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1 of phenotypes observed in the absence of B23/nucleophosmin.
2 a subnucleolar compartment that contains B23/nucleophosmin.
3 sting that avrainvillamide targets cys275 of nucleophosmin.
4 chaperone phosphoproteins, nucleoplasmin and nucleophosmin.
5 bility of genes, such as GAP43, p27(Kip) and nucleophosmin.
6 by somatic mutations in NPM1, which encodes nucleophosmin.
8 ith the interaction of R-DPRs with nucleolar nucleophosmin 1 (NPM1) and underscore that R-DPRs intera
14 ding to aberrant cytoplasmic localization of Nucleophosmin 1 (NPM1) have been recently identified as
17 bset analyses revealed that AML with mutated Nucleophosmin 1 (NPM1) may particularly benefit from VPA
20 of mutant level, size, and interaction with nucleophosmin 1 (NPM1) mutations remains controversial.
22 onally up-regulated targets of U2AF1-S34F is Nucleophosmin 1 (NPM1), which is a major driver of myelo
23 targeting a "public" neoantigen derived from nucleophosmin 1 (NPM1), which is mutated in approximatel
27 olar localization, perturb nucleolar protein nucleophosmin 1 and suppress nascent protein synthesis.
28 scribe how peptides derived from the mutated nucleophosmin 1 gene (NPM1(mut)) can elicit in vitro CD4
32 e prognosis for relapsed or refractory (R/R) nucleophosmin 1-mutated (NPM1m) acute myeloid leukemia (
33 kemias, including KMT2A-rearranged (KMT2Ar), nucleophosmin 1-mutated (NPM1m), and NUP98-rearranged (N
35 in were increased, nm23/H1, peroxiredoxin 2, nucleophosmin 1/B23, and inorganic pyrophosphatase were
36 S-like tyrosine kinase receptor-3 (FLT3) and Nucleophosmin-1 (NPM1) are most frequent alterations in
38 nditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells
39 and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly v
40 cilitates chromatin transcription (FACT) and nucleophosmin-1 (previously implicated in transcriptiona
42 with clinical activity in AML patients with nucleophosmin-1 mutation (NPM1m) or lysine methyltransfe
43 terogeneous nuclear ribonucleoprotein F, and nucleophosmin-1) as major proteins exposed after injury.
44 ation factor 2, protein disulfide isomerase, nucleophosmin-1, chaperonin, actin, protein tyrosine pho
45 involved in subnuclear architecture, notably nucleophosmin, a 38-kDa nucleolar phosphoprotein that is
46 induced a decrease in the phosphorylation of nucleophosmin, a major nuclear phosphoprotein, and that
49 eosarcoma cells, nucleostemin interacts with nucleophosmin, a nucleolar protein believed to possess o
50 tive effects, binds to the nuclear chaperone nucleophosmin, a proposed oncogenic protein that is over
51 e the anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most commo
52 astic lymphoma kinase (ALK) fusion proteins (nucleophosmin-ALK [NPM-ALK] and other variants) are expr
53 utes a part of the oncogenic fusion proteins nucleophosmin-ALK and echinoderm microtubule-associated
57 irst discovered as the constitutively active nucleophosmin-ALK oncoprotein in anaplastic large cell l
59 suggest that the mTOR pathway contributes to nucleophosmin-ALK/PI3K/AKT-mediated tumorigenesis and th
60 tion t(2;5) and the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are d
61 of the constitutively active tyrosine kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expre
64 s in the production of the nucleolar protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) prote
65 nduces the formation of the chimeric protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), whic
74 ormation mediated by the oncogenic, chimeric nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) tyros
75 NPM1c, result in cytoplasmic dislocation of nucleophosmin and are associated with distinctive transc
76 t CTCF copurifies with the nucleolar protein nucleophosmin and both are present at insulator sites in
79 EXIM1 interacts with two key p53 regulators, nucleophosmin and human double minute-2 protein (HDM2),
80 ic ligands binding to cell surface nucleolin/nucleophosmin and known as HB 19 for the lead compound a
81 hen evaluated whether nucleolar proteins B23/nucleophosmin and nucleolin, previously shown to interac
83 emonstrate that GRK5 phosphorylates Ser-4 in nucleophosmin and regulates the sensitivity of cells to
84 ian cells; within nucleoli it interacts with nucleophosmin and rRNA through N-terminal Lys residues,
86 athway involving AKT, ROCK and CDK2/Cyclin E-nucleophosmin) and in mouse tissues, and increased in vi
87 action of ARF with the nucleolar protein B23(nucleophosmin) and promotes a transient p53-independent
88 ive and stain positively with nucleolar (B23/nucleophosmin) and stem/progenitor cell markers (SPRR1A
92 of protamine-DNA complexes: NAP-1, NLP, and nucleophosmin are previously characterized histone chape
95 such as heat shock proteins, prohibitin, or nucleophosmin, as well as to the up-regulation of NF-kap
97 two-dimensional gels showed that the form of nucleophosmin B23 that is up-regulated in melanoma repre
98 r, hepatoma-derived growth factor (HDGF) and nucleophosmin B23 were strongly correlated with melanoma
103 nucleolar and ribosomal proteins, including nucleophosmin/B23 (NPM), a protein thought to foster the
104 tants that do not efficiently associate with nucleophosmin/B23 are unstable and functionally impaired
109 nd the hepatocellular carcinoma autoantigen, nucleophosmin/B23, as a model system to define the uniqu
113 ffinity-isolation of a protein identified as nucleophosmin by MS sequencing and Western-blotting.
114 f the three cysteine residues of a truncated nucleophosmin coexpressed with native nucleophosmin in C
116 are basic functions with, the nucleoplasmin/ nucleophosmin family of molecular chaperone proteins.
118 e tyrosine kinase 3 gene (Flt3(ITD)) and the nucleophosmin gene (Npm1(c)) to induce AML in vivo, and
120 leukaemia 1 gene (KMT2Ar) or mutation of the nucleophosmin gene (NPM1) require the chromatin adapter
123 causing aberrant cytoplasmic localization of nucleophosmin have been demonstrated to be the most freq
124 idic, synthetic small molecules that bind to nucleophosmin have not been described, prior to this rep
125 ations, and that siRNA-promoted depletion of nucleophosmin in a population of HeLa S3 cells leads to
126 the similarity of Npm3 to nucleoplasmin and nucleophosmin in amino acid sequence, protein features,
127 ncated nucleophosmin coexpressed with native nucleophosmin in COS-7 cells revealed that the mutation
128 n localization determines the specificity of nucleophosmin in sorting nascent ribosomal subunits and
130 udy, we examined the underlying mechanism of nucleophosmin induction and showed that hyperproliferati
140 We find that the Schizosaccharomyces pombe nucleophosmin-like protein Fkbp39 localizes to rDNA site
141 echanistic link between TSC1/mTOR signaling, nucleophosmin-mediated nuclear export of ribosome subuni
143 However, the oncogenic potential of this nucleophosmin mutant (NPMc+) has never been established,
144 2A (KMT2A or MLL1)-rearranged (KMT2A-r) and nucleophosmin-mutant (NPM1c) acute myeloid leukemia (AML
146 FLT3 internal tandem duplication (ITD) and nucleophosmin mutations occurred at a similar frequency
147 y, involving interferon regulatory factor-1, nucleophosmin, NFkappaB, and CRE binding in cell surviva
153 anslocation that forms a fusion gene between nucleophosmin (NPM) and MDS/myeloid leukemia factor 1 (M
155 eport the purification and identification of nucleophosmin (NPM) and nucleolin as two genotoxic stres
156 s the center of ribosome synthesis, with the nucleophosmin (NPM) and p19(ARF) proteins antagonizing o
158 yelocytic leukemia (APL) fuses the genes for nucleophosmin (NPM) and the retinoic acid receptor alpha
159 ion of anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM) and the subsequent expression of the
161 ing, and biochemical approaches, we identify Nucleophosmin (NPM) as a novel functional target of RASS
163 le in p53-null cells by hyperphosphorylating nucleophosmin (NPM) at Thr199, as evidenced by observati
165 stic lymphoma kinase (ALK) gene fuses to the nucleophosmin (NPM) gene as a result of a (2;5) transloc
166 in the fusion of the ubiquitously expressed nucleophosmin (NPM) gene at 5q35 to the anaplastic lymph
167 35) chromosomal translocation that fuses the nucleophosmin (NPM) gene on chromosome 5q35 to a novel p
169 rming capability when truncated and fused to nucleophosmin (NPM) in the t(2;5) chromosomal rearrangem
174 inal portion of the nucleolar phosphoprotein nucleophosmin (NPM) joined to the entire cytoplasmic por
175 cid residues of the nucleolar phosphoprotein nucleophosmin (NPM) joined to the entire cytoplasmic por
176 ogenesis through increased expression of the nucleophosmin (NPM) nuclear-cytoplasmic shuttling protei
178 consensus sequence were abolished, with the nucleophosmin (NPM) reporter gene and used them for in v
180 es the gene for the nucleolar phosphoprotein nucleophosmin (NPM) to the retinoic acid receptor alpha
187 PKR-modulating proteins we report here that nucleophosmin (NPM), a protein frequently overexpressed
191 the most frequently mutated genes in AML is nucleophosmin (NPM), and this is associated with low CD3
192 F inhibited the interaction between DDX5 and nucleophosmin (NPM), preventing association of DDX5 with
193 ed here indicate that the nucleolar protein, nucleophosmin (NPM), redistributes from the nucleolus fo
194 nalysis of CXCR4 immune complexes identified nucleophosmin (NPM), which was confirmed by reciprocal c
195 ptase polymerase chain reaction (RT-PCR) for Nucleophosmin (NPM)-ALK during treatment identifies pati
198 ylation is accurately recapitulated in a new nucleophosmin (NPM)-ALK transgenic mouse model of lympho
199 human cell lines, primary human tumours and nucleophosmin (NPM)-ALK-induced murine tumours demonstra
200 ssing the oncogenic chimeric tyrosine kinase nucleophosmin (NPM)-anaplastic lymphoma kinase [ALK; ALK
207 In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant f
208 hat T-cell lymphoma (TCL) cells carrying the nucleophosmin (NPM)/ALK fusion protein (ALK+ TCL) strong
209 sformation caused by the oncogenic, chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) rem
210 nisms of cell transformation mediated by the nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) tyr
212 e describe a nuclear PI(3,4,5)P(3) receptor, nucleophosmin (NPM)/B23, that mediates the antiapoptotic
213 ns of p19(Arf) with Mdm2, or separately with nucleophosmin (NPM, B23) that localizes and stabilizes p
214 ain of the multifunctional nucleolar protein nucleophosmin (Npm-N) are central to its function, with
218 yclin E triggers centrosome duplication, and nucleophosmin (NPM/B23) is found to be one of its target
220 leus as a physical and functional partner of nucleophosmin (NPM/B23), a major nucleolar phosphoprotei
222 of p53-independent ARF targets, we isolated nucleophosmin (NPM/B23), a protein we show is required f
223 omal biogenesis through its interaction with nucleophosmin (NPM/B23), RNA helicase DDX5 and RNA polym
224 f many cellular proteins, including Mdm2 and nucleophosmin (NPM/B23), with which p19(Arf) physically
225 inal portion of the nucleolar phosphoprotein nucleophosmin(NPM) joined to the entire cytoplasmic port
226 or fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%)
227 Furthermore, the nucleolar phosphoprotein nucleophosmin (NPM1) acts as a scaffold for PIDD and is
228 ts were the same in all 3 cases, between the nucleophosmin (NPM1) and fms-related tyrosine kinase 4 (
229 ds were investigated using redistribution of nucleophosmin (NPM1) as a marker of nucleolar stress.
232 5 is able to interact with and phosphorylate nucleophosmin (NPM1) both in vitro and in intact cells.
243 olyadenylation, the multi-functional protein nucleophosmin (NPM1) is deposited onto all cellular mRNA
250 ed in CN-AML patients harboring mutations in nucleophosmin (NPM1) that are associated with favorable
252 eoli, co-localize with the nucleolar protein nucleophosmin (NPM1), and alter the phase separation beh
257 arker (e.g., a mutation in the gene encoding nucleophosmin [NPM1]) could improve prognostication by i
258 r nuclear transport include oncogenic mutant nucleophosmin (NPM1c) and mutant PI3K catalytic subunit
259 four-nucleotide duplication in the oncogene nucleophosmin (NPM1c), which creates a neoepitope presen
260 eading to aberrant cytoplasmic expression of nucleophosmin (NPMc(+)) are the most frequent genetic le
262 AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) accounts for about one-third o
263 a-associated antigens, prototypically mutant nucleophosmin (NPMc+) that upon mutation translocates fr
265 ia gene, promyelocytic leukemia zinc finger, nucleophosmin, nuclear matrix protein, and signal transd
267 nactive, unphosphorylated CPC interacts with nucleophosmin/nucleoplasmin proteins, which are known to
270 rotein-protein interaction and verified that nucleophosmin only bound to activated conformationally a
272 some inhibition, siRNA-mediated knockdown of nucleophosmin potentiated nucleolar accumulation and inc
277 ajor upstream inhibitor of mTOR, resulted in nucleophosmin protein induction through increased transl
278 ation and proximity assays confirmed the Bax-nucleophosmin protein-protein interaction and verified t
281 , we demonstrate that overexpression of NPM (nucleophosmin) significantly suppresses 12-O-tetradecano
283 ence of p53, ARF can be stabilized by NS and nucleophosmin to serve as an alternative tumor-suppresso
284 ecognized including topoisomerases I and II, nucleophosmin, Translin, EGR1, dek, pim-1, TFG, and MLL.
285 ell-based apoptosis model, demonstrated that nucleophosmin translocation from nucleolus to cytosol pr
286 cellular fractionation studies verified that nucleophosmin translocation occurred within 3 h, at a ti
289 etion of SENP3 and SENP5 or depletion of B23/nucleophosmin, we observed accumulation of SUMO proteins
290 also discuss the role of TIF-IA, COMMD1, and nucleophosmin, which are key players in this crosstalk,
291 ied including FMS-like tyrosine kinase-3 and nucleophosmin, which will enhance our ability to more ac
292 ransport of tumor suppressors (e.g., p53 and nucleophosmin) whose function is altered in cancer becau
293 n that juxtaposes the dimerization domain of nucleophosmin with anaplastic lymphoma kinase (ALK).