Protein Variants | Comment | Organism |
---|---|---|
additional information | Cd39-/- mice phenotype with increased levels of macrophages and neutrophils, cerebral ischemia effects, overview. 50% increase in the number of alphaMbeta2-integrin high-expressing monocytes in Cd39-/- mice compared with wild-type controls. Although an acute rescue from CD39 deficiency can be obtained through administration of an apyrase or solCD39 analog, a permanent rescue can be obtained via bone marrow reconstitution with CD39-bearing cells | Mus musculus |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
cell surface | - |
Mus musculus | 9986 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + 2 H2O | Mus musculus | dissipation of ATP by CD39 reduces P2X7 receptor stimulation and thereby suppresses baseline leukocyte alphaMbeta2-integrin expression. As alphaMbeta2-integrin blockade reverses the postischemic, inflammatory phenotype of Cd39-/- mice. Phosphohydrolytic activity on the leukocyte surface suppresses cell-cell interactions that would otherwise promote thrombosis or inflammation | AMP + 2 phosphate | - |
? | |
additional information | Mus musculus | CD39 can regulate platelet activation from either the endothelial or leukocyte compartment. CD39 on monocytes and neutrophils regulates their own sequestration into ischemic cerebral tissue, by catabolizing nucleotides released by injured cells, thereby inhibiting their chemotaxis, adhesion, and transmigration. Leukocyte ectoapyrases modulate the ambient vascular nucleotide milieu. Dissipation of ATP by CD39 reduces P2X7 receptor stimulation and thereby suppresses baseline leukocyte alphaMbeta2-integrin expression. As alphaMbeta2-integrin blockade reverses the postischemic, inflammatory phenotype of Cd39-/- mice | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
bone marrow | - |
Mus musculus | - |
endothelium | - |
Mus musculus | - |
leukocyte | - |
Mus musculus | - |
monocyte | - |
Mus musculus | - |
neutrophil | - |
Mus musculus | - |
RAW-264.7 cell | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + 2 H2O | - |
Mus musculus | AMP + 2 phosphate | - |
? | |
ATP + 2 H2O | dissipation of ATP by CD39 reduces P2X7 receptor stimulation and thereby suppresses baseline leukocyte alphaMbeta2-integrin expression. As alphaMbeta2-integrin blockade reverses the postischemic, inflammatory phenotype of Cd39-/- mice. Phosphohydrolytic activity on the leukocyte surface suppresses cell-cell interactions that would otherwise promote thrombosis or inflammation | Mus musculus | AMP + 2 phosphate | - |
? | |
additional information | CD39 can regulate platelet activation from either the endothelial or leukocyte compartment. CD39 on monocytes and neutrophils regulates their own sequestration into ischemic cerebral tissue, by catabolizing nucleotides released by injured cells, thereby inhibiting their chemotaxis, adhesion, and transmigration. Leukocyte ectoapyrases modulate the ambient vascular nucleotide milieu. Dissipation of ATP by CD39 reduces P2X7 receptor stimulation and thereby suppresses baseline leukocyte alphaMbeta2-integrin expression. As alphaMbeta2-integrin blockade reverses the postischemic, inflammatory phenotype of Cd39-/- mice | Mus musculus | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
CD39 | - |
Mus musculus |
ectoapyrase | - |
Mus musculus |