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The involvement of caspase‐11 in TPEN‐induced apoptosis
Author(s) -
Lee Jong-Min,
Kim Yu-Jin,
Ra Hana,
Kang Shin-Jung,
Han SeungJin,
Koh Jae-Young,
Kim Yang-Hee
Publication year - 2008
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/j.febslet.2008.04.056
Subject(s) - apoptosis , cycloheximide , caspase , caspase 3 , caspase 8 , caspase 9 , microbiology and biotechnology , chemistry , inhibitor of apoptosis domain , caspase 2 , biology , programmed cell death , biochemistry , protein biosynthesis
The depletion of intracellular zinc with N , N , N ′, N ′‐tetrakis(2‐pyridylmethyl)ethylenediamine (TPEN) induces protein synthesis‐dependent apoptosis. Here we examined the involvement of caspase induction in apoptosis. Among the examined caspases, only caspase‐11 was increased by TPEN. Caspase‐11 activity also increased, which resulted in caspase‐3 activation. Cycloheximide or actinomycin D blocked caspase‐11 induction, reduced caspase‐11 and ‐3 activation, and attenuated TPEN‐induced neuronal apoptosis. Blockade of caspase‐11 by a chemical inhibitor or genetic deletion attenuated TPEN‐induced apoptosis, indicating a critical role of caspase‐11 in TPEN‐induced apoptosis. Although mitochondria‐mediated caspase‐9/‐3 activation also contributed to TPEN‐induced apoptosis, caspase‐11 is likely a key inducible apoptosis‐inducing protein.