Expression of RB C pocket fragments in HSF induces delayed cell cycle progression and sensitizes to apoptosis upon cellular stresses
- Affiliated Author(s)
- 백원기; 서성일; 서민호; 권택규; 박종욱
- Alternative Author(s)
- Baek, Won Ki; Suh, Seong Il; Suh, Min Ho; Kwon, Taeg Kyu; Park, Jong Wook
- Journal Title
- Cell Proliferation
- Issued Date
- The retinoblastoma protein (RB) plays an important role in growth suppression through the formation of multiple protein complexes with its target proteins using A/B and C pockets. Even though the A/B and C pockets co-operate for growth suppression, the function of RB in growth arrest is inhibited by the coexpression of RB C fragments with full length RB in the absence of p53, which implies that C pocket fragments are likely to act as a dominant-negative inhibitor of RB function. In contrast, the loss of the RB functions in the presence of p53 triggers a cell cycle arrest or apoptosis by p53-dependent pathways. Thus, it still remains to be elucidated whether the expression of RB C pocket fragments in the presence of p53 induces delayed cell cycle progression and sensitizes cells to apoptosis through p53-dependent pathways. Our results show that the expression of RB C pocket fragments not only induces delayed cell cycle progression, which is mediated by the down-regulation of cyclin A, cyclin E, and E2F-1, but also sensitizes cells to apoptosis through p53-dependent pathways.
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