| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-90 |
Sentence |
denotes |
The metalloprotease ADAM10 generates soluble interleukin-2 receptor alpha (sCD25) in vivo. |
| T1 |
0-90 |
Sentence |
denotes |
The metalloprotease ADAM10 generates soluble interleukin-2 receptor alpha (sCD25) in vivo. |
| T2 |
91-273 |
Sentence |
denotes |
The cytokine interleukin-2 (IL-2) plays a critical role in controlling the immune homeostasis by regulating the proliferation and differentiation of immune cells, especially T cells. |
| T2 |
91-273 |
Sentence |
denotes |
The cytokine interleukin-2 (IL-2) plays a critical role in controlling the immune homeostasis by regulating the proliferation and differentiation of immune cells, especially T cells. |
| T3 |
274-404 |
Sentence |
denotes |
IL-2 signaling is mediated via the IL-2 receptor (IL-2R) complex, which consists of the IL-2Rα (CD25), the IL-2Rβ, and the IL-2Rγ. |
| T3 |
274-404 |
Sentence |
denotes |
IL-2 signaling is mediated via the IL-2 receptor (IL-2R) complex, which consists of the IL-2Rα (CD25), the IL-2Rβ, and the IL-2Rγ. |
| T4 |
405-528 |
Sentence |
denotes |
While the latter are required for signal transduction, IL-2Rα controls the ligand-binding affinity of the receptor complex. |
| T4 |
405-528 |
Sentence |
denotes |
While the latter are required for signal transduction, IL-2Rα controls the ligand-binding affinity of the receptor complex. |
| T5 |
529-684 |
Sentence |
denotes |
A soluble form of the IL-2Rα (sIL-2Rα) is found constitutively in human serum, though its levels are increased under various pathophysiological conditions. |
| T5 |
529-684 |
Sentence |
denotes |
A soluble form of the IL-2Rα (sIL-2Rα) is found constitutively in human serum, though its levels are increased under various pathophysiological conditions. |
| T6 |
685-857 |
Sentence |
denotes |
The sIL-2Rα originates partly from activated T cells through proteolytic cleavage, but neither the responsible proteases nor stimuli that lead to IL-2Rα cleavage are known. |
| T6 |
685-857 |
Sentence |
denotes |
The sIL-2Rα originates partly from activated T cells through proteolytic cleavage, but neither the responsible proteases nor stimuli that lead to IL-2Rα cleavage are known. |
| T7 |
858-1049 |
Sentence |
denotes |
Here, we show that the metalloproteases ADAM10 and ADAM17 can cleave the IL-2Rα and generate a soluble ectodomain, which functions as a decoy receptor that inhibits IL-2 signaling in T cells. |
| T7 |
858-1049 |
Sentence |
denotes |
Here, we show that the metalloproteases ADAM10 and ADAM17 can cleave the IL-2Rα and generate a soluble ectodomain, which functions as a decoy receptor that inhibits IL-2 signaling in T cells. |
| T8 |
1050-1207 |
Sentence |
denotes |
We demonstrate that ADAM10 is mainly responsible for constitutive shedding of the IL-2Rα, while ADAM17 is involved in IL-2Rα cleavage upon T cell activation. |
| T8 |
1050-1207 |
Sentence |
denotes |
We demonstrate that ADAM10 is mainly responsible for constitutive shedding of the IL-2Rα, while ADAM17 is involved in IL-2Rα cleavage upon T cell activation. |
| T9 |
1208-1339 |
Sentence |
denotes |
In vivo, we found that mice with a CD4-specific deletion of ADAM10, but not ADAM17, show reduced steady-state sIL-2Rα serum levels. |
| T9 |
1208-1339 |
Sentence |
denotes |
In vivo, we found that mice with a CD4-specific deletion of ADAM10, but not ADAM17, show reduced steady-state sIL-2Rα serum levels. |
| T10 |
1340-1620 |
Sentence |
denotes |
We propose that the identification of proteases involved in sIL-2Rα generation will allow for manipulation of IL-2Rα cleavage, especially as constitutive and induced cleavage of IL-2Rα are executed by different proteases, and thus offer a novel opportunity to alter IL-2 function. |
| T10 |
1340-1620 |
Sentence |
denotes |
We propose that the identification of proteases involved in sIL-2Rα generation will allow for manipulation of IL-2Rα cleavage, especially as constitutive and induced cleavage of IL-2Rα are executed by different proteases, and thus offer a novel opportunity to alter IL-2 function. |