HCSGD entry for NUCB2
1. General information
Official gene symbol | NUCB2 |
---|---|
Entrez ID | 4925 |
Gene full name | nucleobindin 2 |
Other gene symbols | NEFA |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0003677 | DNA binding | IEA | molecular_function |
GO:0005509 | Calcium ion binding | IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005615 | Extracellular space | TAS | cellular_component |
GO:0005640 | Nuclear outer membrane | IEA | cellular_component |
GO:0005783 | Endoplasmic reticulum | IEA | cellular_component |
GO:0005793 | Endoplasmic reticulum-Golgi intermediate compartment | IDA | cellular_component |
GO:0005794 | Golgi apparatus | IDA | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0005886 | Plasma membrane | TAS | cellular_component |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.9183239960 | 0.0105823601 | 0.9999902473 | 0.2031643326 |
- 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 | Down | -0.1115753966 |
GSE13712_SHEAR | Down | -0.2710738663 |
GSE13712_STATIC | Down | -0.3340881298 |
GSE19018 | Up | 0.2927553283 |
GSE19899_A1 | Down | -1.1950169986 |
GSE19899_A2 | Down | -1.0631218375 |
PubMed_21979375_A1 | Down | -0.8533327433 |
PubMed_21979375_A2 | Down | -1.8816888522 |
GSE35957 | Down | -0.8325852471 |
GSE36640 | Down | -0.1446943632 |
GSE54402 | Down | -0.5813801923 |
GSE9593 | Down | -0.3244747290 |
GSE43922 | Down | -0.9678387033 |
GSE24585 | Up | 0.2221413462 |
GSE37065 | Up | 0.1075169001 |
GSE28863_A1 | Up | 0.2058355067 |
GSE28863_A2 | Up | 0.2922304680 |
GSE28863_A3 | Up | 0.0370048879 |
GSE28863_A4 | Up | 0.2917314194 |
GSE48662 | Down | -0.3635829764 |
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-193b-3p | MIMAT0002819 | MIRT016539 | Proteomics | Functional MTI (Weak) | 21512034 |
hsa-miR-215-5p | MIMAT0000272 | MIRT024896 | Microarray | Functional MTI (Weak) | 19074876 |
hsa-miR-192-5p | MIMAT0000222 | MIRT026936 | Microarray | Functional MTI (Weak) | 19074876 |
hsa-miR-26b-5p | MIMAT0000083 | MIRT030199 | Microarray | Functional MTI (Weak) | 19088304 |
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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: 2 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
25565110 | Isoflavones significantly blocked activations of senescence-associated beta-galactosidase and PPARgamma/p53/p21 by NEFA |
25565110 | Finally, replicative senescent osteoblastic cells and bone marrow mesenchymal ST2 cells exhibited similar behavior to cells treated with NEFA and in vivo bone cells in rats fed HF-Cas diet |
25565110 | These results suggest that: 1) high concentrations of NEFA occurring with HF intake are mediators of osteoblast cell senescence leading to impairment of bone development and acquisition; 2) the molecular mechanisms underlying the SPI-protective effects involve isoflavone-induced inhibition of osteoblastic cell senescence to prevent HF-induced bone impairments |
25490147 | Isoflavones significantly blocked activations of senescence-associated beta-galactosidase and PPARgamma/p53/p21 by NEFA |
25490147 | Finally, replicative senescent osteoblastic cells and bone marrow mesenchymal ST2 cells exhibited behavior similar to that of cells treated with NEFA and in vivo bone cells in rats fed the HF-Cas diet |
25490147 | These results suggest that (1) high concentrations of NEFA occurring with HF intake are mediators of osteoblast cell senescence leading to impairment of bone development and acquisition and (2) the molecular mechanisms underlying the SPI-protective effects involve isoflavone-induced inhibition of osteoblastic cell senescence to prevent HF-induced bone impairments |
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