ライフサイエンスコーパス: nuclear body

1 toimmune antigen and is a constituent of the nuclear body.

2 its featured subcellular structure, the PML nuclear body.

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

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

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

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

7 associate with promyelocytic leukemia (PML) nuclear bodies.

8 assemble, maintain, and regulate particular nuclear bodies.

9 xtaposed with promyelocytic leukemia protein nuclear bodies.

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

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

12 oplasm to subnuclear foci called phytochrome nuclear bodies.

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

14 Maf localization into promyelocytic leukemia nuclear bodies.

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

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

17 and compartments, collectively described as nuclear bodies.

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

19 ic nuclear fission with reduced formation of nuclear bodies.

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

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

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

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

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

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

26 labeling appeared to colocalize with the PML nuclear bodies.

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

28 with Nbs1 or promyelocytic leukemia protein nuclear bodies.

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

30 1, was able to target YFP to the nucleus and nuclear bodies.

31 of SOP-2 partially restores localization to nuclear bodies.

32 ociation with promyelocytic leukemia protein nuclear bodies.

33 ND10 or promyelocytic leukemia protein (PML) nuclear bodies.

34 from the cytoplasm to promyelocytic leukemia nuclear bodies.

35 main and localizes in promyelocytic leukemia nuclear bodies.

36 associate with promyelocytic leukemia (PML) nuclear bodies.

37 r) causes the accumulation of E7 in discrete nuclear bodies.

38 -cell differentiation and retained LIN-11 in nuclear bodies.

39 g ABI5 for ubiquitin-mediated degradation in nuclear bodies.

40 ting it to multiprotein complexes termed PML-nuclear bodies.

41 by recruiting it to nuclear foci termed PML nuclear bodies.

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

43 and phytochromes colocalize and interact in nuclear bodies.

44 localizes to promyelocytic leukemia-adjacent nuclear bodies.

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

46 so disorganizes promyelocytic leukemia (PML) nuclear bodies.

47 ounteract RNF4 to inhibit the dissolution of nuclear bodies.

48 distribution of the chromatin into apoptotic nuclear bodies.

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

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

51 d chromatin does not localize into apoptotic nuclear bodies.

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

53 d their localizations using markers of known nuclear bodies.

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

55 and provide key information for research on nuclear bodies.

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

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

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

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

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

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

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

63 SP100 is localized to nuclear bodies and ETS1 expression alters the nuclear bo

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

65 ucleolus-associated structures, nucleoplasm, nuclear bodies and extra-nuclear-is provided.

66 ntial for its localization to characteristic nuclear bodies and for its in vivo function in the repre

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

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

69 214, although mostly cytoplasmic, also forms nuclear bodies and inhibits nuclear protein but not poly

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

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

72 itiation whereas in the nucleus, eIF4E forms nuclear bodies and promotes the nucleo-cytoplasmic expor

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

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

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

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

77 erferon increases the size and number of PML nuclear bodies and stimulates transcription of several g

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

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

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

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

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

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

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

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

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

87 BNA3CDelta343-545 colocalized with SUMO-1 in nuclear bodies and was modified by SUMO-2, SUMO-3, and S

88 5K-induced p53 sumoylation, tethering in PML nuclear bodies, and E1B-55K inhibition of p53 activity.

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

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

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

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

93 modification of LEF-1, sequestering it into nuclear bodies, and SUMO-1 ligation to c-Myb, modulating

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

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

96 These nuclear bodies are detergent insoluble and contain polyu

97 Nuclear bodies are discrete suborganelle structures that

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

99 Nuclear bodies are dynamic structures that form at sites

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

101 PML nuclear bodies are implicated in transcriptional regulat

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

103 Nuclear bodies are protein- and RNA-containing structure

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 cytic leukaemia (APL) accumulates in the PML nuclear body, but cytoplasmic PML isoforms of unknown fu

123 14 (RBM14), all reported to be components of nuclear bodies called paraspeckles.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 We suggest that E7 relocates to specific nuclear bodies for proteolysis in HPV-containing epithel

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

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

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

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

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

150 rans-retinoic acid, or IFN-gamma induced PML-nuclear body formation.

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

152 to a specific type of promyelocytic leukemia nuclear body found in immortalized cells that maintain t

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

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

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

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

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

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

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

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

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

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

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

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

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

166 of SOP-2 is required for its localization to nuclear bodies in vivo and for its physiological repress

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

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

169 Nuclear bodies including nucleoli, Cajal bodies, nuclear

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

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

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

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

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

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

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

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

178 The function of these nuclear bodies is unknown.

179 The promyelocytic leukemia protein (PML)-nuclear body is a cellular structure that is disrupted d

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

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

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

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

184 were also required for EBNA3C sumolation and nuclear body localization but were dispensable for coact

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 uclear bodies and ETS1 expression alters the nuclear body morphology in living cells.

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

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

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

192 -life by inhibiting its degradation in a PML-nuclear body (NB)-dependent manner.

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

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

195 of the promyelocytic leukemia protein (PML) nuclear bodies (NBs) and interacts with a number of tran

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

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

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

199 Nuclear bodies (NBs) are structures that concentrate pro

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

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

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

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

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

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

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

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

208 crete speckled nuclear structures termed PML nuclear bodies (NBs).

209 cription of p53 targets by recruiting p53 to nuclear bodies (NBs).

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

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

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

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

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

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

216 sociation kinetics are unaltered in residual nuclear bodies of coilin knockout cells.

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

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

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

220 ctures known as PML (promyelocytic leukemia) nuclear bodies or ND10, while the immediate-early (IE) p

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

222 Promyelocytic leukemia protein (PML) nuclear bodies or nuclear domain 10s (ND10s) are multipr

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

224 tant of Arabidopsis with altered phytochrome nuclear body patterns.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 es a multiprotein nuclear structure, the PML-nuclear body (PML-NB), whose proper formation and functi

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

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

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

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

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

255 rr virus (EBV) replication and Sp110b, a PML nuclear body protein, was investigated.

256 Moreover, some PML nuclear body proteins colocalize at sites of viral DNA s

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

258 transcription of several genes encoding PML nuclear body proteins.

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

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

261 Large nuclear bodies remained but with some concomitant reduct

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

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

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

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

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

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

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

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

272 ic leukemia (PML) protein is aggregated into nuclear bodies that are associated with diverse nuclear

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

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

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

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

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

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

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

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

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

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

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

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

285 these structures and that the absence of PML-nuclear bodies was a feature of N- and I-type, but not S

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

287 examine the composition and function of PML-nuclear bodies, we observed that the human neuroblastoma

288 PML-nuclear bodies were not detected in tissue sections prep

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

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

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

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

293 known chromatin regulator, HIRA, enters PML nuclear bodies, where it transiently colocalizes with HP

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

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

299 6AP expressed elevated levels of PML and PML-nuclear bodies with a concomitant increase in markers of

300 or for seedling deetiolation, colocalizes in nuclear bodies with CONSTITUTIVELY PHOTOMORPHOGENIC (COP