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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.


B23, NPM, NPM1
This gene encodes a phosphoprotein which moves between the nucleus and the cytoplasm. The gene product is thought to be involved in several processes including regulation of the ARF/p53 pathway. A number of genes are fusion partners have been characterized, in particular the anaplastic lymphoma kinase gene on chromosome 2. Mutations in this gene are associated with acute myeloid leukemia. More than a dozen pseudogenes of this gene have been identified. Alternative splicing results in multiple transcript variants.[provided by RefSeq, Nov 2009] (from NCBI)
Top mentioned proteins: FLT3, HAD, CAN, AGE, iMpact
Papers using B23 antibodies
Frequent pathway mutations of splicing machinery in myelodysplasia.
Pelicci Pier Giuseppe et al., In Frontiers in Oncology, 2010
... The cytoplasmic NPM mutant induces myeloproliferation in a transgenic mouse model.
The survival-promoting peptide Y-P30 enhances binding of pleiotrophin to syndecan-2 and -3 and supports its neuritogenic activity.
Bogyo Matthew, In PLoS ONE, 2007
... sc-8334; Santa Cruz Biotechnology, Heidelberg, Germany); α-GST (glutathione S-transferase, sc-57753; Santa Cruz Biotechnology, Heidelberg, Germany); α-NPM1 (nucleophosmin, #3542 Cell Signaling); α-Tasp ...
Nucleolar trafficking is essential for nuclear export of intronless herpesvirus mRNA.
Glaunsinger Britt A., In PLoS Pathogens, 2005
... Antibodies against SC-35, Flag, Myc and Aly (Sigma), GFP and mCherry (Clontech), B23 (Santa Cruz), KSHV gB (Abcam) and GAPDH (Abcam) were ...
Systematic functional analysis of the Caenorhabditis elegans genome using RNAi.
Burns Jorge Sans, In PLoS ONE, 2002
... Mouse anti-GFP (Covance Research Products) anti-myc (myc-Tag 9B11) (DSHB), anti-B23/Nucleophosmin (AB10530; Abcam) and anti-UBF (H00007343-M01), goat ...
Rapid and simple phenotypic assay for drug susceptibility of human immunodeficiency virus type 1 using CCR5-expressing HeLa/CD4+ cell clone 1–10 (MAGIC-5)
Speck Roberto F., In PLoS ONE, 2000
... approved by the Ethics Committee for Animal Care and Use of Kumamoto University (Approval ID, B23-181 R1: Analysis of immune responses against viral diseases by using humanized and HLA transgenic mice) ...
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Papers on B23
Assessment of Minimal Residual Disease in Standard-Risk AML.
UK National Cancer Research Institute AML Working Group et al., Nottingham, United Kingdom. In N Engl J Med, Feb 2016
Sensitive detection of a leukemia-specific marker (e.g., a mutation in the gene encoding nucleophosmin [NPM1]) could improve prognostication by identifying submicroscopic disease during remission.
Minimal Residual Disease in NPM1-Mutated AML.
Burke, Milwaukee, United States. In N Engl J Med, Feb 2016
UNASSIGNED: One of the most important discoveries in the treatment of acute leukemia is that the presence of minimal residual disease is an independent prognostic factor for the duration of remission and survival.
The leukemic oncoprotein NPM1-RARA inhibits TP53 activity.
Redner et al., Pittsburgh, United States. In Leuk Lymphoma, Feb 2016
UNASSIGNED: The variant acute promyelocytic leukemia (APL) translocation t(5;17)(q35;q21) fuses the N-terminus of nucleophosmin (NPM1) to the retinoic acid receptor alpha (RARA).
Benefit of high dose daunorubicin in AML induction extends across cytogenetic and molecular groups: updated analysis of E1900.
Luger et al., Philadelphia, United States. In Blood, Feb 2016
Patients with FLT3-ITD (24%), DNMT3A (24%), and NPM1 (26%) mutant AML all benefited from HD daunorubicin (HR, 0.61, P = .009;
Molecular therapy for acute myeloid leukaemia.
Levine et al., New York City, United States. In Nat Rev Clin Oncol, Jan 2016
Indeed, risk status in patients with this disease has classically been based on cytogenetic findings; however, additional molecular characteristics have been shown to inform risk assessment, including FLT3, NPM1, KIT, and CEBPA mutation status.
Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress.
Turner et al., Paris, France. In Nat Commun, Dec 2015
Here we present a model of peripheral ALCL pathogenesis where the malignancy is initiated in early thymocytes, before T-cell receptor (TCR) β-rearrangement, which is bypassed in CD4/NPM-ALK transgenic mice following Notch1 expression.
Design and synthesis of novel selective anaplastic lymphoma kinase inhibitors.
Hood et al., San Diego, United States. In Bioorg Med Chem Lett, Dec 2015
Expression of ALK in normal human tissues is only found in a subset of neural cells, however it is involved in the genesis of several cancers through genetic aberrations involving translocation of the kinase domain with multiple fusion partners (e.g., NPM-ALK in anaplastic large cell lymphoma ALCL or EML4-ALK in non-small cell lung cancer) or activating mutations in the full-length receptor resulting in ligand-independent constitutive activation (e.g., neuroblastoma).
Pathology Consultation on Gene Mutations in Acute Myeloid Leukemia.
Education Committee of the Academy of Clinical Laboratory Physicians and Scientists et al., San Francisco, United States. In Am J Clin Pathol, Oct 2015
RESULTS: Current laboratory studies of gene mutations in AML include analysis of NPM1, FLT3, CEBPA, and KIT.
Simpson's Paradox and the Impact of Different DNMT3A Mutations on Outcome in Younger Adults With Acute Myeloid Leukemia.
Linch et al., Cardiff, United Kingdom. In J Clin Oncol, Jul 2015
RESULTS: DNMT3A mutations (DNMT3A(MUT)) were identified in 272 patients (30%) and associated with a poorer prognosis than wild-type DNMT3A, but the difference was only seen when the results were stratified according to NPM1 genotype.
Mutations in the BCR-ABL1 Kinase Domain and Elsewhere in Chronic Myeloid Leukemia.
Martinelli et al., Bologna, Italy. In Clin Lymphoma Myeloma Leuk, Jun 2015
Mutations in genes other than BCR-ABL1 include ASXL1, TET2, RUNX1, DNMT3A, EZH2, and TP53 in chronic phase patients and RUNX1, ASXL1, IKZF1, WT1, TET2, NPM1, IDH1, IDH2, NRAS, KRAS, CBL, TP53, CDKN2A, RB1, and GATA-2 mutations in advanced phase patients.
Prognostic significance of NPM1 mutations in the absence of FLT3-internal tandem duplication in older patients with acute myeloid leukemia: a SWOG and UK National Cancer Research Institute/Medical Research Council report.
Stirewalt et al., Seattle, United States. In J Clin Oncol, May 2015
PURPOSE: Younger patients with acute myeloid leukemia (AML) harboring NPM1 mutations without FLT3-internal tandem duplications (ITDs; NPM1-positive/FLT3-ITD-negative genotype) are classified as better risk; however, it remains uncertain whether this favorable classification can be applied to older patients with AML with this genotype.
Allogeneic stem-cell transplantation in patients with NPM1-mutated acute myeloid leukemia: results from a prospective donor versus no-donor analysis of patients after upfront HLA typing within the SAL-AML 2003 trial.
Ehninger et al., Berlin, Germany. In J Clin Oncol, Mar 2015
PURPOSE: The presence of a mutated nucleophosmin-1 gene (NPM1(mut)) in acute myeloid leukemia (AML) is associated with a favorable prognosis.
Goryainova, In Lik Sprava, 2014
In addition to the conventional risk factors molecular genetic alterations, such as mutations of NPM1, CEBPA, c-KIT, AML1/RUNX1, WT1, FLT3 and others, are also important prognostic factors in AML patients.
Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer Cells.
Schatz et al., Miami, United States. In Biomark Cancer, 2014
This is highlighted in particular by recent studies of mutant-BRAF in melanoma and the fusion kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) in anaplastic large cell lymphoma.
Adenoviral protein V promotes a process of viral assembly through nucleophosmin 1.
Curiel et al., Birmingham, United States. In Virology, 2012
Adenoviral protein V participates in a process of viral assembly through NPM1.
Mutated regions of nucleophosmin 1 elicit both CD4(+) and CD8(+) T-cell responses in patients with acute myeloid leukemia.
Schmitt et al., Ulm, Germany. In Blood, 2012
NPM1(mut) induces specific T-cell responses of CD4(+) and CD8(+) T cells and therefore is a promising target for specific immunotherapies in acute myeloid leukemia.
Structure of nucleophosmin DNA-binding domain and analysis of its complex with a G-quadruplex sequence from the c-MYC promoter.
Federici et al., Sesto Fiorentino, Italy. In J Biol Chem, 2012
present the solution structure of the NPM1-C70 domain and NMR analysis of its interaction with a c-MYC-derived G-quadruplex. These data were used to calculate an experimentally restrained molecular docking model for the complex
In silico studies of potential phosphoresidues in the human nucleophosmin/B23: its kinases and related biological processes.
Pons et al., Havana, Cuba. In J Cell Biochem, 2012
study suggesst that B23 phosphorylation is related to cellular processes such as apoptosis, cell survival, cell proliferation, and response to DNA damage stimulus, in which these kinases are involved
Nucleophosmin (NPM1/B23) interacts with activating transcription factor 5 (ATF5) protein and promotes proteasome- and caspase-dependent ATF5 degradation in hepatocellular carcinoma cells.
Liu et al., State College, United States. In J Biol Chem, 2012
a mechanistic link between elevated NPM1 expression and depressed ATF5 in HCC and suggests that regulation of ATF5 by NPM1 plays an important role in the proliferation and survival of HCC.
Molecular and cytogenetic abnormalities in acute myeloid leukemia: review and case studies.
Pinho et al., São Paulo, Brazil. In Einstein (sao Paulo), 2011
METHODS: Thirty samples of patients with acute myeloid leukemia were studied, in which FLT3-ITD, FLT3-TKD and NPM1 mutations were investigated.
More papers using B23 antibodies
A quantitative assay for HIV DNA integration in vivo.
Vij Neeraj, In PLoS ONE, 2000
... Rabbit polyclonal anti-HA antibodies were purchased from Santa Cruz Biotechnology, mouse anti-B23 (nucleophosmin) antibody from Abcam, Alexa 568 conjugated goat ...
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