes to nuclear bodies, but not to PML-NBs.

115 oes not indefinitely support the emulsion of nuclear bodies, but only kinetically stabilizes them by

116 s the nuclear membrane, other chromosomes or nuclear bodies, but the resulting forces cannot be direc

117 in part, by the presence of specialized PML nuclear bodies called ALT-associated PML bodies (APBs).

118 14 (RBM14), all reported to be components of nuclear bodies called paraspeckles.

119 cells, light can induce de novo formation of nuclear bodies called photobodies (PBs) composed of the

120 tional promyelocytic leukaemia protein (PML) nuclear bodies co-ordinate PTEN localization by opposing

121 ear bodies in vivo, which indicates that FCA nuclear bodies compartmentalize 3'-end processing factor

122 recent progress in our understanding of how nuclear body components come together, what happens when

123 Thus, GFP-MuMx1 nuclear bodies comprised phase-separated condensates.

124 Nuclear domains called ND10 or PML nuclear bodies contain interferon (IFN)-upregulated prot

125 Both proteins colocalize to nuclear bodies containing histone deacetylases, which ar

126 far-red light led to the appearance of small nuclear bodies containing phyB.

127 cause colocalization and merger of ICP0 with nuclear bodies containing Sp100 and Daxx is ineffective,

128 SET-Nup214 nuclear bodies containing the nuclear export receptor CR

129 e11, Daxx, as well as the integrity of these nuclear bodies contribute to the transformation process.

130 The deficiency of SMN-containing sub-nuclear bodies correlates with the severity of SMA.

131 A component of promyelocytic leukemia nuclear bodies, Daxx is a transcriptional corepressor th

132 evealed that E1B-55K tethering of p53 in PML nuclear bodies decreases the in vivo nuclear mobility of

133 t for the dissociation of ATRX and Daxx from nuclear bodies during de novo infection of primary B lym

134 ures known as ND10 or promyelocytic leukemia nuclear bodies during the early stages of lytic infectio

135 ion forks outside the promyelocytic leukemia nuclear bodies during the S-phase arrest of the cell cyc

136 n of PML in neuroblastoma cells restored PML-nuclear bodies, enhanced responsiveness to all-trans-ret

137 malian genes localize near nuclear speckles, nuclear bodies enriched in ribonucleic acid-processing f

138 ssociating with promyelocytic leukemia (PML) nuclear bodies, ensuring its availability upon mitotic o

139 pool of phyB and the size of the associated nuclear bodies, even in daylight.

140 ls that the contents of many (membrane-free) nuclear bodies exchange rapidly with the soluble pool wh

141 zes with p53 in promyelocytic leukemia (PML) nuclear bodies following cellular stress.

142 Paraspeckles are nuclear bodies form around the long non-coding RNA, Neat

143 cation, causing mitotic abnormalities, 53BP1 nuclear body formation in the ensuing G1 phase, and G1 a

144 ecular self-organization is thought to drive nuclear body formation, but whether this occurs stochast

145 us, we uncover a DNA under replication-53BP1 nuclear body formation-G1 arrest axis as an unanticipate

146 ing that ordered assembly can play a role in nuclear body formation.

147 Paraspeckles are nuclear bodies formed by a set of specialized proteins a

148 and base excision repair, is recruited into nuclear bodies formed in response to replication-related

149 lear actin network that prevents liquid-like nuclear bodies from immediate sedimentation and coalesce

150 n adenoviruses is the ability to disrupt PML nuclear bodies from their normally punctate appearance i

151 our experiments identify a mechanism linking nuclear body growth and size with gene expression.

152 The formation of a specific nuclear body has been suggested to follow a stochastic o

153 tin modifiers and other machineries, various nuclear bodies have been shown to sequester and modify p

154 t RNF4 continues to rapidly shuttle into PML nuclear bodies in a SUMO-dependent manner.

155 re that DCL1 and HYL1 colocalize in discrete nuclear bodies in addition to being present in a low-lev

156 TiPARP forms distinct nuclear condensates or nuclear bodies in an ADP ribosylation-dependent manner.

157 sed regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic co

158 d1 localizes to ProMyelocytic Leukemia (PML) nuclear bodies in breast cancer and cultured cells.

159 components are distributed into at least two nuclear bodies in D. melanogaster.

160 ition caused DNA damage to manifest as 53BP1 nuclear bodies in daughter G(1) cells leading to G(1) ar

161 on data related to the configuration of PML nuclear bodies in mammalian fibroblast cells.

162 CRY2-GFP, but not GFP-CRY2, formed distinct nuclear bodies in response to blue light.

163 SMN and promotes accumulation of SMN in sub-nuclear bodies in SMA patient fibroblasts.

164 DNA elimination occurs, Wag1p forms multiple nuclear bodies in the developing macronuclei that do not

165 In cells, MORC4 mediates formation of nuclear bodies in the nucleus and has a role in the prog

166 hat both GFP-CRY2 and endogenous CRY2 formed nuclear bodies in the presence of the 26S-proteasome inh

167 n assays and are localized to aggregated PML-nuclear bodies in undifferentiated pluripotent human NTe

168 ssing components colocalized with FCA in the nuclear bodies in vivo, which indicates that FCA nuclear

169 gene, implicating the participation of this nuclear body in an innate antiviral response.

170 indicate that E1B-55K's association with PML nuclear bodies inactivates p53 by first sequestering it

171 Nuclear bodies including nucleoli, Cajal bodies, nuclear

172 dentified 325 proteins localized to distinct nuclear bodies, including nucleoli (148), promyelocytic

173 omponents of the histone locus body (HLB), a nuclear body involved in the expression of replication-d

174 gests a unifying model in which formation of nuclear bodies is driven by nonrandom, biologically dete

175 etween the 3D organization of the genome and nuclear bodies is essential to fully uncover the regulat

176 This initial recruitment of PML into nuclear bodies is not dependent on RNF4, but RNF4 quickl

177 proposed functions of promyelocytic leukemia nuclear bodies is regulation of gene transcription, we s

178 The classic archetypal function of nuclear bodies is to accelerate specific reactions withi

179 sm of E4-ORF3-mediated reorganization of PML nuclear bodies is unknown.

180 The function of these nuclear bodies is unknown.

181 The largest and most well-known nuclear body is the nucleolus, an organelle whose primar

182 h as Cajal bodies (CBs), nucleoli, and other nuclear bodies, is dynamic and can change in response to

183 pes simplex virus 1 (HSV-1) DNA localizes to nuclear bodies known as ND10.

184 me instability such as micronuclei and 53BP1 nuclear bodies, known consequences of persistently stall

185 O binding affects Daxx-PML interactions, PML nuclear body localization, and Daxx-mediated repression

186 Thus, the distinct HYL1- and DCL1-containing nuclear bodies may be miRNA precursor processing sites.

187 response to blue light, suggesting that the nuclear bodies may result from accumulation of photoexci

188 ized to promyelocytic leukemia protein (PML) nuclear bodies (NB).

189 nforces promyelocytic leukemia protein (PML) nuclear body (NB) formation and partner protein recruitm

190 The mechanisms underlying nuclear body (NB) formation and their contribution to ge

191 ell death upon gamma-irradiation through PML-nuclear body (NB)-mediated control of p53 acetylation.

192 d that the entire C terminus is required for nuclear-body (NB) localization.

193 een proposed to control the formation of PML nuclear bodies (NBs) and is crucial for PML-dependent ce

194 Promyelocytic leukemia protein (PML) nuclear bodies (NBs) are dynamic subnuclear compartments

195 PML nuclear bodies (NBs) are nuclear structures that have be

196 Nuclear bodies (NBs) are structures that concentrate pro

197 Persistent TopBP1 foci transition into 53BP1 nuclear bodies (NBs) in G1 and precise temporal depletio

198 of dynamic, reversible, liquid droplet-like nuclear bodies (NBs) in response to stress.

199 ntalization of RNA biosynthetic factors into nuclear bodies (NBs) is a ubiquitous feature of eukaryot

200 h disruption of promyelocytic leukemia (PML) nuclear bodies (NBs) mediated by the PML-retinoic acid r

201 Promyelocytic leukemia protein (PML) nuclear bodies (NBs) recruit multiple partners, includin

202 Promyelocytic leukemia (PML) nuclear bodies (NBs) recruit partner proteins, including

203 lved and the substrates into uncharacterized nuclear bodies (NBs) remains poorly understood.

204 locytic leukemia (PML) protein organizes PML nuclear bodies (NBs), which are stress-responsive domain

205 otein (PML) is an essential organizer of PML nuclear bodies (NBs), which carry out a variety of activ

206 However, ZIKV NS5 formed discrete punctate nuclear bodies (NBs), while DENV NS5 was uniformly dispe

207 disrupt promyelocytic leukemia protein (PML) nuclear bodies (NBs).

208 mponent of sub-nuclear structures called PML nuclear bodies (NBs).

209 e the assembly of NS5 proteins into discrete nuclear bodies (NBs).

210 , disruption of functions connected with PML nuclear bodies (ND10), and inhibition of cellular histon

211 The identification of these nuclear bodies now permits a broad range of questions to

212 h PIAS3 and SUMO-1 in promyelocytic leukemia nuclear bodies, nuclear domains involved in regulation o

213 with E1B-55K in promyelocytic leukemia (PML) nuclear bodies, nuclear domains with a high concentratio

214 demonstrated that AtEFR4 accumulated in the nuclear bodies of Arabidopsis cells.

215 umber of the snoRNAs and the localization to nuclear bodies of two putative scaRNAs was confirmed by

216 nown as promyelocytic leukemia protein (PML) nuclear bodies or ND10 and disrupts their integrity by i

217 cellular nuclear substructures known as PML nuclear bodies or ND10, is one of the most notable prote

218 nown as promyelocytic leukemia protein (PML) nuclear bodies or ND10.

219 ce, GFP-GmHSP40.1 was exclusively present in nuclear bodies or speckles.

220 tant of Arabidopsis with altered phytochrome nuclear body patterns.

221 Cellular bodies such as P bodies and PML nuclear bodies (PML NBs) appear to be phase-separated li

222 Using promyelocytic leukemia nuclear bodies (PML NBs) as a model, we used immuno-TRAP

223 ML) protein is an essential component of PML nuclear bodies (PML NBs) frequently lost in cancer.

224 Promyelocytic leukemia nuclear bodies (PML NBs) have been proposed to be involv

225 remodeling of promyelocytic leukemia protein nuclear bodies (PML NBs), an important constituent of nu

226 otein associated with promyelocytic leukemia nuclear bodies (PML NBs), is a target of herpes simplex

227 omponents of nuclear structures known as PML nuclear bodies (PML NBs), or ND10.

228 rred by components of promyelocytic leukemia nuclear bodies (PML NBs), which respond to infection by

229 cleavage of SATB1 at promyelocytic leukemia nuclear bodies (PML NBs).

230 se kinases at promyelocytic leukemia protein nuclear bodies (PML NBs).

231 ociated with structures known as ND10 or PML nuclear bodies (PML NBs).

232 hat are components of promyelocytic leukemia nuclear bodies (PML NBs, also known as ND10) have restri

233 Promyelocytic leukemia nuclear bodies (PML-NB) are sub-nuclear organelles that

234 is innate process are promyelocytic leukemia nuclear bodies (PML-NBs), which are subnuclear structure

235 traffics, in part, to promyelocytic leukemia-nuclear bodies (PML-NBs).

236 lasts by dissociating promyelocytic leukemia nuclear bodies (PML-NBs).

237 localizes to promyelocytic leukemia protein nuclear bodies (PML-NBs).

238 nd capacity to recruit other proteins to PML nuclear bodies (PML-NBs).

239 Promyelocytic leukemia nuclear bodies (PML-NBs)/nuclear domain 10s (ND10s) are

240 estigated its role in the recruitment of PML nuclear body (PML NB) components to viral genomes.

241 Promyelocytic Leukemia nuclear body (PML NB) proteins mediate an intrinsic cell

242 LP interacts with the promyelocytic leukemia nuclear body (PML NB)-associated protein Sp100 and displ

243 unity are mediated by promyelocytic leukemia nuclear body (PML-NB) constituent proteins.

244 V-infected cells, the promyelocytic leukemia nuclear body (PML-NB) protein Daxx silences viral immedi

245 e defense mediated by promyelocytic leukemia nuclear body (PML-NB) proteins such as Daxx and histone

246 t to reorganize a nuclear subdomain, the PML nuclear body (PML-NB), from punctate structures into elo

247 lear macromolecular structure called the PML nuclear body (PML-NB).

248 tumorigenesis, other promyelocytic leukemia nuclear body (PML-NB)/PML oncogenic domain (POD)-associa

249 with p63, (ii) p63 is localized into the PML nuclear-bodies (PML-NBs) in vivo, and (iii) PML regulate

250 ts binding partner, PRPF38A, in droplet-like nuclear bodies precedes formation of nuclear speckles du

251 A haplotype within the SP110 nuclear body protein (SP110) was present in 40% of affec

252 SP110 is a nuclear body protein involved in the regulation of gene

253 ining canonical promyelocytic leukemia (PML) nuclear body protein SP100 concentrated in a peripheral

254 sensor of pathogen DNA, and also of the PML nuclear body proteins PML and hDaxx, as revealed by live

255 nd G1-specific p53-binding protein 1 (53BP1) nuclear bodies provide a mechanism for resolving unrepli

256 The TiPARP nuclear bodies recruit both HIF-1alpha and an E3 ubiquit

257 d PML/RARA degradation is blunted, as is PML nuclear body reformation and activation of P53 signaling

258 TD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradic

259 and how they facilitate the stabilization of nuclear bodies, remain unknown.

260 Large nuclear bodies remained but with some concomitant reduct

261 onal forces also cause creep displacement of nuclear bodies, resulting in their asymmetric nuclear di

262 Promyelocytic leukemia (PML) nuclear bodies selectively associate with transcriptiona

263 GFP-MuMx1 filaments, but not those with only nuclear bodies, showed antiviral activity toward VSV.

264 YFP-DCL1 fusion proteins colocalize to small nuclear bodies similar to Cajal bodies but lacking the C

265 e foci containing SREBP-2 are electron-dense nuclear bodies, similar or identical to structures conta

266 s form reversible, transient species such as nuclear bodies, stress granules, and myo-granules.

267 f of ICP22 is needed for its localization to nuclear body structures.

268 on, and elevated levels of 53BP1-positive G1 nuclear bodies, suggesting that defects in chromosome se

269 l as another component of the PML-containing nuclear body, SUMO-1, and SREBP-2 within these nuclear s

270 s involved in transcription transactivation, nuclear body targeting, and dimerization.

271 ddition of a SV40 NLS to MFD domain restored nuclear body targeting.

272 onstrate that NAC-1 is localized in discrete nuclear bodies (tentatively named NAC-1 bodies), and the

273 ng foci constitute newly recognized PML-like nuclear bodies that accrete and locally deliver essentia

274 Speckles are nuclear bodies that contain pre-mRNA splicing factors an

275 P0 to nuclear domain 10 (ND10), the discrete nuclear bodies that impose restrictions on viral express

276 in in PARG mutants, but accumulates in large nuclear bodies that may be involved in protein recycling

277 HeLa cells leads to the formation of similar nuclear bodies that recruit CRM1, export cargo proteins,

278 ntagonizes the formation and function of PML nuclear bodies that regulate numerous signaling pathways

279 protein, and fibrillarin occur together in a nuclear body that is closely associated with the nucleol

280 l. show that formation of the paraspeckle, a nuclear body that regulates gene expression, requires lo

281 us body (HLB) is an evolutionarily conserved nuclear body that regulates the transcription and proces

282 protein and the accumulation of SnoN in PML nuclear bodies, thus allowing SnoN to stabilize p53 and

283 mation within the chains and the presence of nuclear bodies to quantify the extent to which these mec

284 is responsible for BNRF1 localization to PML-nuclear bodies typically associated with host-antiviral

285 HIPK2 partially colocalized with AIRE in nuclear bodies upon cotransfection and in human mTECs in

286 ng (FRAP) assays revealed that the GFP-MuMx1 nuclear bodies upon photobleaching showed a slow partial

287 Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RAR

288 The appearance of small nuclear bodies was rapid, stable, and reversible upon th

289 These GFP-MuMx1 nuclear bodies were rapidly disassembled by exposing cel

290 SATB1 localized into promyelocytic leukemia nuclear bodies where enhanced SATB1 cleavage was detecte

291 RNF4, but RNF4 quickly follows PML into the nuclear bodies where it is responsible for ubiquitylatio

292 ia (PML) protein and is recruited to the PML nuclear bodies where it stabilizes p53, leading to prema

293 on of arsenic, PML immediately transits into nuclear bodies where it undergoes SUMO modification.

294 The nuclear bodies, which are structures that appear to be c

295 Sp100 is a prototypical protein of ND10/PML nuclear bodies, which colocalizes with Daxx and the prot

296 in the expression of promyelocytic leukemia nuclear bodies, which decreases GluA1 (also called Gria1

297 ligomerization promote the assembly of large nuclear bodies, which sequester SRSF7 transcripts at the

298 r U7 small nuclear RNP resides in a separate nuclear body, which we call the histone locus body (HLB)

299 ntial architectural component of paraspeckle nuclear bodies, whose pathophysiological relevance remai

300 6AP expressed elevated levels of PML and PML-nuclear bodies with a concomitant increase in markers of