Ectonucleoside Triphosphate diphosphohydrolase 1 Protéines (ENTPD1)

Zebrafish Ectonucleoside Triphosphate diphosphohydrolase 1 (ENTPD1) interaction partners

1. Extracellular ATP hydrolysis via NTPDase1 action inhibits synaptic transmission by pannexin 1 (Montrer PANX1 Protéines)-mediated increase in pH buffering of the synaptic cleft.

Human Ectonucleoside Triphosphate diphosphohydrolase 1 (ENTPD1) interaction partners

1. ur results demonstrate that CD39 is upregulated on conventional CD4 (Montrer CD4 Protéines)+ and CD8 (Montrer CD8A Protéines)+ T cells at sites of acute infection and inflammation, and that CD39 dampens responses to bacterial infection.

2. this paper shows that simultaneous overexpression of human E5NT and ENTPD1 protects porcine endothelial cells against H2O2-induced oxidative stress and cytotoxicity in vitro

3. The peripheral blood mononuclear cells (PBMC) from the transgenic pigs were more resistant to lysis by pooled complement-preserved normal human serum than that from wild type (WT) pig. Accordingly, GGTA1 (Montrer GGTA1 Protéines) mutated piglets expressing hCD39 will provide a new organ source for xenotransplantation research

4. Phosphoantigens (pAgs) induced expression of the ecto-ATPase CD39, which, however, not only hydrolyzed ATP but also abrogated the gammadelta T cell receptor (TCR) agonistic activity of self and microbial pAgs.

5. These studies showed that the G allele of rs3176891 marks a haplotype associated with increased clotting and platelet aggregation attributable to a promoter variant associated with increased transcription, expression, and activity of NTPDase1.

6. Transgenic expression of human CD39 is associated with increased renal fibrosis after ischemia in mice.

7. CD39 overexpression protects against cerebral ischemia in a transgenic mouse model.

8. Ablation of CD73 minimally effects in vivo thrombosis, but increased CD39 expression on hematopoietic-derived cells, especially monocytes, attenuates in vivo arterial thrombosis.

9. Data show that Th17(CD39+) cells are markedly diminished and fail to generate AMP (Montrer APRT Protéines)/adenosine, thereby limiting control of both target cell proliferation and IL-17 (Montrer IL17A Protéines) production in juvenile autoimmune liver disease (AILD).

10. concluded that CD39 and CD73 are molecular targets for the development of drugs for ALF (Montrer GTF2A1L Protéines) patients care

Mouse (Murine) Ectonucleoside Triphosphate diphosphohydrolase 1 (ENTPD1) interaction partners

1. Furthermore, our results suggest a crucial role for the enzyme CD39 in limiting P2X7 receptor (Montrer P2RX7 Protéines) proinflammatory responses since CD39(-/-) septic mice exhibited higher levels of IL-1beta (Montrer IL1B Protéines) in the brain.

2. CD39 expression in macrophages limits P2X7 (Montrer P2RX7 Protéines)-mediated pro-inflammatory responses, scavenging extracellular ATP and ultimately generating adenosine. CD39 genetic deletion exacerbates sepsis-induced experimental liver injury.

3. complete deletion of Cd39 paradoxically attenuates development of atherosclerosis in hyperlipidemic mice

4. Deletion of CD39 and CD73 or both caused an inhibition of the microglia ramified phenotype in the brain with a reduction in the length of processes, branching frequency and number of intersections with Sholl spheres. In vitro, unlike wild-type microglia, cd39-/- and cd73-/- microglial cells were less complex and did not respond to ATP with the transformation into a more ramified phenotype.

5. CD39 expression by Th17 cells allows the depletion of ATP and is crucial for IL-10 (Montrer IL10 Protéines) production and survival during the resolution of intestinal inflammation.

6. Cardiac-specific expression of CD39 reduces myocardial dysfunction and infarct size following ischemia-reperfusion injury

7. Data indicate that adenosine and CGS21680 upregulate CD39 and CD73 via E2F-1 (Montrer E2F1 Protéines) and CREB (Montrer CREB1 Protéines).

8. Acute cigarette smoke exposure induced CD39 upregulation in murine lungs and BALF cells. CD39 inhibition and deficiency led to augmented lung inflammation.

9. T Lymphocyte Inhibition by Tumor-Infiltrating Dendritic Cells Involves Ectonucleotidase CD39 but Not Arginase-1 (Montrer ARG1 Protéines).

10. CD39 role in neuroinflammation: CD39 defines regulatory phenotypes in CD4 (Montrer CD4 Protéines)-positive T cells.

Pig (Porcine) Ectonucleoside Triphosphate diphosphohydrolase 1 (ENTPD1) interaction partners

1. CD39 and CD73 and their enzymatic activities that convert extracellular nucleotides are highly expressed and could have special function in the valve