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We have linked a deleterious mutation in HS6ST1 to familial self-limited delayed puberty and show that heterozygous Hs6st1 loss causes delayed puberty in mice. In this study, the observed overlap in potentially pathogenic mutations contributing to the phenotypes of self-limited delayed puberty and hypogonadotropic hypogonadism was limited to this one gene.
RT-PCR analysis showed that the overall transcriptional activity of the main Heparan Sulfate biosynthesis-involved genes (EXT1, EXT2, NDST1, NDST2, GLCE, HS2ST1, HS3ST1, HS3ST2, HS6ST1, HS6ST2, SULF1, SULF2, HPSE) was decreased by 1.5-2-fold in Grade II-III glioma.
HS6ST-1 and HS6ST-2 have roles in regulating the angiogenic program in ovarian cancer cells affecting HB-EGF signaling and subsequent expression of angiogenic cytokines by cancer cells
Hs6st1 and Hs2st generate conditions conducive to corpus callosum development.
idiopathic hypogonadotrophic hypogonadism--associated HS6ST1 mutations display reduced activity in vitro and in vivo, suggesting that HS6ST1 and the complex modifications of extracellular sugars are critical for normal development
we have characterized HS6ST-2 and HS6ST-1 human isologues, including their chromosomal localizations,HS6STs could also transfer sulphate to N -sulphoglucosamine residues located at the non-reducing terminal of HS with high affinity.
Distinct expression patterns of Sulf1 and Hs6st1 spatially regulate heparan sulfate sulfation during prostate development.
both HS6ST-1 and HS6ST-2 are involved in 6-O-sulfation of heparin and that the proper packaging and storage of tryptase
6OST1 is predominantly transcribed in epithelial and neural-derived tissues during development
Data show that high expression of 6-O-sulfotransferase (6-OST)-1, 2, or 3 resulted in increased 6-O-sulfation of N-sulfated and N-acetylated glucosamine units, and in altered heparan sulfate domain structure.
Hs2st and/or Hs6st1 expression coincides with Slit expression domains at locations where retinal ganglion cell(RGC) axons make navigation errors in Hs2st-/- and Hs6st1-/- mutants, and Hs6st1-/-RGC axons are less sensitive to Slit2 repulsion.
there is a critical role for HS 6-O sulfation by Hs6st1 in postnatal processes
The protein encoded by this gene is a member of the heparan sulfate biosynthetic enzyme family. Heparan sulfate biosynthetic enzymes are key components in generating a myriad of distinct heparan sulfate fine structures that carry out multiple biological activities. This enzyme is a type II integral membrane protein and is responsible for 6-O-sulfation of heparan sulfate. This enzyme does not share significant sequence similarity with other known sulfotransferases. A pseudogene located on chromosome 1 has been found for this gene.
, heparan-sulfate 6-O-sulfotransferase 1
, heparan-sulfate 6-sulfotransferase
, Heparan-sulfate 6-O-sulfotransferase 1
, heparan sulfate 6-sulfotransferase
, HS 6-OST-1A
, heparan sulfate 6-O-sulfotransferase 1
, heparan-sulfate 6-O-sulfotransferase 1-A