3.6.1.19: nucleoside-triphosphate diphosphatase
This is an abbreviated version!
For detailed information about nucleoside-triphosphate diphosphatase, go to the full flat file.
Word Map on EC 3.6.1.19
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3.6.1.19
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thiopurine
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ribavirin
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azathioprine
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virological
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purinergic
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pegylated
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pharmacogenetic
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rbv-induced
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ribavirin-induced
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ecto-nucleotidase
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s-methyltransferase
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dihydrate
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ecto-5'-nucleotidase
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apyrase
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peg-ifn
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ntpdase3
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mercaptopurine
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ectonucleoside
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xanthosine
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deoxyinosine
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ecto-enzymes
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mutt
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molecular biology
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medicine
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biotechnology
- 3.6.1.19
-
thiopurine
- ribavirin
- azathioprine
-
virological
-
purinergic
-
pegylated
-
pharmacogenetic
-
rbv-induced
-
ribavirin-induced
- ecto-nucleotidase
-
s-methyltransferase
-
dihydrate
- ecto-5'-nucleotidase
- apyrase
-
peg-ifn
- ntpdase3
- mercaptopurine
-
ectonucleoside
- xanthosine
- deoxyinosine
-
ecto-enzymes
-
mutt
- molecular biology
- medicine
- biotechnology
deleted, now included with EC 3.6.1.9
ECTree
Advanced search results
Results in table
2 Expression 6 General Information 46 kcat/KM [mM/s] 61 PDB ID
General Information
General Information on EC 3.6.1.19 - nucleoside-triphosphate diphosphatase
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malfunction
physiological function
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ITPA deficiency causes disruption of the sarcomeric structure and dysfunction of car-diomyocytes. Itpa-deficient mice exhibit peri-orpostnatal lethality dependent on the genetic background. The heart of the Itpa-deficient mouse is structurally and functionally abnormal. Significantly higher levels of deoxyinosine and inosine are detected in nuclear DNA and RNA prepared from Itpa-deficient embryos compared to wild type embryos. Accumulation of ITP and dITP is responsible for the harmful effects observed in the Itpa-deficient mouse
malfunction
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enzyme knockdown sensitizes HeLa cells to 6-N-hydroxylaminopurine-induced DNA breaks and apoptosis, and results in elevated mutagenesis in response to 6-N-hydroxylaminopurine treatment. Individuals with defective ITPase are predisposed to genome damage by impurities in nucleotide pools. They are also at an elevated risk for degenerative diseases and cancer
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the enzyme prevents 6-N hydroxylaminopurine-induced apoptosis, DNA damage and mutagenesis in human cells
physiological function
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extracellular ATP, by upregulating ecto-nucleoside triphosphate diphosphohydrolase 2 and ecto-5'-nucleotidase and altering the enzyme membrane topology, affects local kinetics of ATP metabolism and signal transduction
physiological function
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parasites with high enzymic activity show increased survival rate in LPS/IFN-gamma-activated mouse cells, by inhibiting the host-cell NO production. Inhibition of enzyme activity reduces the parasite survival rates, an effect associated with increased macrophage NO production. Enzymic activity generates substrate for the production of extracellular adenosine, which binds to A2B receptors and reduces IL-12 and TNF-alpha produced by activated macrophages, thus inhibiting NO production
physiological function
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upon combined expression of human ecto-5'-nucleotidase and ecto-nucleoside triphosphate diphosphohydrolase 1 in pig endothelial cells using F2A sequence bearing construct, addition of AMP increases production of adenosine in the medium to 14.2 microM while it remains below 1 microM in controls. A marked increase of adenosine formation from ADP or ATP is observed only in cells transfected with both enzymes
ECTree
Advanced search results
Results | in table |
---|---|
2 | Expression |
6 | General Information |
46 | kcat/KM [mM/s] |
61 | PDB ID |
General Information
General Information on EC 3.6.1.19 - nucleoside-triphosphate diphosphatase
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
malfunction
physiological function
-
ITPA deficiency causes disruption of the sarcomeric structure and dysfunction of car-diomyocytes. Itpa-deficient mice exhibit peri-orpostnatal lethality dependent on the genetic background. The heart of the Itpa-deficient mouse is structurally and functionally abnormal. Significantly higher levels of deoxyinosine and inosine are detected in nuclear DNA and RNA prepared from Itpa-deficient embryos compared to wild type embryos. Accumulation of ITP and dITP is responsible for the harmful effects observed in the Itpa-deficient mouse
malfunction
-
enzyme knockdown sensitizes HeLa cells to 6-N-hydroxylaminopurine-induced DNA breaks and apoptosis, and results in elevated mutagenesis in response to 6-N-hydroxylaminopurine treatment. Individuals with defective ITPase are predisposed to genome damage by impurities in nucleotide pools. They are also at an elevated risk for degenerative diseases and cancer
-
the enzyme prevents 6-N hydroxylaminopurine-induced apoptosis, DNA damage and mutagenesis in human cells
physiological function
-
extracellular ATP, by upregulating ecto-nucleoside triphosphate diphosphohydrolase 2 and ecto-5'-nucleotidase and altering the enzyme membrane topology, affects local kinetics of ATP metabolism and signal transduction
physiological function
-
parasites with high enzymic activity show increased survival rate in LPS/IFN-gamma-activated mouse cells, by inhibiting the host-cell NO production. Inhibition of enzyme activity reduces the parasite survival rates, an effect associated with increased macrophage NO production. Enzymic activity generates substrate for the production of extracellular adenosine, which binds to A2B receptors and reduces IL-12 and TNF-alpha produced by activated macrophages, thus inhibiting NO production
physiological function
-
upon combined expression of human ecto-5'-nucleotidase and ecto-nucleoside triphosphate diphosphohydrolase 1 in pig endothelial cells using F2A sequence bearing construct, addition of AMP increases production of adenosine in the medium to 14.2 microM while it remains below 1 microM in controls. A marked increase of adenosine formation from ADP or ATP is observed only in cells transfected with both enzymes