Id |
Subject |
Object |
Predicate |
Lexical cue |
TextSentencer_T1 |
0-113 |
Sentence |
denotes |
Mice deficient in heparan sulfate 3-O-sulfotransferase-1: normal hemostasis with unexpected perinatal phenotypes. |
TextSentencer_T2 |
114-330 |
Sentence |
denotes |
Heparan sulfate that contains antithrombin binding sites is designated as anticoagulant heparan sulfate (HS(act)) since, in vitro, it dramatically enhances the neutralization of coagulation proteases by antithrombin. |
TextSentencer_T3 |
331-491 |
Sentence |
denotes |
Endothelial cell production of HS(act) is controlled by the Hs3st1 gene, which encodes the rate limiting enzyme-heparan sulfate 3-O-sulfotransferase-1 (Hs3st1). |
TextSentencer_T4 |
492-590 |
Sentence |
denotes |
It has long been proposed that levels of endothelial HS(act) may tightly regulate hemostatic tone. |
TextSentencer_T5 |
591-683 |
Sentence |
denotes |
This potential in vivo role of HS(act) was assessed by generating Hs3st1(-/-) knockout mice. |
TextSentencer_T6 |
684-804 |
Sentence |
denotes |
Hs3st1(-/-) and Hs3st1(+/+) mice were evaluated with a variety of methods, capable of detecting altered hemostatic tone. |
TextSentencer_T7 |
805-852 |
Sentence |
denotes |
However, both genotypes were indistinguishable. |
TextSentencer_T8 |
853-980 |
Sentence |
denotes |
Instead, Hs3st1(-/-) mice exhibited lethality on a specific genetic background and also showed intrauterine growth retardation. |
TextSentencer_T9 |
981-1033 |
Sentence |
denotes |
Neither phenotypes result from a gross coagulopathy. |
TextSentencer_T10 |
1034-1162 |
Sentence |
denotes |
So although this enzyme produces the majority of tissue HS(act), Hs3st1(-/-) mice do not show an obvious procoagulant phenotype. |
TextSentencer_T11 |
1163-1326 |
Sentence |
denotes |
These results suggest that the bulk of HS(act) is not essential for normal hemostasis and that hemostatic tone is not tightly regulated by total levels of HS(act). |
TextSentencer_T12 |
1327-1477 |
Sentence |
denotes |
Moreover, the unanticipated non-thrombotic phenotypes suggest structure(s) derived from this enzyme might serve additional/alternative biologic roles. |
T1 |
0-113 |
Sentence |
denotes |
Mice deficient in heparan sulfate 3-O-sulfotransferase-1: normal hemostasis with unexpected perinatal phenotypes. |
T2 |
114-330 |
Sentence |
denotes |
Heparan sulfate that contains antithrombin binding sites is designated as anticoagulant heparan sulfate (HS(act)) since, in vitro, it dramatically enhances the neutralization of coagulation proteases by antithrombin. |
T3 |
331-491 |
Sentence |
denotes |
Endothelial cell production of HS(act) is controlled by the Hs3st1 gene, which encodes the rate limiting enzyme-heparan sulfate 3-O-sulfotransferase-1 (Hs3st1). |
T4 |
492-590 |
Sentence |
denotes |
It has long been proposed that levels of endothelial HS(act) may tightly regulate hemostatic tone. |
T5 |
591-683 |
Sentence |
denotes |
This potential in vivo role of HS(act) was assessed by generating Hs3st1(-/-) knockout mice. |
T6 |
684-804 |
Sentence |
denotes |
Hs3st1(-/-) and Hs3st1(+/+) mice were evaluated with a variety of methods, capable of detecting altered hemostatic tone. |
T7 |
805-852 |
Sentence |
denotes |
However, both genotypes were indistinguishable. |
T8 |
853-980 |
Sentence |
denotes |
Instead, Hs3st1(-/-) mice exhibited lethality on a specific genetic background and also showed intrauterine growth retardation. |
T9 |
981-1033 |
Sentence |
denotes |
Neither phenotypes result from a gross coagulopathy. |
T10 |
1034-1162 |
Sentence |
denotes |
So although this enzyme produces the majority of tissue HS(act), Hs3st1(-/-) mice do not show an obvious procoagulant phenotype. |
T11 |
1163-1326 |
Sentence |
denotes |
These results suggest that the bulk of HS(act) is not essential for normal hemostasis and that hemostatic tone is not tightly regulated by total levels of HS(act). |
T12 |
1327-1477 |
Sentence |
denotes |
Moreover, the unanticipated non-thrombotic phenotypes suggest structure(s) derived from this enzyme might serve additional/alternative biologic roles. |