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1 sting that avrainvillamide targets cys275 of nucleophosmin.
2 chaperone phosphoproteins, nucleoplasmin and nucleophosmin.
3 bility of genes, such as GAP43, p27(Kip) and nucleophosmin.
4 by somatic mutations in NPM1, which encodes nucleophosmin.
5 of phenotypes observed in the absence of B23/nucleophosmin.
6 a subnucleolar compartment that contains B23/nucleophosmin.
10 ding to aberrant cytoplasmic localization of Nucleophosmin 1 (NPM1) have been recently identified as
13 bset analyses revealed that AML with mutated Nucleophosmin 1 (NPM1) may particularly benefit from VPA
14 of mutant level, size, and interaction with nucleophosmin 1 (NPM1) mutations remains controversial.
15 scribe how peptides derived from the mutated nucleophosmin 1 gene (NPM1(mut)) can elicit in vitro CD4
19 in were increased, nm23/H1, peroxiredoxin 2, nucleophosmin 1/B23, and inorganic pyrophosphatase were
21 nditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells
22 and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly v
23 cilitates chromatin transcription (FACT) and nucleophosmin-1 (previously implicated in transcriptiona
25 terogeneous nuclear ribonucleoprotein F, and nucleophosmin-1) as major proteins exposed after injury.
26 ation factor 2, protein disulfide isomerase, nucleophosmin-1, chaperonin, actin, protein tyrosine pho
27 involved in subnuclear architecture, notably nucleophosmin, a 38-kDa nucleolar phosphoprotein that is
28 induced a decrease in the phosphorylation of nucleophosmin, a major nuclear phosphoprotein, and that
31 eosarcoma cells, nucleostemin interacts with nucleophosmin, a nucleolar protein believed to possess o
32 tive effects, binds to the nuclear chaperone nucleophosmin, a proposed oncogenic protein that is over
33 e the anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most commo
34 astic lymphoma kinase (ALK) fusion proteins (nucleophosmin-ALK [NPM-ALK] and other variants) are expr
35 utes a part of the oncogenic fusion proteins nucleophosmin-ALK and echinoderm microtubule-associated
39 irst discovered as the constitutively active nucleophosmin-ALK oncoprotein in anaplastic large cell l
41 suggest that the mTOR pathway contributes to nucleophosmin-ALK/PI3K/AKT-mediated tumorigenesis and th
42 tion t(2;5) and the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are d
43 of the constitutively active tyrosine kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expre
46 s in the production of the nucleolar protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) prote
47 nduces the formation of the chimeric protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), whic
55 ormation mediated by the oncogenic, chimeric nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) tyros
56 NPM1c, result in cytoplasmic dislocation of nucleophosmin and are associated with distinctive transc
57 t CTCF copurifies with the nucleolar protein nucleophosmin and both are present at insulator sites in
60 EXIM1 interacts with two key p53 regulators, nucleophosmin and human double minute-2 protein (HDM2),
61 ic ligands binding to cell surface nucleolin/nucleophosmin and known as HB 19 for the lead compound a
62 hen evaluated whether nucleolar proteins B23/nucleophosmin and nucleolin, previously shown to interac
64 emonstrate that GRK5 phosphorylates Ser-4 in nucleophosmin and regulates the sensitivity of cells to
65 ian cells; within nucleoli it interacts with nucleophosmin and rRNA through N-terminal Lys residues,
67 athway involving AKT, ROCK and CDK2/Cyclin E-nucleophosmin) and in mouse tissues, and increased in vi
68 action of ARF with the nucleolar protein B23(nucleophosmin) and promotes a transient p53-independent
69 ive and stain positively with nucleolar (B23/nucleophosmin) and stem/progenitor cell markers (SPRR1A
73 of protamine-DNA complexes: NAP-1, NLP, and nucleophosmin are previously characterized histone chape
76 such as heat shock proteins, prohibitin, or nucleophosmin, as well as to the up-regulation of NF-kap
78 two-dimensional gels showed that the form of nucleophosmin B23 that is up-regulated in melanoma repre
79 r, hepatoma-derived growth factor (HDGF) and nucleophosmin B23 were strongly correlated with melanoma
84 nucleolar and ribosomal proteins, including nucleophosmin/B23 (NPM), a protein thought to foster the
85 tants that do not efficiently associate with nucleophosmin/B23 are unstable and functionally impaired
90 nd the hepatocellular carcinoma autoantigen, nucleophosmin/B23, as a model system to define the uniqu
94 ffinity-isolation of a protein identified as nucleophosmin by MS sequencing and Western-blotting.
95 f the three cysteine residues of a truncated nucleophosmin coexpressed with native nucleophosmin in C
97 are basic functions with, the nucleoplasmin/ nucleophosmin family of molecular chaperone proteins.
99 e tyrosine kinase 3 gene (Flt3(ITD)) and the nucleophosmin gene (Npm1(c)) to induce AML in vivo, and
103 causing aberrant cytoplasmic localization of nucleophosmin have been demonstrated to be the most freq
104 idic, synthetic small molecules that bind to nucleophosmin have not been described, prior to this rep
105 ations, and that siRNA-promoted depletion of nucleophosmin in a population of HeLa S3 cells leads to
106 the similarity of Npm3 to nucleoplasmin and nucleophosmin in amino acid sequence, protein features,
107 ncated nucleophosmin coexpressed with native nucleophosmin in COS-7 cells revealed that the mutation
108 udy, we examined the underlying mechanism of nucleophosmin induction and showed that hyperproliferati
117 echanistic link between TSC1/mTOR signaling, nucleophosmin-mediated nuclear export of ribosome subuni
119 However, the oncogenic potential of this nucleophosmin mutant (NPMc+) has never been established,
121 FLT3 internal tandem duplication (ITD) and nucleophosmin mutations occurred at a similar frequency
122 y, involving interferon regulatory factor-1, nucleophosmin, NFkappaB, and CRE binding in cell surviva
128 anslocation that forms a fusion gene between nucleophosmin (NPM) and MDS/myeloid leukemia factor 1 (M
130 eport the purification and identification of nucleophosmin (NPM) and nucleolin as two genotoxic stres
131 s the center of ribosome synthesis, with the nucleophosmin (NPM) and p19(ARF) proteins antagonizing o
133 yelocytic leukemia (APL) fuses the genes for nucleophosmin (NPM) and the retinoic acid receptor alpha
134 ion of anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM) and the subsequent expression of the
137 le in p53-null cells by hyperphosphorylating nucleophosmin (NPM) at Thr199, as evidenced by observati
139 stic lymphoma kinase (ALK) gene fuses to the nucleophosmin (NPM) gene as a result of a (2;5) transloc
140 in the fusion of the ubiquitously expressed nucleophosmin (NPM) gene at 5q35 to the anaplastic lymph
141 35) chromosomal translocation that fuses the nucleophosmin (NPM) gene on chromosome 5q35 to a novel p
142 rming capability when truncated and fused to nucleophosmin (NPM) in the t(2;5) chromosomal rearrangem
147 inal portion of the nucleolar phosphoprotein nucleophosmin (NPM) joined to the entire cytoplasmic por
148 cid residues of the nucleolar phosphoprotein nucleophosmin (NPM) joined to the entire cytoplasmic por
149 ogenesis through increased expression of the nucleophosmin (NPM) nuclear-cytoplasmic shuttling protei
150 consensus sequence were abolished, with the nucleophosmin (NPM) reporter gene and used them for in v
152 es the gene for the nucleolar phosphoprotein nucleophosmin (NPM) to the retinoic acid receptor alpha
159 PKR-modulating proteins we report here that nucleophosmin (NPM), a protein frequently overexpressed
163 the most frequently mutated genes in AML is nucleophosmin (NPM), and this is associated with low CD3
164 F inhibited the interaction between DDX5 and nucleophosmin (NPM), preventing association of DDX5 with
165 ed here indicate that the nucleolar protein, nucleophosmin (NPM), redistributes from the nucleolus fo
166 nalysis of CXCR4 immune complexes identified nucleophosmin (NPM), which was confirmed by reciprocal c
167 ptase polymerase chain reaction (RT-PCR) for Nucleophosmin (NPM)-ALK during treatment identifies pati
170 ylation is accurately recapitulated in a new nucleophosmin (NPM)-ALK transgenic mouse model of lympho
171 human cell lines, primary human tumours and nucleophosmin (NPM)-ALK-induced murine tumours demonstra
178 In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant f
179 hat T-cell lymphoma (TCL) cells carrying the nucleophosmin (NPM)/ALK fusion protein (ALK+ TCL) strong
180 sformation caused by the oncogenic, chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) rem
181 nisms of cell transformation mediated by the nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) tyr
183 e describe a nuclear PI(3,4,5)P(3) receptor, nucleophosmin (NPM)/B23, that mediates the antiapoptotic
184 ns of p19(Arf) with Mdm2, or separately with nucleophosmin (NPM, B23) that localizes and stabilizes p
185 ain of the multifunctional nucleolar protein nucleophosmin (Npm-N) are central to its function, with
189 yclin E triggers centrosome duplication, and nucleophosmin (NPM/B23) is found to be one of its target
191 leus as a physical and functional partner of nucleophosmin (NPM/B23), a major nucleolar phosphoprotei
193 of p53-independent ARF targets, we isolated nucleophosmin (NPM/B23), a protein we show is required f
194 omal biogenesis through its interaction with nucleophosmin (NPM/B23), RNA helicase DDX5 and RNA polym
195 f many cellular proteins, including Mdm2 and nucleophosmin (NPM/B23), with which p19(Arf) physically
196 inal portion of the nucleolar phosphoprotein nucleophosmin(NPM) joined to the entire cytoplasmic port
197 or fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%)
198 Furthermore, the nucleolar phosphoprotein nucleophosmin (NPM1) acts as a scaffold for PIDD and is
199 ts were the same in all 3 cases, between the nucleophosmin (NPM1) and fms-related tyrosine kinase 4 (
200 5 is able to interact with and phosphorylate nucleophosmin (NPM1) both in vitro and in intact cells.
208 olyadenylation, the multi-functional protein nucleophosmin (NPM1) is deposited onto all cellular mRNA
210 ed in CN-AML patients harboring mutations in nucleophosmin (NPM1) that are associated with favorable
213 arker (e.g., a mutation in the gene encoding nucleophosmin [NPM1]) could improve prognostication by i
214 eading to aberrant cytoplasmic expression of nucleophosmin (NPMc(+)) are the most frequent genetic le
216 AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) accounts for about one-third o
218 ia gene, promyelocytic leukemia zinc finger, nucleophosmin, nuclear matrix protein, and signal transd
220 nactive, unphosphorylated CPC interacts with nucleophosmin/nucleoplasmin proteins, which are known to
223 rotein-protein interaction and verified that nucleophosmin only bound to activated conformationally a
225 some inhibition, siRNA-mediated knockdown of nucleophosmin potentiated nucleolar accumulation and inc
230 ajor upstream inhibitor of mTOR, resulted in nucleophosmin protein induction through increased transl
231 ation and proximity assays confirmed the Bax-nucleophosmin protein-protein interaction and verified t
233 , we demonstrate that overexpression of NPM (nucleophosmin) significantly suppresses 12-O-tetradecano
235 ence of p53, ARF can be stabilized by NS and nucleophosmin to serve as an alternative tumor-suppresso
236 ecognized including topoisomerases I and II, nucleophosmin, Translin, EGR1, dek, pim-1, TFG, and MLL.
237 ell-based apoptosis model, demonstrated that nucleophosmin translocation from nucleolus to cytosol pr
238 cellular fractionation studies verified that nucleophosmin translocation occurred within 3 h, at a ti
241 etion of SENP3 and SENP5 or depletion of B23/nucleophosmin, we observed accumulation of SUMO proteins
242 ied including FMS-like tyrosine kinase-3 and nucleophosmin, which will enhance our ability to more ac
243 ransport of tumor suppressors (e.g., p53 and nucleophosmin) whose function is altered in cancer becau
244 n that juxtaposes the dimerization domain of nucleophosmin with anaplastic lymphoma kinase (ALK).
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