| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-71 |
Sentence |
denotes |
Regulation of c-Rel nuclear localization by binding of Ca2+/calmodulin. |
| T2 |
72-288 |
Sentence |
denotes |
The NF-kappa B/Rel family of transcription factors participates in the control of a wide array of genes, including genes involved in embryonic development and regulation of immune, inflammation, and stress responses. |
| T3 |
289-376 |
Sentence |
denotes |
In most cells, inhibitory I kappa B proteins sequester NF-kappa B/Rel in the cytoplasm. |
| T4 |
377-565 |
Sentence |
denotes |
Cellular stimulation results in the degradation of I kappa B and modification of NF-kappa B/Rel proteins, allowing NF-kappa B/Rel to translocate to the nucleus and act on its target genes. |
| T5 |
566-714 |
Sentence |
denotes |
Calmodulin (CaM) is a highly conserved, ubiquitously expressed Ca(2+) binding protein that serves as a key mediator of intracellular Ca(2+) signals. |
| T6 |
715-834 |
Sentence |
denotes |
Here we report that two members of the NF-kappa B/Rel family, c-Rel and RelA, interact directly with Ca(2+)-loaded CaM. |
| T7 |
835-1056 |
Sentence |
denotes |
The interaction with CaM is greatly enhanced by cell stimulation, and this enhancement is blocked by addition of I kappa B. c-Rel and RelA interact with CaM through a similar sequence near the nuclear localization signal. |
| T8 |
1057-1326 |
Sentence |
denotes |
Compared to the wild-type protein, CaM binding-deficient mutants of c-Rel exhibit increases in both nuclear accumulation and transcriptional activity on the interleukin 2 and granulocyte macrophage colony-stimulating factor promoters in the presence of a Ca(2+) signal. |
| T9 |
1327-1487 |
Sentence |
denotes |
Conversely, for RelA neither nuclear accumulation nor transcriptional activity on these promoters is increased by mutation of the sequence interacting with CaM. |
| T10 |
1488-1687 |
Sentence |
denotes |
Our results suggest that CaM binds c-Rel and RelA after their release from I kappa B and can inhibit nuclear import of c-Rel while letting RelA translocate to the nucleus and act on its target genes. |
| T11 |
1688-1794 |
Sentence |
denotes |
CaM can therefore differentially regulate the activation of NF-kappa B/Rel proteins following stimulation. |
| T1 |
0-71 |
Sentence |
denotes |
Regulation of c-Rel nuclear localization by binding of Ca2+/calmodulin. |
| T2 |
72-288 |
Sentence |
denotes |
The NF-kappa B/Rel family of transcription factors participates in the control of a wide array of genes, including genes involved in embryonic development and regulation of immune, inflammation, and stress responses. |
| T3 |
289-376 |
Sentence |
denotes |
In most cells, inhibitory I kappa B proteins sequester NF-kappa B/Rel in the cytoplasm. |
| T4 |
377-565 |
Sentence |
denotes |
Cellular stimulation results in the degradation of I kappa B and modification of NF-kappa B/Rel proteins, allowing NF-kappa B/Rel to translocate to the nucleus and act on its target genes. |
| T5 |
566-714 |
Sentence |
denotes |
Calmodulin (CaM) is a highly conserved, ubiquitously expressed Ca(2+) binding protein that serves as a key mediator of intracellular Ca(2+) signals. |
| T6 |
715-834 |
Sentence |
denotes |
Here we report that two members of the NF-kappa B/Rel family, c-Rel and RelA, interact directly with Ca(2+)-loaded CaM. |
| T7 |
835-1056 |
Sentence |
denotes |
The interaction with CaM is greatly enhanced by cell stimulation, and this enhancement is blocked by addition of I kappa B. c-Rel and RelA interact with CaM through a similar sequence near the nuclear localization signal. |
| T8 |
1057-1326 |
Sentence |
denotes |
Compared to the wild-type protein, CaM binding-deficient mutants of c-Rel exhibit increases in both nuclear accumulation and transcriptional activity on the interleukin 2 and granulocyte macrophage colony-stimulating factor promoters in the presence of a Ca(2+) signal. |
| T9 |
1327-1487 |
Sentence |
denotes |
Conversely, for RelA neither nuclear accumulation nor transcriptional activity on these promoters is increased by mutation of the sequence interacting with CaM. |
| T10 |
1488-1687 |
Sentence |
denotes |
Our results suggest that CaM binds c-Rel and RelA after their release from I kappa B and can inhibit nuclear import of c-Rel while letting RelA translocate to the nucleus and act on its target genes. |
| T11 |
1688-1794 |
Sentence |
denotes |
CaM can therefore differentially regulate the activation of NF-kappa B/Rel proteins following stimulation. |