Id |
Subject |
Object |
Predicate |
Lexical cue |
T2 |
0-82 |
Sentence |
denotes |
Protein degradation by the proteasome generates functional intracellular peptides. |
T2 |
0-82 |
Sentence |
denotes |
Protein degradation by the proteasome generates functional intracellular peptides. |
T3 |
83-223 |
Sentence |
denotes |
Pep5, a peptide derived from Cyclin D2, induces cell death in tumor cell lines and reduces the volume of rat C6 glioblastoma tumors in vivo. |
T3 |
83-223 |
Sentence |
denotes |
Pep5, a peptide derived from Cyclin D2, induces cell death in tumor cell lines and reduces the volume of rat C6 glioblastoma tumors in vivo. |
T4 |
224-374 |
Sentence |
denotes |
Here, we chose the human MDA-MB-231 breast cancer cells to evaluate the mechanism of cell death induced by pep5 in different phases of the cell cycle. |
T4 |
224-374 |
Sentence |
denotes |
Here, we chose the human MDA-MB-231 breast cancer cells to evaluate the mechanism of cell death induced by pep5 in different phases of the cell cycle. |
T5 |
375-542 |
Sentence |
denotes |
Fluorescently labeled pep5, monitored by real time confocal microscopy, entered the MDA-MB-231 cells 3min after application and localized to the nucleus and cytoplasm. |
T5 |
375-542 |
Sentence |
denotes |
Fluorescently labeled pep5, monitored by real time confocal microscopy, entered the MDA-MB-231 cells 3min after application and localized to the nucleus and cytoplasm. |
T6 |
543-698 |
Sentence |
denotes |
Pep5-induced cell death was increased when the MDA-MB-231 cell population was arrested at the G1/S transition or in S phase compared to asynchronous cells. |
T6 |
543-698 |
Sentence |
denotes |
Pep5-induced cell death was increased when the MDA-MB-231 cell population was arrested at the G1/S transition or in S phase compared to asynchronous cells. |
T7 |
699-837 |
Sentence |
denotes |
Pep5 induced permanent extracellular signal-regulated kinase (ERK1/2) phosphorylation in MDA-MB-231 cells synchronized in G1/S or S phase. |
T7 |
699-837 |
Sentence |
denotes |
Pep5 induced permanent extracellular signal-regulated kinase (ERK1/2) phosphorylation in MDA-MB-231 cells synchronized in G1/S or S phase. |
T8 |
838-1027 |
Sentence |
denotes |
Affinity chromatography followed by mass spectrometry identified CLIC1 and Plectin as the only two proteins that interacted with pep5 in both asynchronous and synchronized MDA-MB-231 cells. |
T8 |
838-1027 |
Sentence |
denotes |
Affinity chromatography followed by mass spectrometry identified CLIC1 and Plectin as the only two proteins that interacted with pep5 in both asynchronous and synchronized MDA-MB-231 cells. |
T9 |
1028-1230 |
Sentence |
denotes |
These interactions could explain the long-lasting ERK1/2 phosphorylation and the cytoskeleton perturbations in the MDA-MB-231 cells, in which the stress fibers' integrity is affected by pep5 treatments. |
T9 |
1028-1230 |
Sentence |
denotes |
These interactions could explain the long-lasting ERK1/2 phosphorylation and the cytoskeleton perturbations in the MDA-MB-231 cells, in which the stress fibers' integrity is affected by pep5 treatments. |
T10 |
1231-1365 |
Sentence |
denotes |
These data suggest that pep5 has potential therapeutic properties for treating specific types of cancers, such as breast cancer cells. |
T10 |
1231-1365 |
Sentence |
denotes |
These data suggest that pep5 has potential therapeutic properties for treating specific types of cancers, such as breast cancer cells. |