Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-110 |
Sentence |
denotes |
Hereditary alpha 2-plasmin inhibitor deficiency caused by a transport-deficient mutation (alpha 2-PI-Okinawa). |
T2 |
111-189 |
Sentence |
denotes |
Deletion of Glu137 by a trinucleotide deletion blocks intracellular transport. |
T3 |
190-343 |
Sentence |
denotes |
alpha 2-Plasmin inhibitor is the most important physiological inhibitor of fibrinolysis; hence, its deficiency results in a severe hemorrhagic diathesis. |
T4 |
344-466 |
Sentence |
denotes |
We have cloned and characterized a mutant alpha 2-plasmin inhibitor gene from an individual homozygous for the deficiency. |
T5 |
467-629 |
Sentence |
denotes |
By sequencing all the coding exons and exon-intron boundaries of the gene, a trinucleotide deletion in exon VII that results in deletion of Glu137 was identified. |
T6 |
630-699 |
Sentence |
denotes |
We have designated this variant as alpha 2-plasmin inhibitor Okinawa. |
T7 |
700-912 |
Sentence |
denotes |
Using DNA samples amplified with the polymerase chain reaction, hybridization analysis by oligonucleotide probes confirmed the presence of this mutation in all the affected family members, including both parents. |
T8 |
913-1158 |
Sentence |
denotes |
To elucidate the mechanism by which this mutation leads to the deficiency, a eukaryotic expression plasmid for alpha 2-plasmin inhibitor containing this mutation was constructed and transfected into COS-7 cells for transient expression analysis. |
T9 |
1159-1458 |
Sentence |
denotes |
Immunoprecipitation analysis and enzyme-linked immunosorbent assay revealed that the mutant alpha 2-plasmin inhibitor synthesized is mostly retained within the cells as an endoglycosidase H-sensitive form, and only a small portion of it is secreted into the medium as a neuraminidase-sensitive form. |
T10 |
1459-1658 |
Sentence |
denotes |
These results suggest that the Glu137 deletion leads to the alpha 2-plasmin inhibitor deficiency by causing a block in its intracellular transport from the endoplasmic reticulum to the Golgi complex. |
T1 |
0-110 |
Sentence |
denotes |
Hereditary alpha 2-plasmin inhibitor deficiency caused by a transport-deficient mutation (alpha 2-PI-Okinawa). |
T2 |
111-189 |
Sentence |
denotes |
Deletion of Glu137 by a trinucleotide deletion blocks intracellular transport. |
T3 |
190-343 |
Sentence |
denotes |
alpha 2-Plasmin inhibitor is the most important physiological inhibitor of fibrinolysis; hence, its deficiency results in a severe hemorrhagic diathesis. |
T4 |
344-466 |
Sentence |
denotes |
We have cloned and characterized a mutant alpha 2-plasmin inhibitor gene from an individual homozygous for the deficiency. |
T5 |
467-629 |
Sentence |
denotes |
By sequencing all the coding exons and exon-intron boundaries of the gene, a trinucleotide deletion in exon VII that results in deletion of Glu137 was identified. |
T6 |
630-699 |
Sentence |
denotes |
We have designated this variant as alpha 2-plasmin inhibitor Okinawa. |
T7 |
700-912 |
Sentence |
denotes |
Using DNA samples amplified with the polymerase chain reaction, hybridization analysis by oligonucleotide probes confirmed the presence of this mutation in all the affected family members, including both parents. |
T8 |
913-1158 |
Sentence |
denotes |
To elucidate the mechanism by which this mutation leads to the deficiency, a eukaryotic expression plasmid for alpha 2-plasmin inhibitor containing this mutation was constructed and transfected into COS-7 cells for transient expression analysis. |
T9 |
1159-1458 |
Sentence |
denotes |
Immunoprecipitation analysis and enzyme-linked immunosorbent assay revealed that the mutant alpha 2-plasmin inhibitor synthesized is mostly retained within the cells as an endoglycosidase H-sensitive form, and only a small portion of it is secreted into the medium as a neuraminidase-sensitive form. |
T10 |
1459-1658 |
Sentence |
denotes |
These results suggest that the Glu137 deletion leads to the alpha 2-plasmin inhibitor deficiency by causing a block in its intracellular transport from the endoplasmic reticulum to the Golgi complex. |