EC Number   |
General Information |
Reference |
|---|
   3.1.4.39 | evolution |
mouse and human enzymes show high structural homology |
728853 |
| 3.1.4.39 | evolution |
the enzyme belongs to the ENPP family, but ATX/ENPP2 is a unique lysoPLD with no functional redundancy within the ENPP family, overview. The enzyme and its ENPP family members can be divided into two main subgroups, namely ENPP1-3 and ENPP4-7. ATX/ENPP2 and its closest relatives, ENPP1 and ENPP3, have two N-terminal somatomedin B (SMB)-like domains, a central phosphodiesterase (PDE) domain and a C-terminal nuclease (NUC)-like domain. The second subgroup (ENPP4-7) has only the PDE domain in common. ATX/NPP2 is a secreted protein, while the other ENPPs are transmembrane proteins, either type-I (ENPP4-7) or type-II (ENPP1-3) |
728930 |
| 3.1.4.39 | malfunction |
a recombinant ATX mutant, lacking lysoPLD activity, or heat-inactived ATX also induces lung epithelial cell migration |
714106 |
| 3.1.4.39 | malfunction |
adipocyte-specific knockout FATX-KO mice or mice treated with the lysophosphatidic acid receptor antagonist Ki16425 gain more weight and accumulate more adipose tissue than wild-type or control mice fed a high fat diet |
729338 |
| 3.1.4.39 | malfunction |
ATX inhibitor bithionol remarkably decreases lymphocyte migration to the intestine and ameliorates both dextran sodium sulfate-induced colitis and CD4-induced ileocolitis, administration of bithionol or 1-bromo-3(s)-hydroxy-4-(palmitoyloxy) butylphosphonate significantly decreases transmigration of splenocytes through high-endothelial-like vessels induced by TNF-alpha |
-, 730301 |
| 3.1.4.39 | malfunction |
ATX SMB2 mutants with impaired binding to beta3 integrins display reduced LPA generating capacity. Mutation of a charged, surface-exposed residue at the N-terminus of the ATX SMB2 domain significantly reduces binding of ATX to platelet integrins. The effects of ATX on platelet and cell-associated LPA production, but not hydrolysis of small molecule or detergent-solubilized substrates, are attenuated by point mutations in the SMB2 that impair integrin binding |
715637 |
| 3.1.4.39 | malfunction |
down-regulation of endogenous autotaxin expression in 4T1 cells inhibits osteolytic bone metastasis formation independently of primary tumor growth in vivo |
706456 |
| 3.1.4.39 | malfunction |
E9.5 ATX null mutants exhibit a failure of neural tube closure, most likely independent of the circulatory failure, which correlates with decreased cell proliferation and increased cell death, obligatory deletion results to embryonic lethality most likely due to aberrant vascular branching morphogenesis and chorio-allantoic fusion |
703366 |
| 3.1.4.39 | malfunction |
fasting decreases enzyme activity. Nutritional deficiency of 18 : 2- and 18 : 1-containing phosphatidylcholines causes selective reduction of corresponding unsaturated lysophosphatidylcholines relative to other species in the blood circulation. Prolonged fasting of rats causes a greater decrease in the level of lysophosphatidylcholine in the liver than that of phosphatidylethanolamine |
-, 729349 |
| 3.1.4.39 | malfunction |
in Enpp2 knockout mouse embryos, lysosomes in the visceral endoderm cells are fragmented |
704588 |
