HCSGD entry for NUDT6


1. General information

Official gene symbolNUDT6
Entrez ID11162
Gene full namenudix (nucleoside diphosphate linked moiety X)-type motif 6
Other gene symbolsASFGF2 FGF-AS FGF2AS GFG-1 GFG1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0005575Cellular_componentNDcellular_component
GO:0005634NucleusIEAcellular_component
GO:0005739MitochondrionIEAcellular_component
GO:0008083Growth factor activityTASmolecular_function
GO:0008150Biological_processNDbiological_process
GO:0016787Hydrolase activityIEAmolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.05822570190.20010859010.52290296830.8651541064

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.1696620391
GSE13712_SHEARDown-0.2524186645
GSE13712_STATICDown-0.3105651625
GSE19018Down-0.2224008725
GSE19899_A1Up0.1158265982
GSE19899_A2Up1.4227911212
PubMed_21979375_A1Up3.0523297281
PubMed_21979375_A2Up0.1177576816
GSE35957Down-0.5059943171
GSE36640Up1.2268378220
GSE54402Up0.8236213755
GSE9593Down-0.2889079596
GSE43922Up0.0089044358
GSE24585Up0.4371730528
GSE37065Up0.0227929248
GSE28863_A1Down-0.2465962187
GSE28863_A2Down-0.3167576657
GSE28863_A3Down-0.1820680507
GSE28863_A4Down-0.3661007745
GSE48662Down-0.1857383274

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase
No target information from mirTarBase
  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 13 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25952632Under these conditions, the anti-senescence genes TERT, bFGF, VEGF, and ANG were increased, whereas the senescence-related genes ATM, p21, and p53 were decreased
25375819The influence of the culture media alpha-MEM, low-glucose DMEM, and high-glucose DMEM, used in cell isolation and expansion, was investigated in the presence and absence of basic fibroblast growth factor (bFGF)
25375819Initial cell yield was not affected by culturing medium, but MSCs expanded best in alpha-MEM supplemented with bFGF
24491556Proliferation and differentiation potentials of BMSCs treated with these growth factors for 2 months were evaluated and compared to BMSCs treated with FGF-2, which increased proliferation of BMSCs
24491556FGF-2 and -4 increased proliferation potentials at high levels, about 76- and 26-fold, respectively, for 2 months, while EGF and HGF increased proliferation of BMSCs by less than 2
24491556Treatment with FGF-2 rapidly induced activation of AKT and later induced ERK activation
24491556The basal level of phosphorylated ERK increased during serial passage of BMSCs treated with FGF-2
24491556But FGF-2 and FGF-4 suppressed LC3-II expression and down-regulated senescent cells during long-term (i
24491556Taken together, depletion of growth factors during serial passage could induce autophagy, senescence and down-regulation of stemness (proliferation via FGF-2/-4 and differentiation via HGF) through suppression of AKT and ERK signaling
24269635FOXO1 and FOXO3 phosphorylation was increased by IL-1beta, PDGF, bFGF, IGF-1, and the oxidant t-BHP
20627123Dynamic SUMO regulation controls the biological outcomes initiated by various growth factors involved in cartilage homeostasis, including basic fibroblast growth factors (bFGF or FGF-2), transforming growth factor-beta (TGF-beta) and insulin-like growth factor-1 (IGF-1)
19085240Proliferation, cell viability, mineralization assays, and mRNA levels were assessed for type I and III collagen, platelet-derived growth factor (PDGF)-1, basic fibroblast growth factor (bFGF), metalloproteinase (MMP)-2 and-8, and tissue inhibitor of metalloproteinases (TIMP)-1 and-2
19085240Gene expression analysis further showed that mRNA levels for bFGF, PDGF-1, and TIMP-2 were not affected by aging (p > 0
18313665TRAIL-stimulated production of several cytokines, IL-8, RANTES, MCP-1 and bFGF, and activation of caspases 1 and 8 was essential for this effect
18313665Antibodies to IL-8, RANTES, and bFGF blocked TRAIL-induced cell proliferation and further stimulated apoptosis
17532297Fibroblast growth factor-2 (FGF-2) stimulates the growth of hMSCs in vitro, but its mechanisms have not been clarified yet
17532297In this study, we investigated whether cellular senescence was involved in the stimulation of hMSCs growth by FGF-2 and the expression levels of transforming growth factor-beta1 and -beta2 (TGF-betas)
17532297Because hMSCs were induced cellular senescence due to long-term culture, FGF-2 decreased the percentage of senescent cells and suppressed G1 cell growth arrest through the suppression of p21(Cip1), p53, and p16(INK4a) mRNA expression levels
17532297Furthermore, the levels of TGF-betas mRNA expression in hMSCs were increased by long-term culture, but FGF-2 suppressed the increase of TGF-beta2 mRNA expression due to long-term culture
17532297These results suggest that FGF-2 suppresses the hMSCs cellular senescence dependent on the length of culture through down-regulation of TGF-beta2 expression
16755088Angiogenic growth factors secreted by EPCs, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b-FGF), hepatocyte growth factor (HGF), and macrophage chemoattractant protein (MCP-1) from the culture medium were also measured by enzyme-linked immunosorbent assay
16755088There was no significant difference of angiogenic growth factors (VEGF, HGF, b-FGF, and MCP-1) secreted by EPCs between the two groups
16609829In this study, venous ulcer fibroblasts are examined for cell cycle protein expression and modulation by basic fibroblast growth factor (bFGF)
16609829After 24 hr, one culture set was treated with bFGF (20 ng/mL) and the other was kept in culture medium only (untreated)
16609829Treatment with bFGF resulted in significant downregulation of p21 levels for fb-D (p = 0
16609829Treatment with bFGF increased ppRb significantly in fb-D (p = 0
16609829The aberrations seen in the cell cycle proteins in fb-D are similar to those seen in senescent cells; however, bFGF can modulate important cell cycle regulatory proteins, promoting a proliferative environment in fb-D that is not possible in a senescent cell
16609829The role of bFGF may be useful in the clinical treatment of venous ulcer pathology
16280018RESULTS: There was no correlation between age and hepatocyte growth factor (HGF), stem cell factor (SCF), and basic fibroblast growth factor (bFGF) secretion by fibroblasts
12704538Basic fibroblast growth factor (bFGF) has been shown to improve growth rates in these fibroblasts
12704538In bFGF-treated fibroblasts, levels of fibronectin and matrix metaloproteinase-2 (MMP-2), known to be up-regulated in senescence, were examined to determine whether bFGF induces changes in these markers of senescence with rescue of cellular proliferation
12704538Cells were plated at 3000 cells/plate and treated with bFGF (20 ng/mL) on days 1, 5, 8, and 11
12704538Total cell number was obtained on days 5 and 12 using the Coulter particle counter, and concurrently cells were plated at 10,000 cells/plate and treated with bFGF on the same schedule; cell lysate was harvested on day 12 for immunoblot analysis for MMP-2 and fibronectin
127045383-fold increase in growth in response to bFGF, and immunoblot analysis demonstrated an up-regulation of fibronectin and MMP-2 in response to bFGF
12704538This represents the possibility that by stimulating growth, bFGF may drive cells toward senescence
12704538This suggests clinical implication for the use of bFGF and other growth factors in general
12676798In this study, we examined the relationship between telomerase activity and endothelial cell proliferation as well as the regulation of this enzyme by fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor-A (VEGF)
12676798Treatment of quiescent HUVECs with FGF-2 restored telomerase activity in a time- and dose-dependent manner, whereas VEGF had no such effect, although both factors induced comparable mitogenic responses
12676798Serial passage in the presence of individual growth factors accelerated the accumulation of senescent cells in VEGF-treated cultures compared with cultures treated with FGF-2
12676798CONCLUSIONS: FGF-2, but not VEGF, restores telomerase activity and maintains the replicative capacity of endothelial cells
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