ライフサイエンスコーパス: PML

1 PML and PML NBs can also regulate mTOR and cell fate dec

2 PML is a tumour suppressor and regulator of cell differe

3 PML is frequently downregulated in many cancer types, in

4 PML NBs coordinate chromosomal regions via modification

5 PML nuclear bodies are druggable and could be harnessed

6 PML results when oligodendrocytes within immunocompromis

7 PML-NB constituent proteins mediate aspects of intrinsic

8 PML-RARalpha is recognized to be insufficient for develo

9 s with t(11q23)/MLL rearrangements, t(15;17)/PML-RARA, FLT3-ITD, and/or NPM1 mutations.

10 Our results showed that E1B-55K/PML binding is not required for p53, Mre11 and Daxx inte

11 f PML in HSV-1 replication, we constructed a PML(-/-) human cell line.

12 We performed mutational analysis to define a PML interaction motif within the E1B-55K polypeptide.

13 The t(15;17) translocation generates a PML-RARalpha fusion protein causative for acute promyelo

14 Here, we identify a PML ubiquitination pathway that is mediated by WD repeat

15 3A, but not DNMT3B, is required for aberrant PML-RARA-driven self-renewal ex vivo and that DNMT3A is

16 aches for treating lung cancer with aberrant PML degradation.

17 t's data are available until 12 months after PML diagnosis.

18 e that the PML retinoic acid receptor-alpha (PML-RARalpha) oncofusion protein, which causes acute pro

19 e arsenic-binding site of PML/RARA, but also PML, have been detected in therapy-resistant patients, d

20 Although PML silencing did reduce the sensitivity of U2OS cells t

21 eplicates equally well in parental HEp-2 and PML(-/-) cells infected at 5 pfu wild-type virus per cel

22 Stat1/2/3 and PML are IFNalpha downstream effectors and are pivotal re

23 Physical interaction between SIM362-364 and PML II is necessary but not sufficient for PML II degrad

24 Cellular bodies such as P bodies and PML nuclear bodies (PML NBs) appear to be phase-separate

25 ) with chronic mucocutaneous candidiasis and PML was reported previously.

26 y recognize two of its substrates, PML I and PML II.

27 ociated E1B-55K by SUMO-dependent PML-IV and PML-V interaction have so far remained elusive.

28 eristics of inflammatory NTZ-PML lesions and PML-IRIS to determine differentiating and overlapping fe

29 PML and PML NBs can also regulate mTOR and cell fate decisions i

30 ng SOX3, TNFAIP3, TRAFD1, POU3F3, STAT2, and PML that govern the expression of a large collection of

31 ub-networks regulated by TNFAIP3, TRAFD1 and PML are involved in innate immune response, suggesting t

32 Targeting the interaction of TRIB3 and PML-RARalpha using peptide technology provides a novel t

33 Annual PML risks (per 12 natalizumab infusions) for patients wi

34 suppressant use (n=18 616), estimated annual PML risks per 1000 patients, conditional on having no PM

35 by components of nuclear structures known as PML nuclear bodies (PML NBs), or ND10.

36 s that create oncogenic fusion genes such as PML-RARA, RUNX1-RUNX1T1, and MLL-AF9.

37 the nucleic acid component of ALT-associated PML bodies.

38 ng in patients with varying index-associated PML risks are also discussed.

39 erosis, who developed natalizumab-associated PML or GCN with regard to JC viral load and JCV-specific

40 I of 26 patients with natalizumab-associated PML presenting with lesions suggestive of PML-IRIS durin

41 mmon earliest sign of natalizumab-associated PML-IRIS with a frequent imaging pattern of contrast-enh

42 ive diagnosis of asymptomatic NTZ-associated PML (NTZ PML, 18 brain lesions) underwent 3-T MR imaging

43 n of inflammation (90% at diagnosis, 100% at PML-IRIS).

44 cifically induce HIRA/PML co-localization at PML nuclear bodies and HIRA recruitment to IFN target ge

45 We show that PIAS1 localizes at PML-NBs in a SUMO interaction motif (SIM)-dependent mann

46 diagnosis was similar to the pattern seen at PML-IRIS, with contrast enhancement representing the mos

47 ee water masses of the Central Arctic Basin (PML, intermediate Atlantic Water Layer, and the Arctic D

48 o revealed a significant correlation between PML and DDIT4 expression in several cancer types (e.g. l

49 The interplay between PML, Stat1/Stat2, and Stat3 contributes to IFNalpha-medi

50 However, physiological links between PML and oxidative stress response in vivo remain unexplo

51 Through NB biogenesis, PML therefore couples ROS sensing to p53 responses, shed

52 Instead, bipartite PML I binding domains located in the N-terminal half of

53 el to investigate their impact on full-blown PML-IRIS latency; (2) an analysis of variance ANOVA to i

54 their prophylactic use to prevent full-blown PML-IRIS seems to negatively impact on the longitudinal

55 ies such as P bodies and PML nuclear bodies (PML NBs) appear to be phase-separated liquids organized

56 n essential component of PML nuclear bodies (PML NBs) frequently lost in cancer.

57 with promyelocytic leukemia nuclear bodies (PML NBs), is a target of herpes simplex virus 1 (HSV-1)

58 lear structures known as PML nuclear bodies (PML NBs), or ND10.

59 ts of promyelocytic leukemia nuclear bodies (PML NBs, also known as ND10) have restrictive effects on

60 Promyelocytic leukemia nuclear bodies (PML-NB) are sub-nuclear organelles that are the hub of n

61 ated by promyelocytic leukemia nuclear body (PML-NB) constituent proteins.

62 , other promyelocytic leukemia nuclear body (PML-NB)/PML oncogenic domain (POD)-associated factors in

63 , and ICP0, a viral E3 ligase, degrades both PML and SP100.

64 sion, ICP0, a viral E3 ligase, degrades both PML and Sp100.

65 2 to 21 years with de novo APL confirmed by PML-RARalpha polymerase chain reaction were stratified a

66 ver, the recruitment of PIAS1 is enhanced by PML.

67 d sufficient to impair senescence induced by PML expression.

68 tes with restoration of tumor suppression by PML.

69 We aimed to calculate PML risk estimates from patient-level risk-factor data a

70 DMF appeared generally safe and no carryover PML among investigated cases was observed.

71 tment mechanisms of other well-characterized PML-NB proteins.

72 requires SUMOylated or SUMOylation-competent PML.

73 the restrictive effects of PML-NB components PML, Sp100, hDaxx, and ATRX while human cytomegalovirus

74 ntify the SUMO ligase PIAS1 as a constituent PML-NB antiviral protein.

75 of activated STAT1 (PIAS1) as a constituent PML-NB protein.

76 phenotypes of hematopoietic cells from Ctsg-PML-RARA mice, which express PML-RARA in early hematopoi

77 e patients in this pooled cohort, cumulative PML risk with or without previous immunosuppressant use

78 ve patients (n=21 696), estimated cumulative PML probability over 6 years (72 infusions of natalizuma

79 ate cancer tissue and shown that cytoplasmic PML and CRM1 co-expression correlates with reduced disea

80 ed model system for studies of JCV-dependent PML.

81 of PML-associated E1B-55K by SUMO-dependent PML-IV and PML-V interaction have so far remained elusiv

82 elapsing-remitting MS patients who developed PML under NTZ therapy (pre-PML) and non-PML NTZ-treated

83 ith MS according to their risk of developing PML during treatment with natalizumab and detect early s

84 - and 2-year treated time points, and during PML were analyzed for gene expression by RNA sequencing

85 a significantly higher EDSS increase during PML (0.09 EDSS points per month; p = 0.04) as compared t

86 study, we have examined the role of the E6AP-PML axis in prostate cancer (PC).

87 ubnuclear PML localization because of either PML-IV or PML-V-binding deficiency was no longer capable

88 reast tumours is accompanied by the elevated PML expression and enhanced sensitivity to its inhibitio

89 This study establishes PML as an important regulator of NF-kappaB and demonstra

90 body-negative patients (n=13 996), estimated PML risk was less than 0.07 per 1000 patients (95% CI 0.

91 whereas the accumulation of other evaluated PML-NB proteins occurs independently of PIAS1.

92 uced PML NB-like foci can fuse with existing PML NBs.

93 We used retroviral vectors to express PML-RARA, RUNX1-RUNX1T1, or MLL-AF9 in bone marrow cells

94 cells from Ctsg-PML-RARA mice, which express PML-RARA in early hematopoietic progenitors and myeloid

95 However, few PML NB-associated genes have been identified.

96 (iii) The ICP0 C terminus is dispensable for PML I degradation.

97 This suggested an essential role for PML in IFNalpha's anti-angiogenic function.

98 d PML II is necessary but not sufficient for PML II degradation.

99 Furthermore, PML promotes turnover of nuclear Stat3, and knockdown of

100 of 37 249 patients in the pooled cohort had PML.

101 l interferons (IFN) specifically induce HIRA/PML co-localization at PML nuclear bodies and HIRA recru

102 Here, we identify PML as a reactive oxygen species (ROS) sensor.

103 and specificity assessments for identifying PML cases in an index cohort.

104 stem by knocking down USP18 altered IFNalpha-PML axis-mediated inhibition of endothelial cell migrati

105 Here, we show that PML isoform II (PML-II) is specifically required for efficient induction

106 s significantly less affected by IFN-beta in PML(-/-) cells than in parental PML(+/+) cells, and (iii

107 at may mediate signaling events important in PML-NB-mediated intrinsic immunity.

108 iii) viral yields are significantly lower in PML(-/-) cells exposed to low ratios of virus per cell c

109 ells than in parental SP100(+/+) cells or in PML(-/-) cells.

110 pfu wild-type virus per cell, but poorly in PML(-/-) cells exposed to 0.1 pfu per cell.

111 Finally, ICP0 accumulation is reduced in PML(-/-) infected at low, but not high, multiplicities o

112 ften hijack the cellular factors resident in PML-NBs to promote their proliferation in host cells.

113 We report that in PML(-/-) cells, Sp100 degradation is delayed, possibly b

114 cess, the newly formed, viral-genome-induced PML NB-like foci can fuse with existing PML NBs.

115 of inflammation at diagnosis ('inflammatory PML'), reminiscent of PML-immune reconstitution inflamma

116 ear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is essential, while RA-triggered tr

117 Here, we investigated PML's role in the regulation of Stat1/2/3 activity.

118 n Pml(-/-) MEF transfected with mutant K487R PML, we observed that BMAL1 and PER2 co-localized with K

119 that BMAL1 and PER2 co-localized with K487R PML in the cytosol.

120 above 150 m depth in the polar mixed layer (PML) and halocline.

121 BDE concentrations in the Polar Mixed Layer (PML; a surface water mass) range from 0.3 to 11.2 pg.L(-

122 mic localization of promyelocytic leukaemia (PML) is mediated by its nuclear export in a chromosomal

123 ced disintegration of promonocytic leukemia (PML) nuclear bodies, an intracellular event critical to

124 Promyelocytic Leukemia (PML) is a nuclear protein that forms sub-nuclear structu

125 Promyelocytic leukemia (PML) is a pleiotropic tumor suppressor, but its role in

126 , with disruption of promyelocytic leukemia (PML) nuclear bodies (NBs) mediated by the PML-retinoic a

127 Promyelocytic leukemia (PML) nuclear bodies (NBs) recruit partner proteins, incl

128 Promyelocytic leukemia (PML) plays a tumor suppressive role by inducing cellular

129 The promyelocytic leukemia (PML) protein is an essential component of PML nuclear bo

130 r suppressor protein promyelocytic leukemia (PML).

131 progressive multifocal leukoencephalopathy (PML) and full-blown immune reconstitution inflammatory s

132 progressive multifocal leukoencephalopathy (PML) carry single amino acid substitutions in the domain

133 progressive multifocal leukoencephalopathy (PML) in multiple sclerosis (MS) patients treated with na

134 progressive multifocal leukoencephalopathy (PML) in patients with multiple sclerosis receiving natal

135 Progressive multifocal leukoencephalopathy (PML) is a debilitating disease resulting from infection

136 Progressive multifocal leukoencephalopathy (PML) is a fatal disease caused by reactivation of JC pol

137 Progressive multifocal leukoencephalopathy (PML) is a rare, severe, otherwise fatal viral infection

138 Progressive multifocal leukoencephalopathy (PML) is an often-fatal demyelinating disease of the cent

139 progressive multifocal leukoencephalopathy (PML) is caused by the infection of particular brain cell

140 progressive multifocal leukoencephalopathy (PML) is of crucial clinical relevance in terms of treatm

141 progressive multifocal leukoencephalopathy (PML) or granule cell neuronopathy (GCN).

142 progressive multifocal leukoencephalopathy (PML), and the occurrence of rebounds or disease activity

143 progressive multifocal leukoencephalopathy (PML).

144 progressive multifocal leukoencephalopathy (PML).

145 is computed from posterior mean liabilities (PML) under a liability threshold model; however, LT-Fam

146 ls to metabolic stress induced by metformin, PML loss did not inhibit the upregulation of DDIT4 in re

147 Moreover, PML targeting hampers breast cancer initiation and metas

148 Moreover, PMLs, once recruited, were highly activated in an MyD88-

149 tive in blocking viral replication in murine PML(+/+) cells than in sibling PML(-/-) cells, reproduce

150 Natural PML NBs and P bodies show analogous partitioning behavio

151 promyelocytic leukemia nuclear body (PML-NB)/PML oncogenic domain (POD)-associated factors including

152 per 1000 patients, conditional on having no PML before that year, ranged from 0.01 (0.00-0.03) in ye

153 oped PML under NTZ therapy (pre-PML) and non-PML NTZ-treated patients (NTZ-ctr) were included in the

154 facilitate the detection of asymptomatic NTZ PML.

155 First, the readers were asked to detect NTZ PML lesions without comparing current images with previo

156 icity of MR imaging for the detection of NTZ PML lesions (from 88% to 100%, P = .05).

157 osis of asymptomatic NTZ-associated PML (NTZ PML, 18 brain lesions) underwent 3-T MR imaging.

158 Second, they reassessed NTZ PML lesions with all the previous MR imaging data availa

159 association of MR imaging features with NTZ PML.

160 re exclusively observed in patients with NTZ PML.

161 Ten out of the 44 NTZ-PML patients included showed signs suggestive of inflamm

162 imaging characteristics of inflammatory NTZ-PML lesions and PML-IRIS to determine differentiating an

163 ation on brain MRI scans of inflammatory NTZ-PML patients.

164 gressive multifocal leukoencephalopathy (NTZ-PML) patients may show imaging signs suggestive of infla

165 al consequences and oncogenic alterations of PML-associated E1B-55K by SUMO-dependent PML-IV and PML-

166 The amounts of PML and SP100 and the number of ND10 structures increase

167 The amounts of PML and the number of ND10 structures increase in cells

168 The association of PML-NB proteins and HBV is being addressed in a number o

169 We identified 3 new unrelated cases of PML in patients with GOF STAT1 mutations, including the

170 No cases of PML were observed in EID group compared with 4 cases in

171 gate the earliest imaging characteristics of PML-IRIS manifestation in natalizumab-treated patients w

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

173 CP0 coordinate to promote the degradation of PML I.

174 e ICP0 C terminus enhance the degradation of PML II.

175 62 to 364 is required for the degradation of PML isoforms II, IV, and VI but not isoform I.

176 biomarker associated with the development of PML in MS patients treated with NTZ.

177 in ICP0 overcomes the restrictive effects of PML-NB components PML, Sp100, hDaxx, and ATRX while huma

178 STAT3 on Ser727, and increased expression of PML, a STAT3 transcriptional target.

179 AS inhibited the expression of PML, c-Myc, NFATc1, NFATc3, and NFATc4, while stimulatin

180 Brain biopsy revealed typical features of PML as well as JC virus-infected neurons.

181 To define more precisely the function of PML in HSV-1 replication, we constructed a PML(-/-) huma

182 concept that disruption of the functions of PML-NB proteins is important for efficient herpesvirus i

183 gh degradation or functional inactivation of PML NB proteins, which are recruited to viral genomes in

184 e stem cell gene SOX9 through interaction of PML with its promoter region.

185 Thus, (i) the interaction of PML with viral components facilitates the initiation of

186 turnover of nuclear Stat3, and knockdown of PML mitigates the effect of LLL12, a selective Stat3 inh

187 Knockdown of PML reduced NFATc1, NFATc2, NFATc3 and NFATc4 expression

188 ompositions could be controlled by levels of PML SUMOylation or cellular mRNA concentration, respecti

189 The occurrence of PML in 4 cases of STAT1 GOF suggests that STAT1 plays a

190 ics were followed up until the occurrence of PML-IRIS.

191 its ND10 fusion ability, affects the rate of PML I degradation.

192 ibutes to the fully efficient recruitment of PML, hDaxx, Sp100, and gammaH2AX to these sites.

193 required for fully efficient recruitment of PML, Sp100, hDaxx, and gammaH2AX to sites associated wit

194 agnosis ('inflammatory PML'), reminiscent of PML-immune reconstitution inflammatory syndrome (PML-IRI

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

196 ects a process that may diminish the risk of PML by counteracting the excess of immunosuppression tha

197 individualised annual prediction of risk of PML in patients receiving natalizumab for multiple scler

198 toring is ongoing to evaluate if the risk of PML is reduced in patients on EID.

199 emitting multiple sclerosis, at high risk of PML, were switched from NTZ to DMF and underwent neurolo

200 tant patients, demonstrating the key role of PML in APL cure.

201 1 and Stat3, indicating an important role of PML in regulating Stat1 and Stat3 activity.

202 sponses, shedding a new light on the role of PML in senescence or stem cell biology.

203 Mutations of the arsenic-binding site of PML/RARA, but also PML, have been detected in therapy-re

204 Studies of PML, however, have been hampered by the lack of an immor

205 ed PML presenting with lesions suggestive of PML-IRIS during follow-up.

206 s the most common imaging sign suggestive of PML-IRIS, seen in 92.3% of the patients (with patchy and

207 ugh mechanisms that are additive to those of PML and cooperative with those of PIAS4.

208 Patterns of inflammation at the time of PML diagnosis and at the PML-IRIS stage overlap but diff

209 art, for the transcriptional upregulation of PML in breast cancer.

210 nts with PML and to review the literature on PML in primary immune defects (PIDs).

211 PML localization because of either PML-IV or PML-V-binding deficiency was no longer capable of mediat

212 itin ligase that degrades the ND10 organizer PML and disperses ND10 to alleviate the repression.

213 Thus, similar to p53, PML exerts basal antioxidant properties but also drives

214 IFN-beta in PML(-/-) cells than in parental PML(+/+) cells, and (iii) viral yields are significantly

215 ios of virus per cell compared with parental PML(+/+) cells.

216 ssed genes in the RNA sequencing between pre-PML and NTZ-ctr patients, pathway analysis revealed a hi

217 lloproteinase 9 (MMP9) was validated; in pre-PML patients, MMP9 protein levels were significantly red

218 eening cohort and a validation cohort of pre-PML and NTZ-ctr patients.

219 nts who developed PML under NTZ therapy (pre-PML) and non-PML NTZ-treated patients (NTZ-ctr) were inc

220 it upregulates the tumor suppressor protein PML.

221 omyelocytic leukemia bodies, and the protein PML-II play a role in nuclear LD formation, suggesting f

222 r-suppressor promyelocytic leukemia protein (PML) for proteasomal degradation.

223 ciation with promyelocytic leukemia protein (PML) in response to DNA damage were also dependent on c-

224 stant [e.g., promyelocytic leukemia protein (PML), SP100, death domain-associated protein (Daxx)] and

225 stant [e.g., promyelocytic leukemia protein (PML), Sp100, death-domain associated protein (Daxx), and

226 uid sample of a 73-year-old woman with rapid PML onset, 3 distinct JCPyV populations could be identif

227 -JC antibodies had similar levels of reduced PML risk to those who were anti-JC negative (OR = 1.55,

228 e of infusions with a hypothesis of reducing PML risk.

229 In our review of the literature regarding PML in primary immune deficiencies we found 26 cases, on

230 as an oncoprotein that negatively regulates PML via ubiquitination to promote lung cancer progressio

231 ion in murine PML(+/+) cells than in sibling PML(-/-) cells, reproduced here with human cells, sugges

232 dex testing and MRI monitoring into standard PML safety protocols, in order to allow some JCV positiv

233 lso observed that E1B-55K lacking subnuclear PML localization because of either PML-IV or PML-V-bindi

234 ferentially recognize two of its substrates, PML I and PML II.

235 with natalizumab and detect early suspected PML using MRI including a diffusion-weighted imaging seq

236 immune reconstitution inflammatory syndrome (PML-IRIS).

237 immune reconstitution inflammatory syndrome (PML-IRIS).

238 ytomegalovirus (HCMV) IE protein IE1 targets PML and Sp100, and its tegument protein pp71 targets hDa

239 We now demonstrate that PML depletion in U2OS cells or TERT-immortalized normal

240 We demonstrate that PML promotes TNFalpha-induced transcriptional responses

241 mary endothelial cells, we demonstrated that PML positively regulates Stat1 and Stat2 isgylation, a u

242 We also demonstrated that PML shared a large cohort of regulatory genes with Stat1

243 regulator of NF-kappaB and demonstrates that PML-RARalpha dysregulates NF-kappaB.

244 ute promyelocytic leukemia, we proposed that PML oxidation promotes NB biogenesis.

245 DNA and RNA immuno-FISH reveal that PML NBs are closely associated with actively transcribed

246 Here we show that PML is a novel target in aggressive breast cancer.

247 Here, we show that PML isoform II (PML-II) is specifically required for eff

248 Earlier studies have shown that PML has three key functions.

249 Together, our studies suggest that PML mediates the binding of PER2 to BMAL1 in the BMAL1/C

250 Together, these findings suggest that PML-RARA requires DNMT3A to initiate APL in mice.

251 roduced here with human cells, suggests that PML acts as an effector of antiviral effects of IFN-beta

252 tion at the time of PML diagnosis and at the PML-IRIS stage overlap but differ in their severity of i

253 Furthermore, both the PML-RARA-driven competitive transplantation advantage an

254 a (PML) nuclear bodies (NBs) mediated by the PML-retinoic acid receptor alpha (RARalpha) oncoprotein.

255 t miR-181a/b expression was activated by the PML/RARalpha oncogene in cells and transgenic knock-in m

256 be essential for the exit of Sp110 from the PML-NB during HBV infection and HBx recruitment on the p

257 goes a deSUMOylation-driven release from the PML-NB in the presence of HBV.

258 evade host immune response by hijacking the PML-NB protein Sp110, and therefore, we propose it to be

259 pg/L) of measured PFOA concentrations in the PML (mean 32 +/- 15 pg/L).

260 p to 1 order of magnitude higher than in the PML.

261 vascular distribution pattern outside of the PML lesion were observed in 33.3% of the patients.

262 as contrast enhancement in the border of the PML lesion with either a patchy or punctuate appearance

263 or punctuate appearance in the border of the PML lesion.

264 l known that certain other components of the PML NB complex play an important role during an intrinsi

265 We also demonstrate that the PML retinoic acid receptor-alpha (PML-RARalpha) oncofusi

266 Here, we report that the PML-NB protein Speckled 110 kDa (Sp110) is SUMO1-modifie

267 ema (10%) at diagnosis, as compared with the PML-IRIS stage (40%).

268 with a more individualised analysis of their PML risk.

269 Clinically, this PML degradation pathway is hyperactivated in lung cancer

270 ifferentially regulates NFAT pathway through PML and p53 and reveal an intricate reciprocal regulator

271 Treatment with PLEX was not associated to PML-IRIS latency (hazard ratio [HR] = 1.05; p = 0.92), b

272 In contrast to PML(-/-) cells, SP100(-/-) cells retain the sensitivity

273 ace is responsible for BNRF1 localization to PML-nuclear bodies typically associated with host-antivi

274 with naked plasmid DNA, HIRA re-localizes to PML bodies, sites of cellular anti-viral activity.

275 rs of DNA methylation reversed resistance to PML-induced senescence.

276 ated the mechanisms underlying resistance to PML-induced senescence.

277 TNFalpha-treated PML(-/-) cells show normal IkappaBalpha degradation and

278 where successful targeting of the underlying PML-RARalpha oncoprotein has eliminated the need for che

279 s fail to engage in complete senescence upon PML activation.

280 counteract the inhibitory effects of various PML NB components.

281 enetically engineered mouse models, the WDR4/PML axis elevates intratumoral Tregs and M2-like macroph

282 The WDR4/PML axis induces a set of cell-surface or secreted facto

283 Pml(-/-) cells accumulate ROS, whereas PML expression decreases ROS levels.

284 It remains to be established whether PML pathogenesis is driven by one or several neurotropic

285 findings uncover a novel mechanism by which PML loss may contribute to mTOR activation and cancer pr

286 ucidated an unappreciated mechanism in which PML, an IFNalpha-inducible effector, possess potent angi

287 /-) MEF, CLOCK was primarily cytosolic while PML and PER2 were nuclear.

288 Because MORC3 associates with PML NBs in uninfected cells and is a target for HSV-1-me

289 herapeutically exploited in combination with PML-based stratification.

290 One patient with PML had a single neurotropic strain with rearranged NCCR

291 tify the molecular defect in 3 patients with PML and to review the literature on PML in primary immun

292 adiological data of 42 Italian patients with PML were analyzed.

293 neurotropic JCPyV strains of 3 patients with PML without the bias caused by assembly of short sequenc

294 STAT1 was sequenced in 3 patients with PML.

295 in the cerebrospinal fluid of patients with PML.

296 d by interaction of the ICP0 N-terminus with PML.

297 oup included 40 patients with MS but without PML who were treated with NTZ.

298 ues, separately for patients with or without PML.

299 natalizumab infusions) for patients without PML in the preceding year were estimated using condition

300 In the presence of WT PML, PER2 co-localized with BMAL1 in the nucleus.