HCSGD entry for NUDT1


1. General information

Official gene symbolNUDT1
Entrez ID4521
Gene full namenudix (nucleoside diphosphate linked moiety X)-type motif 1
Other gene symbolsMTH1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0003924GTPase activityTASmolecular_function
GO:0005634NucleusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005739MitochondrionIDAcellular_component
GO:0005759Mitochondrial matrixIDAcellular_component
GO:0005829CytosolTAScellular_component
GO:0006184GTP catabolic processIDAbiological_process
GO:0006195Purine nucleotide catabolic processIDAbiological_process
GO:0006200ATP catabolic processIDAbiological_process
GO:0006203DGTP catabolic processIDA IEAbiological_process
GO:0006281DNA repairIEAbiological_process
GO:0006298Mismatch repairICbiological_process
GO:0006979Response to oxidative stressTASbiological_process
GO:00084138-oxo-7,8-dihydroguanosine triphosphate pyrophosphatase activityIDA IEAmolecular_function
GO:0030515SnoRNA bindingIEA ISSmolecular_function
GO:0034656Nucleobase-containing small molecule catabolic processTASbiological_process
GO:00355398-oxo-7,8-dihydrodeoxyguanosine triphosphate pyrophosphatase activityIDAmolecular_function
GO:0042262DNA protectionIDAbiological_process
GO:0044281Small molecule metabolic processTASbiological_process
GO:0046061DATP catabolic processIDAbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0047693ATP diphosphatase activityIDAmolecular_function
GO:0050072M7G(5')pppN diphosphatase activityISSmolecular_function
GO:0055086Nucleobase-containing small molecule metabolic processTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.99643331180.00124315190.99999024730.0671438525

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

Data sourceUp or downLog fold change
GSE11954Down-0.3427290559
GSE13712_SHEARDown-0.4328583170
GSE13712_STATICDown-0.6702603207
GSE19018Down-0.1342166938
GSE19899_A1Down-1.0857768631
GSE19899_A2Down-1.8846410938
PubMed_21979375_A1Down-1.4800831065
PubMed_21979375_A2Down-2.5144975705
GSE35957Down-1.5067932004
GSE36640Down-1.8909467800
GSE54402Down-0.4551574625
GSE9593Down-0.3535941852
GSE43922Down-0.0198038789
GSE24585Down-0.3457239486
GSE37065Down-0.0748243246
GSE28863_A1Down-0.2537735091
GSE28863_A2Up0.0089326069
GSE28863_A3Up0.0359579953
GSE28863_A4Up0.0940790239
GSE48662Down-0.0073260582

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: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25921542Accordingly, LPC provoked oxidative DNA injury, whereas the gene expressions of DNA repair enzyme (OGG1, MUTYH, MTH1) remained unchanged
22790201Human Mut T Homolog 1 (MTH1): a roadblock for the tumor-suppressive effects of oncogenic RAS-induced ROS
22790201We have recently shown that oncogenic RAS-induced DNA damage and attendant premature senescence can be prevented by overexpressing human MutT Homolog 1 (MTH1), the major mammalian detoxifier of the oxidized DNA precursor, 8-oxo-dGTP
22790201Within this context, we will discuss the implications of MTH1 upregulation in oncogenic RAS-sustaining cells as a beneficial adaptive change that inhibits ROS-mediated cell senescence and participates in the maintenance of ROS-associated tumor-promoting mechanisms
22790201Accordingly, targeting MTH1 in RAS-transformed tumor cells will not only induce proliferative defects but also potentially enhance therapeutic cytotoxicity by shifting cellular response away from pro-survival mechanisms
19118192Suppression of MTH1 expression, which hydrolyzes 8-oxo-dGTP, was accompanied by increased total cellular 8-oxoguanine levels and caused early-passage primary and telomerase-immortalized human skin fibroblasts to rapidly undergo senescence, doing so without altering cellular ROS levels
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