HCSGD entry for NPM1
1. General information
Official gene symbol | NPM1 |
---|---|
Entrez ID | 4869 |
Gene full name | nucleophosmin (nucleolar phosphoprotein B23, numatrin) |
Other gene symbols | B23 NPM |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
![color bar](img/red_blue.jpg)
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0003676 | Nucleic acid binding | IEA | molecular_function |
GO:0003713 | Transcription coactivator activity | IDA | molecular_function |
GO:0003723 | RNA binding | IDA | molecular_function |
GO:0004860 | Protein kinase inhibitor activity | IDA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005634 | Nucleus | IDA ISS | cellular_component |
GO:0005654 | Nucleoplasm | IDA TAS | cellular_component |
GO:0005730 | Nucleolus | IDA | cellular_component |
GO:0005737 | Cytoplasm | IDA ISS | cellular_component |
GO:0005813 | Centrosome | IDA ISS | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0006281 | DNA repair | IDA | biological_process |
GO:0006334 | Nucleosome assembly | IDA TAS | biological_process |
GO:0006886 | Intracellular protein transport | TAS | biological_process |
GO:0006913 | Nucleocytoplasmic transport | IDA TAS | biological_process |
GO:0006950 | Response to stress | IMP | biological_process |
GO:0007098 | Centrosome cycle | IMP ISS | biological_process |
GO:0007165 | Signal transduction | NAS | biological_process |
GO:0007569 | Cell aging | IMP ISS | biological_process |
GO:0008104 | Protein localization | IDA | biological_process |
GO:0008285 | Negative regulation of cell proliferation | IMP ISS | biological_process |
GO:0010826 | Negative regulation of centrosome duplication | IMP | biological_process |
GO:0016032 | Viral process | TAS | biological_process |
GO:0019901 | Protein kinase binding | IPI | molecular_function |
GO:0030529 | Ribonucleoprotein complex | IDA | cellular_component |
GO:0030957 | Tat protein binding | IDA | molecular_function |
GO:0031616 | Spindle pole centrosome | IDA | cellular_component |
GO:0032071 | Regulation of endodeoxyribonuclease activity | IDA | biological_process |
GO:0034080 | CENP-A containing nucleosome assembly at centromere | TAS | biological_process |
GO:0042255 | Ribosome assembly | TAS | biological_process |
GO:0042393 | Histone binding | IDA | molecular_function |
GO:0042803 | Protein homodimerization activity | IDA | molecular_function |
GO:0043023 | Ribosomal large subunit binding | IDA | molecular_function |
GO:0043024 | Ribosomal small subunit binding | IDA | molecular_function |
GO:0043066 | Negative regulation of apoptotic process | IDA NAS | biological_process |
GO:0044387 | Negative regulation of protein kinase activity by regulation of protein phosphorylation | IDA | biological_process |
GO:0045727 | Positive regulation of translation | IDA | biological_process |
GO:0046599 | Regulation of centriole replication | IMP | biological_process |
GO:0046982 | Protein heterodimerization activity | IMP | molecular_function |
GO:0051059 | NF-kappaB binding | IDA ISS | molecular_function |
GO:0051082 | Unfolded protein binding | IDA ISS | molecular_function |
GO:0051092 | Positive regulation of NF-kappaB transcription factor activity | IMP | biological_process |
GO:0051259 | Protein oligomerization | IDA | biological_process |
GO:0060699 | Regulation of endoribonuclease activity | IDA | biological_process |
GO:0060735 | Regulation of eIF2 alpha phosphorylation by dsRNA | IDA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.9453525398 | 0.0617152806 | 0.9999902473 | 0.4685341506 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Up | 0.0997938546 |
GSE13712_SHEAR | Down | -0.3027288812 |
GSE13712_STATIC | Down | -0.0319874960 |
GSE19018 | Down | -0.5935569382 |
GSE19899_A1 | Down | -0.0218058445 |
GSE19899_A2 | Down | -0.0904331679 |
PubMed_21979375_A1 | Up | 0.0732625694 |
PubMed_21979375_A2 | Up | 0.0308581319 |
GSE35957 | Down | -0.5135853821 |
GSE36640 | Down | -0.4053811172 |
GSE54402 | Up | 0.1915739288 |
GSE9593 | Down | -0.0360199680 |
GSE43922 | Down | -0.0319573240 |
GSE24585 | Down | -0.1347671339 |
GSE37065 | Down | -0.2917459787 |
GSE28863_A1 | Up | 0.0724267922 |
GSE28863_A2 | Down | -0.0191125208 |
GSE28863_A3 | Up | 0.0038307030 |
GSE28863_A4 | Down | -0.1129247658 |
GSE48662 | Down | -0.6928682766 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-296-3p | MIMAT0004679 | MIRT038406 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-93-3p | MIMAT0004509 | MIRT038792 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-421 | MIMAT0003339 | MIRT039386 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-625-5p | MIMAT0003294 | MIRT039598 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-598-3p | MIMAT0003266 | MIRT040495 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-92b-3p | MIMAT0003218 | MIRT040565 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-193b-3p | MIMAT0002819 | MIRT041488 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-320a | MIMAT0000510 | MIRT044729 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-149-5p | MIMAT0000450 | MIRT045680 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-125a-5p | MIMAT0000443 | MIRT045754 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-125b-5p | MIMAT0000423 | MIRT045923 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-23b-3p | MIMAT0000418 | MIRT046377 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-15b-5p | MIMAT0000417 | MIRT046385 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-93-5p | MIMAT0000093 | MIRT048875 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-92a-3p | MIMAT0000092 | MIRT049162 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-25-3p | MIMAT0000081 | MIRT050209 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 5 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
24782448 | Interactions of two highly acetylated proteins, nucleophosmin (NPM1) and nucleolin, with SIRT6 and SIRT7 were confirmed by co-immunoprecipitation |
24782448 | NPM1 was found to be deacetylated by both SIRT6 and SIRT7 |
24782448 | In senescent cells, the acetylation level of NPM1 was increased in conjunction with decreased levels of SIRT6 and SIRT7, suggesting that the acetylation of NPM1 could be regulated by SIRT6 and SIRT7 in the aging process |
23536448 | Nucleophosmin 1, upregulated in adenomas and cancers of the colon, inhibits p53-mediated cellular senescence |
23536448 | Dysregulation of nucleophosmin 1 (NPM1) has been found in numerous solid and hematological malignancies |
23536448 | Our aims were to compare NPM1 expression in normal colon, adenoma and CRC, to correlate their expressions with clinico-pathological parameters, and to assess the biological role of aberrant NPM1 expression in CRC cells |
23536448 | NPM1 transcript levels were studied in human CRC cell lines, whereas a tissue microarray of 57 normal human colon, 40 adenoma and 185 CRC samples were used to analyze NPM1 protein expression by immunohistochemistry |
23536448 | NPM1 transcript levels were 7-11-folds higher in three different human CRC cell lines compared to normal colon cells |
23536448 | NPM1 protein expression was found to be progressively and significantly upregulated in CRC compared to adenomas and in adenomas compared to normal mucosa |
23536448 | Reducing NPM1 expression by siRNA had caused a significant decrease in cell viability, a concomitant increase in cellular senescence and cell cycle arrest |
23536448 | Cellular senescence induced under conditions of forced NPM1 suppression could be prevented by knocking down p53 |
23536448 | The differential expression of NPM1 along the normal colon-adenoma-carcinoma progression and its involvement in resisting p53 related senescent growth arrest in CRC cell lines implicate its role in supporting CRC tumorigenesis |
18316603 | Two nucleolar proteins, p14(ARF)/p19(ARF) and B23, were shown to translocate out of the nucleolus after exposure of cells to DNA-damaging agents |
18316603 | We show that redistribution of B23 and p19(ARF) after the exposure to genotoxic stress occurs preferentially when the c-Jun-NH(2)-kinase (JNK) pathway is activated and is inhibited when the JNK pathway is impaired |
18316603 | Instead, c-Jun interacts with B23 in a dose-dependent manner |
18316603 | Hence, we suggest that c-Jun translocates B23 and ARF from the nucleolus after JNK activation by means of protein interactions |
17967869 | However, little is known about how MLF1 functions upstream of the CSN3-COP1-p53 pathway and how its deregulation by the formation of the fusion protein nucleophosmin (NPM)-MLF1, generated by t(3;5)(q25 |
17967869 | Here we show that MLF1 is a cytoplasmic-nuclear-shuttling protein and that its nucleolar localization on fusing with NPM prevents the full induction of p53 by both genotoxic and oncogenic cellular stress |
17967869 | The fusion of MLF1 with NPM translocated MLF1 to the nucleolus and abolished the growth-suppressing activity |
17546053 | The leukemia-associated cytoplasmic nucleophosmin mutant is an oncogene with paradoxical functions: Arf inactivation and induction of cellular senescence |
17546053 | Mutations leading to aberrant cytoplasmic localization of Nucleophosmin 1 (NPM1) have been recently identified as the most frequent genetic alteration in acute myelogenous leukemia |
17546053 | However, the oncogenic potential of this nucleophosmin mutant (NPMc+) has never been established, which casts doubt on its role in leukemogenesis |
17546053 | By performing classical transformation assays, we find that NPMc+, but not wild-type NPM, cooperates specifically with adenovirus E1A to transform primary mouse embryonic fibroblasts in soft agar |
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