Dephosphorylation of p53 during cell death by N-α-tosyl- -phenylalanyl chloromethyl ketone

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The apoptotic function of N-α-tosyl- -phenylalanyl chloromethyl ketone (TPCK) was investigated in cultured human colorectal carcinoma cells (HCT116). TPCK-induced apoptosis was shown to be p53-dependent in HCT116 cells during the early stage of incubation. The function of p53 was required for TPCK-induced activation of caspase-3 and caspase-7. TPCK promoted dephosphorylation of p53 on serine residues at 6, 9, 46, 376, and 378 in parallel with the activation of p53 transcriptional activity. HCT116 p53−/− cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.
Publisher
Elsevier
Issue Date
2003-07-11
Keywords

TPCK; p53; Dephosphorylation; Apoptosis; Caspase

Citation

Biochemical and Biophysical Research Communications, Vol.306, No.4, pp.954-958

ISSN
0006-291X
DOI
10.1016/S0006-291X(03)01088-X
URI
http://hdl.handle.net/10203/14374
Appears in Collection
BS-Conference Papers(학술회의논문)

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