EC Number   |
Protein Variants |
Reference |
|---|
   2.8.2.8 | K614A |
site-directed mutagenesis of the sulfotransferase domain of the bifunctional enzyme, complete loss of N-sulfotransferase activity |
645937 |
| 2.8.2.8 | more |
CHO cell mutant pgsE 606 with reduced N-sulfotransferase activity shows reduced expression of enzyme form NDST1, but normal expression level of enzyme form NDST2 |
645941 |
| 2.8.2.8 | more |
construction of conditional deficiency of the glycocalyx-modifying enzyme N-deacetylase-N-sulfotransferase-1 (Ndst1f/f TekCre+) which reduces aortic allograft inflammation. Conditional donor allograft Ndst1 deficiency (Ndst1-/-, C57Bl/6 background) is compared to systemic treatment with M-T7, a broad-spectrum chemokine glycosaminoglycan (GAG) inhibitor. Early rejection is significantly reduced in Ndst1-/- kidneys engrafted into wild-type BALB/c mice (Ndst1+/+) and comparable to M-T7 treatment in C57Bl/6 allografts. M-T7 is a 37 kDa Myxomavirus-derived secreted glycoprotein that possesses both broad spectrum, species-independent, C, CC and CXC chemokine inhibitory activity and a rabbit species-specific interferon gamma (IFNgamma) inhibitory activity. M-T7 activity is blunted in Ndst1-deficient mouse donor aortic transplants, a model for chronic TAV and vascular injury, but not in CC chemokine receptor deficient aortic allograft transplants, supporting M-T7 interference with chemokine-GAG interactions. M-T7 loses activity in Ndst1-/- allografts, while M-T7 point mutants with modified GAG chemokine binding display a range of anti-rejection activity. CD3+ T cells, HS and CXC chemokine staining, gene expression in NFkappaB and JAK/STAT pathways, and HS and CS disaccharide content are significantly altered with reduced rejection |
-, 762448 |
| 2.8.2.8 | more |
construction of mutant mice bearing a targeted disruption of the heparan sulfate-generating enzyme Ndst1, the mutant mice show severe developmental defects of the forebrain and the skull, overview, determination of molecular mechanisms leading to frontonasal dysplasia, impaired spinal and cranial neural tube fusion, and skeletal abnormalities in Ndst1 mutant embryos, impaired fibroblast growth factor, Hedgehog, and Wnt function may contribute to some of these phenotypes, organ defect phenotypes, overview |
673248 |
| 2.8.2.8 | more |
construction of NDST1+/- and NDST2-/- mice obtained by crossing NDST2-/- and NDST1 heterozygous mice, genotyping, neither NDST-1-/- nor NDST-2-/- mice display any obvious liver phenotype, deletion of one NDST gene does not influence expression of the other one, overview |
674699 |
| 2.8.2.8 | more |
early lens defects occur in Ndst1-knockout embryos, molecular defects underlying lens induction in Ndst1 mutants and phenotype, overview, Ndst1 knockout does not affect canonical bone morphogenic protein and Wnt signaling in the lens |
673255 |
| 2.8.2.8 | more |
knockout mice construction: mice lacking NDST2 show a phenotype restricted to connective tissue-type mast cells, while NDST1 deficiency is lethal, double-knockouts show early embryonic lethality, in utero effect of NDST3 deficiency |
645944 |
| 2.8.2.8 | more |
lack of NDST1 affects heparan sulfate structure in all tissues tested, with a dramatic reduction in N- and O-sulfation of the polysaccharide. Silencing the expression of NDST1, NDST2, 2-OST, and 3-OST3 by RNA interference efficiently decreases binding and activity of cyclophilin B |
704666 |
| 2.8.2.8 | more |
overexpression of NDST1 or NDST2 in recombinant human embryonic kidney 293 cells gives rise to different heparan sulfate (HS) N-sulfation patterns. The HS produced in cells transfected with NDST1 and NDST2 typically shows increased levels of N-sulfation. However, compared with cells overexpressing NDST1, the HS generated by cells overexpressing NDST2 has longer N-sulfation regions and a higher degree of N-sulfation |
760812 |
| 2.8.2.8 | more |
overexpression of NDST1 or NDST2 in recombinant human embryonic kidney 293 cells gives rise to different heparan sulfate (HS) N-sulfation patterns. The HS produced in cells transfected with NDST1 and NDST2 typically shows increased levels of N-sulfation. However, compared with cells overexpressing NDST1, the HS generated by cells overexpressing NDST2 has longer N-sulfation regions and a higher degree of N-sulfation. Furthermore, the transfection of NDST-deficient COS cells with NDST1 results in the formation of HS with a high affinity for FGF. In contrast, the overexpression of NDST1 in wild-type COS cells has very little effect on the N-acetylation to N-sulfation ratio of HS |
760812 |
