| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-95 |
Sentence |
denotes |
Structural requirements for alpha-latrotoxin binding and alpha-latrotoxin-stimulated secretion. |
| T2 |
96-182 |
Sentence |
denotes |
A study with calcium-independent receptor of alpha-latrotoxin (CIRL) deletion mutants. |
| T3 |
183-374 |
Sentence |
denotes |
Stimulation of neurotransmitter release by alpha-latrotoxin requires its binding to the calcium-independent receptor of alpha-latrotoxin (CIRL), an orphan neuronal G protein-coupled receptor. |
| T4 |
375-684 |
Sentence |
denotes |
CIRL consists of two noncovalently bound subunits, p85, a heptahelical integral membrane protein, and p120, a large extracellular polypeptide with domains homologous to lectin, olfactomedin, mucin, the secretin receptor family, and a novel structural motif common for large orphan G protein-coupled receptors. |
| T5 |
685-908 |
Sentence |
denotes |
The analysis of CIRL deletion mutants indicates that the high affinity alpha-latrotoxin-binding site is located within residues 467-891, which comprise the first transmembrane segment of p85 and the C-terminal half of p120. |
| T6 |
909-1031 |
Sentence |
denotes |
The N-terminal lectin, olfactomedin, and mucin domains of p120 are not required for the interaction with alpha-latrotoxin. |
| T7 |
1032-1255 |
Sentence |
denotes |
Soluble p120 and all its fragments, which include the 467-770 residues, bind alpha-latrotoxin with low affinity suggesting the importance of membrane-embedded p85 for the stabilization of the complex of the toxin with p120. |
| T8 |
1256-1653 |
Sentence |
denotes |
Two COOH-terminal deletion mutants of CIRL, one with the truncated cytoplasmic domain and the other with only one transmembrane segment left of seven, supported both alpha-latrotoxin-induced calcium uptake in HEK293 cells and alpha-latrotoxin-stimulated secretion when expressed in chromaffin cells, although with a different dose dependence than wild-type CIRL and its N-terminal deletion mutant. |
| T9 |
1654-1799 |
Sentence |
denotes |
Thus the signaling domains of CIRL are not critically important for the stimulation of exocytosis in intact chromaffin cells by alpha-latrotoxin. |
| T1 |
0-95 |
Sentence |
denotes |
Structural requirements for alpha-latrotoxin binding and alpha-latrotoxin-stimulated secretion. |
| T2 |
96-182 |
Sentence |
denotes |
A study with calcium-independent receptor of alpha-latrotoxin (CIRL) deletion mutants. |
| T3 |
183-374 |
Sentence |
denotes |
Stimulation of neurotransmitter release by alpha-latrotoxin requires its binding to the calcium-independent receptor of alpha-latrotoxin (CIRL), an orphan neuronal G protein-coupled receptor. |
| T4 |
375-684 |
Sentence |
denotes |
CIRL consists of two noncovalently bound subunits, p85, a heptahelical integral membrane protein, and p120, a large extracellular polypeptide with domains homologous to lectin, olfactomedin, mucin, the secretin receptor family, and a novel structural motif common for large orphan G protein-coupled receptors. |
| T5 |
685-908 |
Sentence |
denotes |
The analysis of CIRL deletion mutants indicates that the high affinity alpha-latrotoxin-binding site is located within residues 467-891, which comprise the first transmembrane segment of p85 and the C-terminal half of p120. |
| T6 |
909-1031 |
Sentence |
denotes |
The N-terminal lectin, olfactomedin, and mucin domains of p120 are not required for the interaction with alpha-latrotoxin. |
| T7 |
1032-1255 |
Sentence |
denotes |
Soluble p120 and all its fragments, which include the 467-770 residues, bind alpha-latrotoxin with low affinity suggesting the importance of membrane-embedded p85 for the stabilization of the complex of the toxin with p120. |
| T8 |
1256-1653 |
Sentence |
denotes |
Two COOH-terminal deletion mutants of CIRL, one with the truncated cytoplasmic domain and the other with only one transmembrane segment left of seven, supported both alpha-latrotoxin-induced calcium uptake in HEK293 cells and alpha-latrotoxin-stimulated secretion when expressed in chromaffin cells, although with a different dose dependence than wild-type CIRL and its N-terminal deletion mutant. |
| T9 |
1654-1799 |
Sentence |
denotes |
Thus the signaling domains of CIRL are not critically important for the stimulation of exocytosis in intact chromaffin cells by alpha-latrotoxin. |