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Literature summary for 3.6.1.5 extracted from
- The differential effect of apyrase treatment and hCD39 overexpression on chronic renal fibrosis after ischemia-reperfusion injury (2017), Transplantation, 101, e194-e204 .
Application
| Application | Comment | Organism |
|---|---|---|
| medicine | augmenting CD39 activity is a potential therapy to improve both short- and long-term outcomes of ischemia-reperfusion injury (IRI) by reducing the extracellular concentration of proinflammatory ATP and promoting adenosine generation. In mouse models of IRI, treatment with soluble CD39 (apyrase) or expression of a human CD39 (hCD39) transgene in mice (CD39Tg mice) reduce the severity of acute kidney injury (AKI) as evidenced by decreased serum creatinine and reduced tubular injury score at 24 hours | Homo sapiens |
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| recombinant expression of human enzyme in C57BL/6 mice | Homo sapiens |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | construction of hCD39 transgene expressing CD39Tg mice from C57BL/6 wild-type expressing human CD39, hCD39 transgene expression in CD39Tg mice reduces ischemia-induced acute renal injury, but exacerbates chronic renal injury. In comparison with wild-type littermates, hCD39 transgenic mice are protected from acute renal injury at 24 hours, but have increased renal fibrosis at 4 weeks post-ischemia-reperfusion injury (IRI), hCD39 transgene expression is localized to the vascular endothelium at baseline and does not affect total renal nucleotide and nucleoside levels during ischemia. But hCD39 transgene is more widespread at 4 weeks post-IRI and is associated with higher renal adenosine levels at 4 weeks post-IRI compared with wild-type littermates | Homo sapiens |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| extracellular | - |
Homo sapiens | - |
- |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ADP + H2O | Homo sapiens | - |
AMP + phosphate | - |
? |  |
| ATP + 2 H2O | Homo sapiens | overall reaction | AMP + 2 phosphate | - |
? | |
| ATP + H2O | Homo sapiens | - |
ADP + phosphate | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | P49961 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| kidney | - |
Homo sapiens | - |
Specific Activity [micromol/min/mg]
| Specific Activity Minimum [µmol/min/mg] | Specific Activity Maximum [µmol/min/mg] | Comment | Organism |
|---|---|---|---|
| additional information | - |
kidney purinergic nucleotide and nucleoside levels (nmol/g wet weight) in vehicle- and apyrase-treated mice at baseline 23.5 minutes of ischemia, and at 24 hours and 4 weeks after ischemia-reperfusion, overview | Homo sapiens |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ADP + H2O | - |
Homo sapiens | AMP + phosphate | - |
? | |
| ATP + 2 H2O | overall reaction | Homo sapiens | AMP + 2 phosphate | - |
? | |
| ATP + H2O | - |
Homo sapiens | ADP + phosphate | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| 5' ectonucleotidase | - |
Homo sapiens |
| CD39 | - |
Homo sapiens |
| ectonucleotidase | - |
Homo sapiens |
| ENTPDase1 | - |
Homo sapiens |
| hCD39 | - |
Homo sapiens |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | differential effect of apyrase treatment and hCD39 overexpression on chronic renal fibrosis after ischemia-reperfusion injury (IRI), overview. Hydrolysis of ATP to adenosine diphosphate (ADP) by the ectonucleotidase CD39 (ENTPDase1) is an important step in reducing the proinflammatory effects of ATP CD39 also hydrolyses ADP to adenosine monophosphate (AMP), which is subsequently converted to adenosine by CD73 (5' ectonucleotidase). Augmenting CD39 activity is a potential therapy to improve both short- and long-term outcomes of IRI by reducing the extracellular concentration of proinflammatory ATP and promoting adenosine generation. hCD39 transgene expression in CD39Tg mice (C57BL/6 wild-type expressing human CD39) reduces ischemia-induced acute renal injury, but exacerbates chronic renal injury. Apyrase does not modify baseline ATP, ADP, AMP, adenosine or inosine levels, but reduces ATP, ADP, and AMP levels during ischemia. Apyrase attenuates the increase in A2BR mRNA levels at week 4 post-IRI | Homo sapiens |
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