ライフサイエンスコーパス: NPM

1 NPM and AurA coimmunoprecipitate and colocalize to centr

2 NPM enhances the expression of p53 target gene p21 and b

3 NPM induces phosphorylation of AurA on serine 89, and th

4 NPM is a potential cotarget in combination with other th

5 NPM is an endogenous inhibitor of HDM2:p53 interaction a

6 NPM is translationally responsive to hyperactive mammali

7 NPM knockdown reduces heat-induced inhibition of DNA DSB

8 NPM mRNA destabilization involves the association of HuR

9 NPM-ALK acts through STAT3, a transcription factor that

10 NPM-ALK co-opts several intracellular signal transductio

11 NPM-ALK induces ICOS expression via STAT3, which trigger

12 NPM-ALK is a chimeric tyrosine kinase, which induces num

13 NPM-ALK L182M, L182V, and L256M mutants displayed kinase

14 NPM-ALK-deregulated kinase activity drives several pathw

15 NPM-Bax complex formation is a novel target for preventi

16 NPM/ALK induces CD274 expression by activating its key s

17 NPM/ALK induces HIF1alpha expression by upregulating its

18 NPM/B23 phosphorylated by CDK2-cyclin E acquires a high

19 te catalyst, [Ru(II)(NPM)(4-pic)2(H2O)](2+) (NPM = 4-t-butyl-2,6-di(1',8'-naphthyrid-2'-yl)pyridine,

20 poptosis inhibition (CASP-9, CASP-7, DFF-45, NPM, YWHAZ, Src, PAX2, MAPK8), cell cycle promotion and

21 ndence by ectopic expression of an activated NPM-ALK fusion oncoprotein.

22 mitochondrial translocation and activation, NPM helps human HCC cells evade death induction independ

23 th previously characterized AurA activators, NPM does not trigger autophosphorylation of AurA on thre

24 In addition, NPM is necessary for the ability of c-Myc to induce rRNA

25 In addition, NPM-ALK uses epigenetic silencing mechanisms to downregu

26 mphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most common.

27 cumulative incidence rates of developing an NPM after stage III melanoma were 1.2% (95% CI, 0.86% to

28 achieved substantial tumor regression in an NPM-ALK driven murine tumor xenograft model when dosed q

29 ways identified as affected by both IL-2 and NPM/ALK.

30 e compared samples of primary NPM-ALK(+) and NPM-ALK(-) ALCL to investigate the role of miR-150 downs

31 Targeting the interaction between FOXM1 and NPM by peptides or small molecules may represent a novel

32 confirmed the interaction between FOXM1 and NPM in cancer and immortal cells.

33 t understanding of the biology of IGF-IR and NPM-ALK and have significant therapeutic implications as

34 l functional interactions between IGF-IR and NPM-ALK.

35 The dynamic behavior of NS and NPM reveal that nucleolar disruption is an early event a

36 Rapid translocation of NS and NPM to the nucleoplasm and suppression of new preribosom

37 ed protein binding, including La, P54nrb and NPM.

38 uch as TEL/ABL, TEL/JAK2, TEL/PDGFbetaR, and NPM/ALK also elevate WRN.

39 the NPM-ALK is not active and sequestered as NPM-ALK/NPM1 heterodimers in the nucleus.

40 Nucleophosmin/B23 (NPM) is a pleiotropic nucleolar protein involved in a va

41 e growth inhibition and cytotoxicity of BaF3/NPM-ALK mutant cells induced by ALK inhibitors were cons

42 WT cells but not those inoculated with BaF3/NPM-ALK L256M cells.

43 he survival of the mice inoculated with BaF3/NPM-ALK WT cells but not those inoculated with BaF3/NPM-

44 indings are of clinical significance because NPM up-regulation and p53 mutations are usually found in

45 (CDK1, CDK2, CDK8, CHEK1, CHEK2, GSK-3 beta, NPM, PAK1, PP2C-alpha).

46 tation revealed a direct interaction between NPM and BAX in the cytoplasm.

47 our previous finding that ARF directly binds NPM, impeding its transit to the cytoplasm and arresting

48 cytosol, NPM-Bax complexes formed, and both NPM and Bax accumulated in mitochondria.

49 thylation is induced in malignant T cells by NPM-ALK.

50 e affected genes were modulated in common by NPM/ALK and IL-2.

51 elocalization of NPM-ALK to the cytoplasm by NPM genetic knockout or knockdown caused ERK1/2 (extrace

52 Phosphorylation of pS(9)-GSK3beta by NPM-ALK was mediated by the PI3K/AKT signaling pathway.

53 ene amplification and is further mediated by NPM-ALK through activation of PI3K/AKT and stabilization

54 Many genes and proteins modulated by NPM-ALK are also involved in evasion of antitumor immune

55 Suppression of NPM by NPM small interfering RNA leads to an increase of p53 le

56 novel actin signaling pathways regulated by NPM-ALK, a comprehensive phosphoproteome analysis of ALC

57 ch syndrome protein (WASp) were regulated by NPM-ALK.

58 tic option in cells that become resistant by NPM-ALK amplification.

59 beta-rearrangement, which is bypassed in CD4/NPM-ALK transgenic mice following Notch1 expression.

60 Cdk2 or Cdk4, we conclude that the Cdk2/Cdk4/NPM pathway is a major guardian of centrosome dysfunctio

61 Our data suggest that in cancer cells NPM interacts with FOXM1 and their interaction is requir

62 were consistent with inhibition of cellular NPM-ALK autophosphorylation.

63 Constitutive expression of the chimeric NPM/ALK fusion protein encoded by the t(2;5)(p32;q35) is

64 synthesis in the nucleolus, and constitutive NPM overexpression stimulates c-Myc-mediated rRNA synthe

65 nucleolar NPM translocated into the cytosol, NPM-Bax complexes formed, and both NPM and Bax accumulat

66 Thus, TAT-delivered NPM peptide may provide a novel therapy for inflammation

67 A Bax peptide that disrupts NPM-Bax interaction significantly reduced cell death cau

68 A subset of the proteins distinguished NPM/ALK-positive ALCLs from NPM/ALK-negative ALCLs and H

69 by the NPM/ALK fusion, we identified diverse NPM/ALK-induced changes affecting cell proliferation, ri

70 e value of Flt-3 internal tandem duplication/NPM-1 status, with inferior survival seen in patients wi

71 , in a clean cell system in which endogenous NPM had been removed by RNA interference.

72 roteins and formed complexes with endogenous NPM and p65 at promoters of several antiapoptotic and in

73 Also, we found that NS can enhance NPM stabilization of ARF.

74 e T198A mutant is fully capable of executing NPM's described roles in nucleocytoplasmic shuttling, ri

75 Endogenous and exogenous NPM directly interact with c-Myc and regulate the expres

76 nhibited in T-cell lymphoma cells expressing NPM-ALK kinase as a result of DNA methylation of the IL-

77 orylation of NPM-Thr198 is not essential for NPM's capacity to drive cell cycle progression and proli

78 estigate the cell's presumed requirement for NPM-Thr198 phosphorylation in promoting the processes of

79 se results demonstrate an essential role for NPM in c-Myc nucleolar localization and c-Myc-mediated r

80 urt-Munster-type protocols were screened for NPM-ALK transcripts at diagnosis; 103 were found to be M

81 ns distinguished NPM/ALK-positive ALCLs from NPM/ALK-negative ALCLs and Hodgkin lymphoma.

82 On the other hand, NPM-ALK L256M exhibited >30-fold lower sensitivity to bo

83 d to cytoplasm in cells with relatively high NPM level, or accumulated in the mitochondria in cells w

84 whereas nontransgenic littermates and hMRP8-NPM transgenic mice remained disease free.

85 milar wild-type NPM trans-genic model (hMRP8-NPM).

86 leukemia was found in hMPR8-NPMc(+) or hMRP8-NPM mice.

87 Remarkably, human NPM-ALK-amplified cell lines resistant to ALK tyrosine k

88 Previous studies have shown that the human NPM's phosphorylation by cyclin E-cyclin-dependent kinas

89 f the Ru-based single site catalyst, [Ru(II)(NPM)(4-pic)2(H2O)](2+) (NPM = 4-t-butyl-2,6-di(1',8'-nap

90 NPM ligand modification results in [Ru(III)(NPM-NO)(4-pic)2(H2O)](3+) and [Ru(III)(NPM-NO,NO)(4-pic)

91 (III)(NPM-NO)(4-pic)2(H2O)](3+) and [Ru(III)(NPM-NO,NO)(4-pic)2](3+) complexes.

92 Importantly, NPM-ALK is capable of transforming primary human CD4(+)

93 In NPM-ALK(+) cell lines, DNA hypermethylation-mediated miR

94 he MIR150 gene was substantially elevated in NPM-ALK(+) biopsies and correlated with reduced miR-150

95 letion of FBP1 caused a dramatic increase in NPM translation and resulted in enhanced overall cell pr

96 Early evaluation of MRD in NPM-ALK-positive ALCL identifies patients with a very hi

97 Thus, we demonstrate that the reduction in NPM protein expression blocks cellular growth and prolif

98 d with wild-type NPM/ALK and kinase-inactive NPM/ALK K210R mutant and by the inhibition of the NPM/AL

99 ld-type NPM/ALK, but not the kinase-inactive NPM/ALK K210R mutant or empty vector alone.

100 t a nucleus-restricted NPM mutant, increased NPM-Bax complex formation, mitochondrial NPM and Bax acc

101 on of HuR stabilizes the NPM mRNA, increases NPM protein levels and inhibits myogenesis, while its ov

102 PPAN depletion induces NPM and upstream-binding factor (UBF) degradation, which

103 we hypothesized that ARF might also inhibit NPM phosphorylation.

104 bic SN-38 was successfully encapsulated into NPM with significantly increased water solubility (up to

105 ar pathways, and provide novel insights into NPM/ALK-positive ALCL pathobiology.

106 monstrate that the oncogenic tyrosine kinase NPM-ALK induces epigenetic silencing of the IL-2Rgamma g

107 se nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressing anaplastic large cell lymphoma are n

108 ound that in ALK-rearranged ALCL cell lines, NPM-ALK was distributed in equal amounts between the cyt

109 he mitochondria in cells with relatively low NPM level and undergoing apoptosis.

110 ssue and used quantitative RT-PCR to measure NPM-ALK fusion transcript in bone marrow and blood sampl

111 A family of mesoporous nonprecious metal (NPM) catalysts for oxygen reduction reaction (ORR) in ac

112 ue class of photonic nanoporphyrin micelles (NPM), the extremely hydrophobic SN-38 was successfully e

113 sed NPM-Bax complex formation, mitochondrial NPM and Bax accumulation, mitochondrial membrane injury,

114 y and hydrophobicity of the nonpolar moiety (NPM) of the anions.

115 The multiple NPM/ALK-deregulated pathways identified by MS analysis a

116 ylation of the cdk2 target residue in murine NPM, Thr198.

117 In murine NPM-ALK(+) xenograft models, miR-150 upregulation induce

118 stable NPM knockdown were restored by mutant NPM-T198A expression.

119 compared with kinase-defective K210R mutant NPM-ALK, but did not affect total GSK3beta levels.

120 Transfection of wild-type or mutant NPM-ALK into 293T cells showed that only wild-type NPM-A

121 ion, in OCI/AML3 leukemia cells where mutant NPM is localized in the cytoplasm we found that typicall

122 pression of a cytosol-restricted NPM mutant (NPM-DeltaNLS), but not a nucleus-restricted NPM mutant,

123 Here we report the identification of a novel NPM-BCL2-associated X protein (BAX) pathway orchestratin

124 During stress, nucleolar NPM translocated into the cytosol, NPM-Bax complexes for

125 Nucleophosmin (NPM) (B23) is an essential protein in mouse development

126 Nucleophosmin (NPM), a multifunctional nucleolar phosphoprotein is dysr

127 Nucleophosmin (NPM), a predominantly nucleolar protein, is also critica

128 Nucleophosmin (NPM), an oligomeric phosphoprotein and nucleolar target

129 Nucleophosmin (NPM/B23) is a multifunctional oncoprotein whose protein

130 Nucleophosmin (NPM/B23) is one of the phosphorylation targets of CDK2-c

131 interaction between DDX5 and nucleophosmin (NPM), preventing association of DDX5 with the rDNA promo

132 es, primary human tumours and nucleophosmin (NPM)-ALK-induced murine tumours demonstrate the TPC freq

133 s centrosome duplication, and nucleophosmin (NPM/B23) is found to be one of its targets.

134 harbor the well-characterized nucleophosmin (NPM)-ALK fusion protein.

135 ed by the oncogenic, chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) remain only partia

136 1 and its downstream effector nucleophosmin (NPM) to rDNA.

137 e chain reaction (RT-PCR) for Nucleophosmin (NPM)-ALK during treatment identifies patients at the hig

138 cells by hyperphosphorylating nucleophosmin (NPM) at Thr199, as evidenced by observations that ablati

139 Recently, we identified nucleophosmin (NPM) as a key factor counteracting death stimuli in huma

140 ently mutated genes in AML is nucleophosmin (NPM), and this is associated with low CD34 expression.

141 Moreover, nucleophosmin (NPM) and c-Myc, both of which are commonly overexpressed

142 y, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ALK expr

143 cal and functional partner of nucleophosmin (NPM/B23), a major nucleolar phosphoprotein with diverse

144 on of the cell cycle promoter nucleophosmin (NPM).

145 of the anti-apoptotic protein nucleophosmin (NPM).

146 e that the nucleolar protein, nucleophosmin (NPM), redistributes from the nucleolus following hyperth

147 We hypothesized that nucleophosmin (NPM), a nucleolar phosphoprotein, is critical for Bax-me

148 homa (TCL) cells carrying the nucleophosmin (NPM)/ALK fusion protein (ALK+ TCL) strongly express hypo

149 ic lymphoma kinase (ALK) with nucleophosmin (NPM) and the subsequent expression of the NPM-ALK fusion

150 NS interacts with nucleophosmin (NPM), a marker of nucleolar stress with cytoprotective p

151 with Mdm2, or separately with nucleophosmin (NPM, B23) that localizes and stabilizes p19(Arf) within

152 through its interaction with nucleophosmin (NPM/B23), RNA helicase DDX5 and RNA polymerase I transcr

153 ues as a fusion protein with nucleophosphin (NPM) and other partners.

154 was performed in the presence or absence of NPM-ALK activity.

155 on the expression and enzymatic activity of NPM-ALK.

156 on the expression and enzymatic activity of NPM/ALK, as demonstrated by inhibition of the NPM/ALK fu

157 on the expression and enzymatic activity of NPM/ALK, as shown in BaF3 cells transfected with wild-ty

158 L2 was found to result in reduced binding of NPM to HDM2, with concomitant defects in p53 accumulatio

159 Coexpression of NPM-DeltaNLS with constitutively active Bax mutants caus

160 ed loss of cell adhesion as a consequence of NPM/ALK expression in a kinase-dependent manner, and sen

161 phoproteomic and metabolomic consequences of NPM-ALK expression and reveals a novel role of ALK in th

162 data were confirmed in vivo, as depletion of NPM by ribonucleic acid interference eliminated phosphor

163 ve studies evaluated the serial detection of NPM-ALK fusion transcripts in patients with ALCL.

164 nvestigate the role of miR-150 downstream of NPM-ALK.

165 r-expression of FOXM1 reversed the effect of NPM knockdown in vitro.

166 The results demonstrate the effect of NPM on p53 localization in mitochondria and apoptosis.

167 The suppressive effect of NPM on p53 mitochondrial localization is also observed i

168 t contributes to the lymphomagenic effect of NPM-ALK.

169 sis also predicted novel biologic effects of NPM/ALK expression.

170 r, these findings indicate that an excess of NPM-ALK activation and signaling induces apoptosis via o

171 Expression of NPM enhances p53 levels in the nucleus but reduces p53 l

172 Expression of NPM-ALK in 293T cells led to an increase of pS(9)-GSK3be

173 sor by reciprocally inhibiting expression of NPM-ALK.

174 Since a mutant form of NPM lacking the G(1) Cdk phosphorylation site (NPM(T199A

175 ediates the phosphorylation of a fraction of NPM at threonine 199, an event required for its proteaso

176 ng Western blotting and/or immunostaining of NPM/ALK-transfected cells and ALK-deregulated lymphomas.

177 ous studies focusing mainly on the impact of NPM/ALK on cell survival and proliferation.

178 Implantation of NPM-ALK-transformed CD4(+) T lymphocytes into immunodefi

179 multiple primaries had a higher incidence of NPM.

180 clinical studies indicate that inhibition of NPM-ALK induces long-lasting complete remissions in a la

181 Furthermore, knockdown of NPM in immortal and cancer cells led to significant down

182 umor cells with a high constitutive level of NPM results in p53 translocation to mitochondria and enh

183 Levels of NPM-ALK decreased during therapy in most patients with A

184 rt for the role of GSK3beta as a mediator of NPM-ALK oncogenesis.

185 entified GSK3beta as a signaling mediator of NPM-ALK.

186 Here, we demonstrate that overexpression of NPM (nucleophosmin) significantly suppresses 12-O-tetrad

187 nd proliferation, whereas phosphorylation of NPM-Thr198 is not essential for NPM's capacity to drive

188 an additional cell-transforming property of NPM/ALK and describe a direct link between an oncoprotei

189 entify a novel cell-transforming property of NPM/ALK, namely its ability to induce the expression of

190 th, and 1-year cumulative incidence rates of NPM after diagnosis of stage IV melanoma were 0.2% (95%

191 Reduction of NPM significantly reduces heat-induced radiosensitizatio

192 Clinically, up-regulation of NPM was significantly associated with advanced tumor sta

193 Overexpression or relocalization of NPM-ALK to the cytoplasm by NPM genetic knockout or knoc

194 FBP1 resulted in translational repression of NPM mRNAs, whereas depletion of FBP1 caused a dramatic i

195 kinase-dependent manner, and sensitivity of NPM/ALK-positive ALCLs to inhibition of the RAS, p42/44E

196 s kinase in the topological sequestration of NPM, linking p53 signaling to the generation of threonin

197 lar fractionation revealed that silencing of NPM expression greatly enhanced mitochondrial translocat

198 Silencing of NPM expression significantly sensitized HCC cells-partic

199 sensitization effect exerted by silencing of NPM in HCC cells.

200 Silencing of NPM significantly sensitized HCC cells to anticancer the

201 ta together show that NSC348884 is an SMI of NPM oligomer formation, upregulates p53, induces apoptos

202 on of STAT3, a major downstream substrate of NPM-ALK, in cooperation with DNA methyltransferase 1 (DN

203 Suppression of NPM by NPM small interfering RNA leads to an increase of

204 Furthermore, suppression of NPM in tumor cells with a high constitutive level of NPM

205 n cells comparable to or higher than that of NPM-ALK wild type (WT) and rendered BaF3 cells into IL-3

206 -derived ALK inhibitor comparable to that of NPM-ALK WT but were dramatically less sensitive to a dia

207 1) interacts specifically with the 3' UTR of NPM to repress translation.

208 The expression dependence on NPM/ALK and IL-2 of the five selected genes-CD25 (IL-2Ra

209 ue features, which are strictly dependent on NPM-ALK activity and expression, include perpetual cell

210 ;q35), which generates the chimeric oncogene NPM-ALK.

211 ents with stage IV melanoma had at least one NPM after diagnosis of stage III or IV disease.

212 stress, whereas expression of active Bax or NPM-DeltaNLS alone did not.

213 Knockdown of FOXM1 or NPM in MIA PaCa-2 pancreatic cancer cells inhibited anch

214 Overexpression of either NS or NPM significantly decreases caspase 8 activity in cultur

215 nd was concomitant with increases in overall NPM expression.

216 es of oncogenic c-Myc and that overexpressed NPM dramatically stimulates c-Myc-induced hyperprolifera

217 amined the effects of a non-phosphorylatable NPM mutant, T198A, in a clean cell system in which endog

218 e generation of threonine 199-phosphorylated NPM.

219 d for the translocation of de-phosphorylated NPM from the nucleolus to the nucleoplasm.

220 The Thr199-phosphorylated NPM/B23 physically interacts with and super-activates th

221 olar stress-response pathway involving PPAN, NPM, and BAX to guarantee cell survival in a p53-indepen

222 Rac1 single deletions, completely prevented NPM-ALK lymphoma dissemination in vivo.

223 Here, we compared samples of primary NPM-ALK(+) and NPM-ALK(-) ALCL to investigate the role o

224 We transplanted sorted fractions of primary NPM-mutated AML into immunodeficient mice to establish w

225 5; p23;q35) that produces the fusion protein NPM-ALK (nucleophosmin-anaplastic lymphoma kinase).

226 ncers interacts with multifunctional protein NPM, which is also overexpressed in a variety of human t

227 ported to the North Pacific margin province (NPM) by East Asian winter monsoon.

228 s rRNA synthesis through a PKCiota-Ect2-Rac1-NPM signaling axis that is required for lung tumorigenes

229 heat-induced radiosensitization, but reduced NPM level does not alter radiation sensitivity per se.

230 selectively bind the NPM 3' UTR and repress NPM translation.

231 Treatment of crizotinib-resistant NPM-ALK(+) KARPAS-299-CR06 cells with decitabine or ecto

232 With regard to inhibitor response, NPM-ALK L182M and L182V exhibited sensitivity to a fused

233 Expression of a cytosol-restricted NPM mutant (NPM-DeltaNLS), but not a nucleus-restricted

234 (NPM-DeltaNLS), but not a nucleus-restricted NPM mutant, increased NPM-Bax complex formation, mitocho

235 M lacking the G(1) Cdk phosphorylation site (NPM(T199A)) prevents centrosome amplification to the sam

236 N-38-encapsulated nanoporphyrin micelles (SN-NPM) enhanced the in vitro antitumor activity by 78 and

237 Due to the relatively small size, SN-NPM possessed superior long tumor retention time (>5days

238 l-, photodynamic- and chemo-therapy) with SN-NPM demonstrated dramatically enhanced in vivo antitumor

239 e proliferative defects observed with stable NPM knockdown were restored by mutant NPM-T198A expressi

240 degradation and maintenance of steady-state NPM levels.

241 Following cell stress, NPM and BAX were induced and exported out of the nucleol

242 another rationale to therapeutically target NPM/ALK and STAT3 in ALK+ TCL.

243 ditional rationale to therapeutically target NPM/ALK and STAT3 in ALK+TCL.

244 Our data demonstrate that NPM is a strong activator of AurA kinase activity at the

245 Our results demonstrate that NPM-ALK regulates the phosphorylation of S(9)-GSK3beta b

246 These results demonstrate that NPM-ALK, acting through STAT3 as the gene transcriptiona

247 Previously, we demonstrated that NPM directly interacts with c-Myc and controls c-Myc-ind

248 rase pull-down experiments demonstrated that NPM forms a complex with FOXM1 and also identified the r

249 It has been found that NPM/B23 phosphorylated on Thr199 by CDK2-cyclin E acquir

250 These findings indicate that NPM/ALK transforms the target CD4(+) T lymphocytes, at l

251 In the present study, we report that NPM is a strong activator of AurA kinase activity.

252 Here, we show that NPM is essential for the activities of oncogenic c-Myc a

253 Here, we show that NPM is necessary for the localization of c-Myc protein t

254 Here we show that NPM-ALK phosphorylates WASp at its known activation site

255 osphoproteomic and metabolomic strategy that NPM-ALK induces a metabolic shift toward aerobic glycoly

256 Also, these results suggest that NPM associates with nuclear matrix attachment region DNA

257 in stress-induced apoptosis and suggest that NPM may protect cells from apoptosis by reducing the mit

258 of FOXM1 from the cytoplasm, suggesting that NPM may also determine intracellular localization of FOX

259 its levels in normal cells, suggesting that NPM might modulate FOXM1 level.

260 The NPM/B23-binding results in superactivation of ROCK II, w

261 through its ability to selectively bind the NPM 3' UTR and repress NPM translation.

262 changes in protein expression caused by the NPM/ALK fusion, we identified diverse NPM/ALK-induced ch

263 port that T-cell lymphoma cells carrying the NPM-ALK fusion protein (ALK(+) TCL) frequently express t

264 species to the uncoordinated nitrogen of the NPM ligand.

265 that the 3' untranslated region (UTR) of the NPM messenger (m)RNA is sufficient to mediate its transl

266 ufficient for maintaining a low level of the NPM mRNA as well as promoting the commitment of muscle c

267 se a model whereby the downregulation of the NPM mRNA, mediated by HuR, KSRP and its associated ribon

268 Despite the importance of the NPM of the anions, neutral solutes were sorbed much less

269 n (NPM) and the subsequent expression of the NPM-ALK fusion protein.

270 Thus, about 50% of the NPM-ALK is not active and sequestered as NPM-ALK/NPM1 he

271 at the SP cells express higher levels of the NPM-ALK oncogene and are sensitive to an ALK inhibitor.

272 f IL-2Rgamma expression leads to loss of the NPM-ALK protein and, consequently, apoptotic cell death

273 aled that WASp is a central component of the NPM-ALK-dependent actin signaling pathway.

274 LK K210R mutant and by the inhibition of the NPM/ALK function in ALK+ TCL cells by a small-molecule A

275 PM/ALK, as demonstrated by inhibition of the NPM/ALK function in ALK+TCL cells by the small molecule

276 In few seconds, the NPM ligand modification results in [Ru(III)(NPM-NO)(4-pi

277 Depletion of HuR stabilizes the NPM mRNA, increases NPM protein levels and inhibits myog

278 These findings reveal that the NPM/ALK alteration affects diverse cellular pathways, an

279 Here we report that the NPM/ALK-carrying T cell lymphoma (ALK+TCL) cells strongl

280 -positive (ALK+) ALCL is associated with the NPM-ALK t(2;5) translocation, which is highly correlated

281 The unprecedented performance of these NPM catalysts in ORR was attributed to their well-define

282 Thus, NPM-Bax interaction enhances mitochondrial Bax accumulat

283 CD24 competitively inhibits ARF binding to NPM, resulting in decreased ARF, increase MDM2 and decre

284 Conversely, high transient NPM expression enhances c-Myc nucleolar localization, le

285 lly, TAT-NPMDeltaC associated with wild-type NPM proteins and formed complexes with endogenous NPM an

286 n parallel, we generated a similar wild-type NPM trans-genic model (hMRP8-NPM).

287 K into 293T cells showed that only wild-type NPM-ALK increased GLI1 protein levels and activated SHH/

288 own in BaF3 cells transfected with wild-type NPM/ALK and kinase-inactive NPM/ALK K210R mutant and by

289 ed BaF3 cells transfected with the wild-type NPM/ALK, but not the kinase-inactive NPM/ALK K210R mutan

290 A proposed [Ru(V)(NPM)(4-pic)2 horizontal lineO](3+) intermediate was not

291 g from doxorubicin treatment in CPC, whereas NPM knockdown alone induces cell death.

292 We examined whether NPM stimulates proliferation and transformation by affec

293 We, therefore, investigated whether NPM-mutated AMLs have LICs restricted to the CD34(+) fra

294 Mechanisms by which NPM-ALK signaling regulates cell migration, invasion and

295 o-localized with NPM in the cytoplasm, while NPM knockdown led to the disappearance of FOXM1 from the

296 F3 cells into IL-3-independent growth, while NPM-ALK L182R, L256R, L256V, L256P, and L256Q displayed

297 The reason why NPM-ALK succeeds in transforming specifically CD4(+) T l

298 ar FOXM1 was predominantly co-localized with NPM in the cytoplasm, while NPM knockdown led to the dis

299 on of normal human CD4(+) T lymphocytes with NPM-ALK results in their malignant transformation.

300 lood and/or bone marrow of 180 patients with NPM-ALK-positive ALCL treated with Berlin-Frankfurt-Muns