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Heparan Sulfate D-glucosaminyl 3-o-sulfotransferase 1 OKDB#: 3662
 Symbols: HS3ST1 Species: human
 Synonyms: 3OST, 3OST1,3OST|3OST1  Locus: 4p16 in Homo sapiens


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General Comment NCBI Summary: Heparan sulfate biosynthetic enzymes are key components in generating a myriad of distinct heparan sulfate fine structures that carry out multiple biologic activities. The enzyme encoded by this gene is a member of the heparan sulfate biosynthetic enzyme family. It possesses both heparan sulfate glucosaminyl 3-O-sulfotransferase activity, anticoagulant heparan sulfate conversion activity, and is a rate limiting enzyme for synthesis of anticoagulant heparan. This enzyme is an intraluminal Golgi resident protein.
General function Enzyme
Comment
Cellular localization Cytoplasmic, Golgi
Comment
Ovarian function
Comment
Expression regulated by
Comment
Ovarian localization
Comment
Follicle stages
Comment
Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name: None
type: null mutation
fertility: fertile
Comment: Normal levels of anticoagulant heparan sulfate are not essential for normal hemostasis. HajMohammadi S et al. Endothelial cell production of anticoagulant heparan sulfate (HS(act)) is controlled by the Hs3st1 gene, which encodes the rate-limiting enzyme heparan sulfate 3-O-sulfotransferase-1 (3-OST-1). In vitro, HS(act) dramatically enhances the neutralization of coagulation proteases by antithrombin. The in vivo role of HS(act) was evaluated by generating Hs3st1(-/-) knockout mice. Hs3st1(-/-) animals were devoid of 3-OST-1 enzyme activity in plasma and tissue extracts. Nulls showed dramatic reductions in tissue levels of HS(act) but maintained wild-type levels of tissue fibrin accumulation under both normoxic and hypoxic conditions. Given that vascular HS(act) predominantly occurs in the subendothelial matrix, mice were subjected to a carotid artery injury assay in which ferric chloride administration induces de-endothelialization and occlusive thrombosis. Hs3st1(-/-) and Hs3st1(+/+) mice yielded indistinguishable occlusion times and comparable levels of thrombin.antithrombin complexes. Thus, Hs3st1(-/-) mice did not show an obvious procoagulant phenotype. Instead, Hs3st1(-/-) mice exhibited genetic background-specific lethality and intrauterine growth retardation, without evidence of a gross coagulopathy. Our results demonstrate that the 3-OST-1 enzyme produces the majority of tissue HS(act). Surprisingly, this bulk of HS(act) is not essential for normal hemostasis in mice. Instead, 3-OST-1-deficient mice exhibited unanticipated phenotypes suggesting that HS(act) or additional 3-OST-1-derived structures may serve alternate biologic roles.

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created: Nov. 25, 2006, 10:03 a.m. by: hsueh   email:
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last update: Nov. 25, 2006, 10:10 a.m. by: hsueh    email:



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