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Podocyte-glomerular basement membrane interactions and cytoskeletal organization are disrupted in the glomeruli of the Ndst1-/- mutant mouse model
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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.
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Targeted ablation of Ndst1 in smooth muscle cells results in altered biomechanical properties of aorta.
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Loss of NDST1 causes defective diaphragm vascular development and congenital diaphragmatic hernia.
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The results of this study suggested that while Chst14 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
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embryonic stem cells lacking both NDST1 and NDST2, expressing a very low sulfated heparan sulfate, can take the initial step toward differentiation into all three germ layers
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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.
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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.
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Inhibitory peptides of the sulfotransferase domain of the heparan sulfate enzyme, N-deacetylase-N-sulfotransferase-1.
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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.
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These findings demonstrate a selective, highly penetrant, cell autonomous effect of Ndst1-mediated sulfation on lobuloalveolar development.
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Structural analyses of heparan sulfate produced by stable human embryonic 293 cells expressing mouse NDST-1 mutants indicate that the deacetylase of one enzyme and the sulfotransferase of another can act on the same glucosamine unit.
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major changes in the heparan sulfate composition in skeletal muscle tissue derived from NDST-1-/- mice and NDST-/- cultured myotubes.
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NDST-1 and C5-epimerase have roles in heparan sulfate structure alterations in mouse tissue
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NDST1 and NDST2 have roles in N-sulfation but not in 6-O-sulfation of heparan sulfate
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findings show that properly synthesized heparan sulfate is required for the normal development of the brain and face, and that Ndst1 is a modifier of heparan sulfate-dependent growth factor/morphogen signalling in those tissues
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analysis of liver NDST1 and NDST2 biosynthesis
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results establish an important role of Ndst1 function in FGF signaling during lens development
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Heparan sulfate Ndst1 gene function variably regulates multiple signaling pathways during mouse development.
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Reduction of N-sulfation due to deficiency in N-deacetylase/N-sulfotransferase-1 attenuated PDGF-BB binding in vitro, and led to pericyte detachment and delayed pericyte migration in vivo.