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| Official Symbol of Gene | Entpd2 |
| Species | Rattus norvegicus |
| Entrez Gene ID | 64467 |
| Official Full Name | ectonucleoside triphosphate diphosphohydrolase 2 |
| Also known as | Cd39l1; NTPDase2 |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSRNOG00000013102 AllianceGenome:RGD:69266 |
| Map Location | 3p13 |
| Detected Sample | spinal cord |
| Sample Detail | N/A |
| Detected Method | Immunofluorescence |
| Disease | EAE |
| Disease subtype | N/A |
| Population | female rats of DA strain |
| Sample Size | counted from at least six sections, from three different animals per each EAE phase |
| Pubmed ID | 29163045 |
| Year | 2017 |
| Title | Down-regulation of NTPDase2 and ADP-sensitive P2 Purinoceptors Correlate with Severity of Symptoms during Experimental Autoimmune Encephalomyelitis |
| Expression | down-regulation |
| Risk type | Disease risk |
| Result | During the course of EAE, the intensity of NTPDase2-ir visibly decreased in the white matter . |
| Mechanism/Pathway | For MS/EAE to develop, the coordinated action of several immune and neural cell types is required.ATP initiates and coordinates a cross-talk between infiltrated T-cells and resident microglia and astrocytes, by recruiting T cells and facilitating their extravasation into the CNS, potentiating the release of cytokines and chemokines and activating and attracting microglia and astrocytes, which govern further pathology in MS.Moreover, ATP activates low-affinity P2X7 receptors and potentiates the release of interleukin-1β and cyclooxygenase induction, causing demyelination,oligodendrocyte death and axonal damage.Extracellular ATP is eliminated by the coordinated action of ectonucleotidase enzyme cascade.An ectonucleotidase, with specific substrate affinity and restricted expression in the brain is ectonucleoside triphosphate diphosphohydrolase-2 (NTPDase2;previously known as Ecto-ATPase, or CD39L1).The enzyme preferentially catalyzes the dephosphorylation of ATP to ADP, generating a ligand for P2Y1, P2Y12 and P2Y13 receptors.There is compelling evidence for the critical involvement of purinergic signaling in the control of different aspects of MS/EAE pathophysiology. |

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