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Inhibition of Bcl‐2‐dependent cell survival by a caspase inhibitor: a possible new pathway for Bcl‐2 to regulate cell death
Author(s) -
Rincheval V,
Renaud F,
Lemaire C,
Mignotte B,
Vayssière J.L
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01345-9
Subject(s) - apoptosis , suppressor , microbiology and biotechnology , caspase , programmed cell death , cleavage (geology) , cell culture , mutant , chemistry , cell survival , caspase 3 , apoptotic cell death , cancer research , biology , biochemistry , genetics , gene , paleontology , fracture (geology)
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.