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TIP47 protects mitochondrial membrane integrity and inhibits oxidative‐stress‐induced cell death
Author(s) -
Hocsak E.,
Racz B.,
Szabo A.,
Mester L.,
Rapolti E.,
Pozsgai E.,
Javor Sz.,
Bellyei Sz.,
Gallyas F.,
Sumegi B.,
Szigeti A.
Publication year - 2010
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.2010.05.027
Subject(s) - mitochondrion , oxidative stress , microbiology and biotechnology , programmed cell death , cytoplasm , inner mitochondrial membrane , biology , oxidative phosphorylation , depolarization , membrane potential , chemistry , biochemistry , apoptosis , biophysics
We found that overexpression of tail interacting protein of 47 kDa (TIP47), but not its truncated form (t‐TIP47) protected NIH3T3 cells from hydrogen‐peroxide‐induced cell death, prevented the hydrogen‐peroxide‐induced mitochondrial depolarization determined by 5,5′,6,6′‐tetrachloro‐1,1′,3,3′‐tetraethyl‐benzimidazolylcarbocyanine iodide (JC1), while suppression of TIP47 in HeLa cells facilitated oxidative‐stress‐induced cell death. TIP47 was located to the cytoplasm of untreated cells, but some was associated to mitochondria in oxidative stress. Recombinant TIP47, but not t‐TIP47 increased the mitochondrial membrane potential (Δψ), and partially prevented Ca 2+ induced depolarization. It is assumed that TIP47 can bind to mitochondria in oxidative stress, and inhibit mitochondria mediated cell death by protecting mitochondrial membrane integrity.