| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-80 |
Sentence |
denotes |
Cardiac troponin T is essential in sarcomere assembly and cardiac contractility. |
| TextSentencer_T2 |
81-307 |
Sentence |
denotes |
Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. |
| TextSentencer_T3 |
308-414 |
Sentence |
denotes |
Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. |
| TextSentencer_T4 |
415-505 |
Sentence |
denotes |
TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. |
| TextSentencer_T5 |
506-623 |
Sentence |
denotes |
Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. |
| TextSentencer_T6 |
624-702 |
Sentence |
denotes |
We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. |
| TextSentencer_T7 |
703-853 |
Sentence |
denotes |
We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. |
| TextSentencer_T8 |
854-1002 |
Sentence |
denotes |
Tnnt2, together with alpha-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. |
| TextSentencer_T9 |
1003-1177 |
Sentence |
denotes |
Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. |
| TextSentencer_T10 |
1178-1466 |
Sentence |
denotes |
This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans. |
| T1 |
0-80 |
Sentence |
denotes |
Cardiac troponin T is essential in sarcomere assembly and cardiac contractility. |
| T2 |
81-307 |
Sentence |
denotes |
Mutations of the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible for 15% of all cases of familial hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. |
| T3 |
308-414 |
Sentence |
denotes |
Mutant proteins are thought to act through a dominant-negative mode that impairs function of heart muscle. |
| T4 |
415-505 |
Sentence |
denotes |
TNNT2 mutations can also lead to dilated cardiomyopathy, a leading cause of heart failure. |
| T5 |
506-623 |
Sentence |
denotes |
Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described. |
| T6 |
624-702 |
Sentence |
denotes |
We show that the zebrafish silent heart (sih) mutation affects the gene tnnt2. |
| T7 |
703-853 |
Sentence |
denotes |
We characterize two mutated alleles of sih that severely reduce tnnt2 expression: one affects mRNA splicing, and the other affects gene transcription. |
| T8 |
854-1002 |
Sentence |
denotes |
Tnnt2, together with alpha-tropomyosin (Tpma) and cardiac troponins C and I (Tnni3), forms a calcium-sensitive regulatory complex within sarcomeres. |
| T9 |
1003-1177 |
Sentence |
denotes |
Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects. |
| T10 |
1178-1466 |
Sentence |
denotes |
This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans. |