Inhibition of Bcl‐2‐dependent cell survival by a caspase inhibitor: a possible new pathway for Bcl‐2 to regulate cell death

FEBS Letters

Vayssière, J.L¹  Rincheval, V¹  Renaud, F¹  Lemaire, C¹  Mignotte, B¹ 

[1] Université de Versailles/St Quentin-en-Yvelines, UPRESA-CNRS 8087, Laboratoire génome, cellule et informatique, 45 avenue des Etats-Unis, 78035 Versailles Cedex, France

关键词: Bcl-2;    Z-VAD-fmk;    Apoptosis;    Large T antigen;    Rb;    LT;    large T antigen;    Tet;    tetracycline;   

DOI  :  10.1016/S0014-5793(99)01345-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The REtsAF cell line expresses a temperature-sensitive mutant of the SV40 large tumor antigen. At restrictive temperature (39.5°C), the cells undergo p53-mediated apoptosis, which can be inhibited by Bcl-2. Here, we show that Z-VAD-fmk, a caspase inhibitor, can suppress the Bcl-2-dependent cell survival at 39.5°C. This result suggests that a caspase-like activity can act as an inhibitor of apoptosis in this model, downstream of Bcl-2. Our results also suggest that this activity may be up-regulated by Bcl-2 and may be responsible for cleavage of the tumor suppressor Rb protein.

【 授权许可】

Unknown