| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-114 |
Sentence |
denotes |
G6PC3 mutations are associated with a major defect of glycosylation: a novel mechanism for neutrophil dysfunction. |
| T1 |
0-114 |
Sentence |
denotes |
G6PC3 mutations are associated with a major defect of glycosylation: a novel mechanism for neutrophil dysfunction. |
| T1 |
0-114 |
Sentence |
denotes |
G6PC3 mutations are associated with a major defect of glycosylation: a novel mechanism for neutrophil dysfunction. |
| TextSentencer_T2 |
115-282 |
Sentence |
denotes |
Glucose-6-phosphatase, an enzyme localized in the endoplasmic reticulum (ER), catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosphate. |
| T2 |
115-282 |
Sentence |
denotes |
Glucose-6-phosphatase, an enzyme localized in the endoplasmic reticulum (ER), catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosphate. |
| T2 |
115-282 |
Sentence |
denotes |
Glucose-6-phosphatase, an enzyme localized in the endoplasmic reticulum (ER), catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosphate. |
| TextSentencer_T3 |
283-383 |
Sentence |
denotes |
In humans, there are three differentially expressed glucose-6-phosphatase catabolic genes (G6PC1-3). |
| T3 |
283-383 |
Sentence |
denotes |
In humans, there are three differentially expressed glucose-6-phosphatase catabolic genes (G6PC1-3). |
| T3 |
283-383 |
Sentence |
denotes |
In humans, there are three differentially expressed glucose-6-phosphatase catabolic genes (G6PC1-3). |
| TextSentencer_T4 |
384-533 |
Sentence |
denotes |
Recently, it has been shown that mutations in the G6PC3 gene result in a syndrome associating congenital neutropenia and various organ malformations. |
| T4 |
384-533 |
Sentence |
denotes |
Recently, it has been shown that mutations in the G6PC3 gene result in a syndrome associating congenital neutropenia and various organ malformations. |
| T4 |
384-533 |
Sentence |
denotes |
Recently, it has been shown that mutations in the G6PC3 gene result in a syndrome associating congenital neutropenia and various organ malformations. |
| TextSentencer_T5 |
534-644 |
Sentence |
denotes |
The enzymatic function of G6PC3 is dependent on G6P transport into the ER, mediated by G6P translocase (G6PT). |
| T5 |
534-644 |
Sentence |
denotes |
The enzymatic function of G6PC3 is dependent on G6P transport into the ER, mediated by G6P translocase (G6PT). |
| T5 |
534-644 |
Sentence |
denotes |
The enzymatic function of G6PC3 is dependent on G6P transport into the ER, mediated by G6P translocase (G6PT). |
| TextSentencer_T6 |
645-733 |
Sentence |
denotes |
Mutations in the gene encoding G6PT result in glycogen storage disease type-1b (GSD-1b). |
| T6 |
645-733 |
Sentence |
denotes |
Mutations in the gene encoding G6PT result in glycogen storage disease type-1b (GSD-1b). |
| T6 |
645-733 |
Sentence |
denotes |
Mutations in the gene encoding G6PT result in glycogen storage disease type-1b (GSD-1b). |
| TextSentencer_T7 |
734-851 |
Sentence |
denotes |
Interestingly, GSD-1b patients exhibit a similar neutrophil dysfunction to that observed in G6PC3-deficient patients. |
| T7 |
734-851 |
Sentence |
denotes |
Interestingly, GSD-1b patients exhibit a similar neutrophil dysfunction to that observed in G6PC3-deficient patients. |
| T7 |
734-851 |
Sentence |
denotes |
Interestingly, GSD-1b patients exhibit a similar neutrophil dysfunction to that observed in G6PC3-deficient patients. |
| TextSentencer_T8 |
852-1061 |
Sentence |
denotes |
To better understand the causes of neutrophil dysfunction in both diseases, we have studied the neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase of patients with G6PC3 and G6PT syndromes. |
| T8 |
852-1061 |
Sentence |
denotes |
To better understand the causes of neutrophil dysfunction in both diseases, we have studied the neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase of patients with G6PC3 and G6PT syndromes. |
| T8 |
852-1061 |
Sentence |
denotes |
To better understand the causes of neutrophil dysfunction in both diseases, we have studied the neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase of patients with G6PC3 and G6PT syndromes. |
| TextSentencer_T9 |
1062-1273 |
Sentence |
denotes |
Unexpectedly, sodium dodecyl sulfate-polyacrylamide gel electrophoresis experiments indicated hypo-glycosylation of gp91(phox), the electron-transporting component of the NADPH oxidase, in all of these patients. |
| T9 |
1062-1273 |
Sentence |
denotes |
Unexpectedly, sodium dodecyl sulfate-polyacrylamide gel electrophoresis experiments indicated hypo-glycosylation of gp91(phox), the electron-transporting component of the NADPH oxidase, in all of these patients. |
| T9 |
1062-1273 |
Sentence |
denotes |
Unexpectedly, sodium dodecyl sulfate-polyacrylamide gel electrophoresis experiments indicated hypo-glycosylation of gp91(phox), the electron-transporting component of the NADPH oxidase, in all of these patients. |
| TextSentencer_T10 |
1274-1487 |
Sentence |
denotes |
Rigorous mass spectrometric glycomic profiling showed that most of the complex-type antennae which characterize the neutrophil N-glycome of healthy individuals were severely truncated in the patients' neutrophils. |
| T10 |
1274-1487 |
Sentence |
denotes |
Rigorous mass spectrometric glycomic profiling showed that most of the complex-type antennae which characterize the neutrophil N-glycome of healthy individuals were severely truncated in the patients' neutrophils. |
| T10 |
1274-1487 |
Sentence |
denotes |
Rigorous mass spectrometric glycomic profiling showed that most of the complex-type antennae which characterize the neutrophil N-glycome of healthy individuals were severely truncated in the patients' neutrophils. |
| TextSentencer_T11 |
1488-1569 |
Sentence |
denotes |
A comparable truncation of the core 2 antenna of the O-glycans was also observed. |
| T11 |
1488-1569 |
Sentence |
denotes |
A comparable truncation of the core 2 antenna of the O-glycans was also observed. |
| T11 |
1488-1569 |
Sentence |
denotes |
A comparable truncation of the core 2 antenna of the O-glycans was also observed. |
| TextSentencer_T12 |
1570-1770 |
Sentence |
denotes |
This aberrant neutrophil glycosylation is predicted to have profound effects on the neutrophil function and merit designation of both syndromes as a new class of congenital disorders of glycosylation. |
| T12 |
1570-1770 |
Sentence |
denotes |
This aberrant neutrophil glycosylation is predicted to have profound effects on the neutrophil function and merit designation of both syndromes as a new class of congenital disorders of glycosylation. |
| T12 |
1570-1770 |
Sentence |
denotes |
This aberrant neutrophil glycosylation is predicted to have profound effects on the neutrophil function and merit designation of both syndromes as a new class of congenital disorders of glycosylation. |