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Validated All-in-One™ qPCR Primer for NPM1(NM_002520.6) Search again
Product ID:
HQP011892
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
B23, NPM
Gene Description:
nucleophosmin 1
Target Gene Accession:
NM_002520.6(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
NPM1 is a ubiquitously expressed nucleolar protein that shuttles between the nucleus and cytoplasm. It is implicated in multiple functions, including ribosomal protein assembly and transport, control of centrosome duplication, and regulation of the tumor suppressor ARF (MIM 600160). NPM1 mutations that relocalize NPM1 from the nucleus into the cytoplasm are associated with development of acute myeloid leukemia (AML; MIM 601626) (Garzon et al., 2008 [PubMed 18308931]).[supplied by OMIM].
Gene References into function
- Protein B23 is an abundant, multifunctional nucleolar phosphoprotein that behaves like a molecular chaperone, an activity that may be related to its role in ribosome biogenesis
- overexpressed in acute myeloid leukemia while translocations associated with this gene are absent
- marker of proliferation activity of human peripheral lymphocytes
- NPM is a crucial regulator of p53
- involvement of NPM/B23 in the acute response of mammalian cells to environmental stress, such as UV rays
- overexpression of NPM suppressed PKR activity, enhanced protein synthesis, and inhibited apoptosis. Fanconi anemia lymphoblasts expressed low levels of NPM, which correlated with high ground-state activation of PKR and hypersensitivity to apoptotic cues
- These findings suggest that an NPM/MLF1 fusion is the primary molecular abnormality in t(3;5) MDS and AML with multilineage dysplasia, and that cases with NPM/MLF1 may be clinically distinct from other MDS-associated disease
- unique B23 conformation in hepatoma
- Src-kinases, particularly pp60(c-src), associate with and are activated by NPM-ALK expression in various cells, and in cell lines established from patients with large cell lymphoma
- Results reveal a molecular mechanism of ARF in regulating ribosome biogenesis and cell proliferation via inhibiting B23.
- NPM/ALK-mediated induction of Bcl-XL
- cleavage of B23 by granzyme b in intact vascular smooth muscle cells is dependent upon both cell type and phenotype
- These data suggest that nucleophosmin is an early responder to DNA damage that prevents premature activation of p53.
- nucleophosmin is an NF-kappaB co-activator for the induction of the human SOD2 gene
- BRCA1-BARD1 catalyzes the polyubiquitination of nucleolar phosphoprotein nucleophosmin/B23
- identification of Ser-4 in B23 as a major physiological substrate of Polo-like kinase 1
- NPM inhibits hypoxia-induced p53 phosphorylation at Ser-15 and interacts with p53 in hypoxic cells; hypoxia-driven cancer progression may require increased expression of NPM to suppress p53 activation and maintain cell survival
- Aloe-emodin caused increase in the amount of proform and fragment of nucleophosmin in cytoplasm may be one of the important events for aloe-emodin-induced H460 cell apoptosis pf mpm-small cell lung cancer.
- c-Myc-mediated expression of NPM decreases during retinoic acid-induced differentiation of HL-60 cells.
- a novel association of B23 and Gadd45a and implicate B23 as an important regulator in Gadd45a nuclear import.
- Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
- CDK2-BRCA1-NPM pathway coordinately functions in cell growth and tumor progression pathways.
- NPM inhibits ARF's p53-dependent activity by targeting it to nucleoli and impairing ARF-Mdm2 association.
- The molecular signature of cytoplasmic NPM+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem-cell phenotype, suggesting that cytoplasmic NPM+ AML may derive from a multipotent hematopoietic progenitor.
- base sequences are given for NPM1 mutated childhood AML patients; consistent deletion/insertion features are presented
- polyamine depletion increased expression of the NPM gene and enhances NPM nuclear translocation and increased NPM interacts with and stabilizes p53, leading to inhibition of IEC-6 cell proliferation
- NPM inhibits ionizing irradiation-induced p53 transactivation, and interacts with p53 in hematopoietic cells.
- the NPM1 mutation is not necessarily an early event during leukemogenesis; the NPM1 mutation was a favorable factor for achieving complete remission but was associated with a high relapse rate
- Nucleophosmin (NPM) may be a Ran-Crm1 substrate that controls centrosome duplication.
- results indicate that HCV core can recruit B23 and p300 to relieve the repression effect of YY1 on B23 promoter activity
- Enforced expression of an NPM cytoplasmic mutant acutely attenuates p53-dependent and -independent functions of Arf tumor suppressor protein, and also affects endogenous NPM localization.
- These findings indicate the involvement of nucleophosmin in the regulation of pre-mRNA processing, and its activity is controlled by CDK2-mediated phosphorylation on Thr(199).
- FRGY2a and YB1 disassemble nucleoli by sequestering B23, which is associated with pre-ribosomes and other structurally important nucleolar components
- both alterations are crucial for acute myeloid leukemia NPM mutant export from nucleus to cytoplasm; NPM leukemic mutants in turn recruit the wild-type NPM from nucleoli to nucleoplasm and cytoplasm
- NPM1 mutations represent a common genetic abnormality in adult acute myeloid leukemia and appears to identify patients with improved response toward treatment.
- The sensitive RQ-PCR assays for NPM1 mutations can now monitor and quantify MRD in AML patients with normal karyotype and NPM1 gene mutations.
- results suggest that B23 plays an important role in the intracellular localization of the core protein and replication of Japanese encephalitis virus
- NPM1 mutations may be also involved in the pathogenesis of myelodysplastic syndromes.
- the functional integrity of the B23 core motif is required for stability, efficient nucleolar localization as well as ARF binding
- constitutive expression of C/EBPbeta in ALK-positive anaplastic large cell lymphoma and its relationship to NPM-ALK
- new exon-12 NPM mutations in acute myeloid leukemia
- These results demonstrate a novel mechanism for transcriptional regulation of E2F1 and identify the functional role of nucleophosmin/B23 in modulating the binding of NF-kappaB, E2F1 and pRB to activate E2F1 promoter.
- NPM/ALK-carrying T cell lymphoma (ALK+TCL) cells secrete IL-10 and TGF-beta and express FoxP3, indicating their T regulatory (Treg) cell phenotype.
- Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
- AUF1 was phosphorylated by ALK in vitro and was hyperphosphorylated in NPM-ALK-expressing cells.
- While complex formation between ARF and NPM retains ARF in the nucleolus and prevents ARF from activating p53, DNA damaging treatments promote a transient subnuclear redistribution of ARF to the nucleoplasm, where promotes p53 activation.
- Ras and c-Myc play important roles in the up-regulation of nucleophosmin/B23 during proliferation of cells associated with a high degree of malignancy, thus outlining a signaling cascade involving these factors in the cancer cells.
- Ddetermination of mutations and promoter methylation status of NPM1 using pyrosequencing in 199 samples of myeloid neoplasia including myeloproliferative disorders (MPD).
- These results provide evidence that phosphorylation at specific sites reduces the affinity of B23 for nucleolar components and might be a factor in regulating its location during the cell cycle.
- Often mutation in acute myeloid leukemia.
- NPM1 gene mutations cause a frame shift in the C-terminus of exon 12, disrupting the NPM nucleolar-localization signal or generating a leucine-rich nuclear export motif, resulting in abnormal cytoplasmic accumulation of NPM.
- A new type of NPM mutation was found, and NPM mutations in MDS patients were demonstrated foe the first time. The results provides new hints for NPM gene mutations in the pathogenesis of AML and MDS.
- In pediatric patients, NPM1 mutations are less common than in adults and tend to affect older patients.
- A novel mechanism of nucleophosmin (NPM) tumorigenesis establishes NPM as a crucial inhibitor of oncogene-induced apoptosis and senescence.
- NPM1 exon 12 mutations is associated with acute myeloid leukemia
- study could not find any NPM gene mutations in pediatric acute myeloid leukemia with normal karyotype
- This study unveils a hitherto unrecognized transcriptional corepressor function of the NPM protein, and highlights a novel mechanism by which NPM regulates cell growth and differentiation.
- Frameshift mutations in exon 12 of the nucleophosmin gene (NPM1) result in aberrant cytoplasmic localization of the NPM protein (NPMc(+); NPMc(+) is relatively rare in childhood AML, particularly in younger children
- Review. NPM1 is translocated or mutated in various lymphomas & leukemias, forming fusion proteins or NPM mutant products. The structural, functional, biological, clinical & pathological features of normal & mutant NPM1 & its malignancies are reviewed.
- data indicate that NPM1 exon 12 is mutated in acute myelogenous leukemias but not in other common human cancers, and suggest that the NPM1 mutation may not play a role in the tumorigenesis of common solid cancers
- B23 sumoylation regulates its subcellular localization, cell proliferation, and survival activities.
- identify splicing factor as a novel NPM/anaplastic lymphoma kinase-binding protein and substrate
- The leukemia-associated NPMc+ is an in vitro oncogene under the appropriate genetic context
- PAI-1 downregulates B23 in LnCAP prostatic cancer.
- Nuclear matrix proteins such as mutant Pyst1 and nucleophosmin 1 were downregulated, whereas eIF6 and beta-tubulin were upregulated during cell differentiation in hepatocarcinoma cells.
- mutated NPM1 leads to dysregulated HOX expression via a different mechanism than MLL rearrangement
- nucleophosmin 1 mutations may cause cells to develop along the myelomonocytic lineage
- B23 functions as a chaperone in the viral chromatin assembly process in infected cells.
- COOH-terminal nuclear export signals of different strength ensure cytoplasmic accumulation of nucleophosmin leukemic mutants
- NPM1 mutations is associated with absence of nucleophosmin leukemic mutants in B and T cells from AML
- NPM1 mutations in acute myeloid leukemia act to achieve maximum nuclear export and cytoplasmic accumulation of NPM1
- Sustained expression of nucleophosmin (NPM1) mutation at late relapse presenting as isolated myeloid sarcoma in a patient with acute myeloid leukemia.
- JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
- mutated NPM peptides can be presented by HLA molecules, suggesting that AML cells carrying cytoplasmic mutated NPM could induce an anti-leukaemic T-cell response
- This study provides evidence for a novel role for NPM as a negative regulator of CXCR4 signaling induced by CXCL12 that may be relevant to the biology of acute myelogenous leukemia.
- NPM1 mutations are associated with residual disease of acute myeloid leukemia
- NPM1 mutations were significantly associated with old age, high peripheral white blood cell count, and the subtypes of French-American-British categories M1/M5, but negatively associated with expression of CD34 and CD117 in a Chinese population.
- crystal structure of human NPM-core (Met9-Asp122)
- Oncogenic NPM1-ALK contains the NPM1 oligomerization motif plus ALK catalytic domain and mediates malignant cell transformation by epigenetic silencing of signal transducer and activator of transcription STAT5A in T-cell anaplastic large cell lymphomas.
- AML cells are a major source of Ang-1 in leukemic bone marrow, especially in patients with NPM1 mutations
- B23 distinctively binds Ebp1 isoforms and regulates cell proliferation and survival through p42 and p48, respectively.
- There was a highly significant trend for worsening in relapse risk (RR) and overall survival (OS) with increasing FLT3/ITD (internal tandem duplication) mutant level.
- nucleolar localization determines the stability of ARF but not its primary function
- correlation of PTPN11 mutations with NPM1 mutations and FLT3/ITD among adult AML patients
- NPM1 mutations were not detected in the 28 patients with myelodysplastic syndrome and acute myeloid leukemia with chromosome 5 abnormalities.
- Fusion protein nucleophosmin (NPM)-ALK activates GTPase Rac1 via phosphatidylkinase 3-kinase (PI3K) and protein-tyrosine kinase c-src (Src) in anaplastic large cell lymphoma patients.
- Could regulate androgen receptor (AR) functions by promoting assembly of AR-containing regulatory complexes; high levels might alter AR functions in prostate cancer.
- NPM1 mutation is a unique genetic event that is specific to Acute myeloid leukemia
- Elderly (range 60-85 yr) but medically fit patients with acute myeloid leukemia (AML) carrying NPM1 mutations demonstrate a higher rate of complete remission compared to NPM1 wildtype AML patients.
- a molecular mechanism of B23 in the mitotic inhibition of GCN5-mediated histone acetylation and transactivation.
- findings point to DR negativity as another phenotypic feature of AML with NPM1 mutation
- In this general and unselected AML patient population, NPM1 mutation was not a prognostic indicator of a favorable outcome.
- NPM1-mutated acute myeloid leukaemia occurring in JAK2-V617F+ primary myelofibrosis.
- The present investigations demonstrate the importance of exposure of the C-terminus of Bax for its interaction with nucleophosmin. These protein-protein interaction assays provide a technical approach for the study of Bax-interacting proteins.
- These results define SENP3 as an essential factor for ribosome biogenesis and suggest that deconjugation of SUMO2 from NPM1 by SENP3 is critically involved in 28S rRNA maturation.
- study confirms in 2562 patients with acute myeloid leukemia the previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities
- NPM1 mutations were observed in 7 of 51 patients presenting as overt therapy-related acute myeloid leukemia as compared to only 3 of 89 patients presenting as therapy-related myelodysplasia
- These results identify a unique miRNA signature associated with Acute myeloid leukemia (AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) and provide evidence that support a role for miRNAs in the regulation of HOX genes.
- c-Jun translocates B23 and ARF from the nucleolus after JNK activation by means of protein interactions
- B23 was found to be associated with the rRNA gene chromatin. Small-interfering-RNA-mediated down-regulation of the B23 expression level resulted in reduction of the transcription rate of the rRNA gene.
- NPMc(+) acute myeloid leukemia represents a primary event rather than a transformation stage of NPMc(-) acute myeloid leukemia
- NPM binds to HEXIM1 in vitro and in vivo, and functions as a negative regulator of HEXIM1.
- Increase sensitivity to chemotherapeutical agents and cytoplasmatic interaction between NPM leukemic mutant and NF-kappaB is associated with acute myeloid leukemia carrying NPM1 mutations
- B23 selectively stores, and protects ribosomal protein S9 in nucleoli and therefore could facilitate ribosome biogenesis.
- Nucleophosmin is a binding partner of nucleostemin in human osteosarcoma cells
- p53-Driven apoptosis limits centrosome amplification and genomic instability downstream of NPM1 phosphorylation
- review of mutations of NPM1 associated with AML and the implications for prognosis
- structural analysis of nucleophosmin mutations in acute myeloid leukemia
- The NPM1-mutated is specific of leukemic cells and shows higher levels at MRD in AML patients presentation.
- detailed cytogenetic analysis of acute myeloid leukaemia with mutated NPM1 in a father and daughter, with different NPM1 mutations
- Model fits with the hypothesis that acute myeloid leukemia arises from an NPM1 mutation with haploinsufficiency of the wild-type NPM1 allele.
- SMT3IP1 desumoylates nucleophosmin and might controls its physiological functions at both the nucleolus and other subcellular compartments.
- NPM1 mutants coexisted mainly with FLT3 mutants
- 38.9% (14/36) patients with NPM1 mutations simultaneously exhibited internal tandem duplications in the FLT3 gene
- NPM is an essential protein not only for the formation of normal nucleolar structure, but also for the maintenance of regular nuclear shape in HeLa cells.
- These findings indicate that nucleophosmin is essential for mitotic progression and cell proliferation.
- Nucleolar protein B23/nucleophosmin regulates the vertebrate SUMO pathway through SENP3 and SENP5 proteases.
- NPM1 mutations confer a favorable prognosis in childhood AML and in cytogenetically normal AML in particular.
- NPM1 expression levels of mRNA and protein in myelodysplastic syndromes were not related to chromosome 5 abnormalities and were almost the same as those in normal bone marrow and acute myeloid leukemia cells
- The ribosomal protein L23 is a negative regulator of Miz1-dependent transactivation.
- A novel interaction between nucleophosmin (NPM1) and APE1 was characterized.