anti-NDST1 (NDST1) Antikörper

Human N-Deacetylase/N-Sulfotransferase (Heparan Glucosaminyl) 1 (NDST1) Interaktionspartner

1. Compound heterozygous mutations in NDST1 were identified, in the heparan sulfate N deacetylatase domain of one allele and the sulfotransferase domain of the other allele. This report expands the phenotypic spectrum of Ndst1 deficiency in humans.

2. Among the genes enriched in this screening, the authors found that TM9SF2 (zeige TM9SF2 Antikörper) is critical for N-sulfation of heparan sulfate and therefore for chikungunya virus infection because it is involved in the proper localization and stability of NDST1.

3. Our data confirm NDST1 mutations as a cause of autosomal recessive intellectual disability with a distinctive phenotype, and support an important function of NDST1 in human development.

4. demonstrate the essential role of domain cooperation within NDST-1 in producing HS with specific domain structures

5. Upregulation of NDST1 is associated with chemoresistance in breast cancer.

6. These findings establish NDST1 as a target of miR (zeige MLXIP Antikörper)-24 and demonstrate how such NDST1 suppression in endothelial cells results in reduced responsiveness to VEGFA (zeige VEGFA Antikörper)

7. MicroRNA-191 targets N-deacetylase/N-sulfotransferase 1 and promotes cell growth in human gastric carcinoma cell line MGC803

8. Inhibitory peptides of the sulfotransferase domain of the heparan sulfate enzyme, N-deacetylase-N-sulfotransferase-1.

9. Altered expression of NDST-1 mRNA in glomerular basement membrane in puromycin aminonucleoside nephrosis.

10. effect of targeted inactivation of the Ndst1 gene on the inflammatory response associated with allergic inflammation

Mouse (Murine) N-Deacetylase/N-Sulfotransferase (Heparan Glucosaminyl) 1 (NDST1) Interaktionspartner

1. Podocyte-glomerular basement membrane interactions and cytoskeletal organization are disrupted in the glomeruli of the Ndst1-/- mutant mouse model

2. Although the renal phenotype of the Ndst1(-/-) mouse is mild, the data show that heparan chain N-sulfation plays a key role in podocyte organization.

3. Targeted ablation of Ndst1 in smooth muscle cells results in altered biomechanical properties of aorta.

4. Loss of NDST1 causes defective diaphragm vascular development and congenital diaphragmatic hernia.

5. The results of this study suggested that while Chst14 (zeige CHST14 Antikörper) and its enzymatic products might be of limited importance for neural development, they may contribute to the regeneration-restricting environment in the adult mammalian nervous system

6. embryonic stem cells lacking both NDST1 and NDST2 (zeige NDST2 Antikörper), expressing a very low sulfated (zeige SULF1 Antikörper) heparan sulfate, can take the initial step toward differentiation into all three germ layers

7. Deletion of N-deacetylase-N-sulfotransferase1 in smooth muscle did not influence any of the blood pressure parameters measured despite significant decrease in aorta and thoracodorsal artery luminal area.

8. Lowered expression of NDST1 also results in a higher sulfate content of the heparin synthesized and is accompanied by increased levels of stored MC proteases.

9. Inhibitory peptides of the sulfotransferase domain of the heparan sulfate enzyme, N-deacetylase-N-sulfotransferase-1.

10. These data provide new evidence that modification of heparan sulfate fine structure through deletion of Ndst1 is sufficient to decrease vascular smooth muscle cell proliferation and alter vascular remodeling.