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Downregulation of peroxiredoxin V stimulates formation of etoposide‐induced double‐strand DNA breaks
Author(s) -
Kropotov Andrei V.,
Grudinkin Pavel S.,
Pleskach Nadezha M.,
Gavrilov Boris A.,
Tomilin Nikolai V.,
Zhivotovsky Boris
Publication year - 2004
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.2004.07.011
Subject(s) - etoposide , dna damage , peroxiredoxin , microbiology and biotechnology , downregulation and upregulation , chemistry , gene knockdown , poly adp ribose polymerase , dna , transcription (linguistics) , ku70 , phosphorylation , biology , apoptosis , biochemistry , gene , enzyme , genetics , polymerase , peroxidase , linguistics , philosophy , chemotherapy
Antioxidant protein Peroxiredoxin V (PrxV) is located in mitochondria and peroxisomes but is also present in the nucleus. Here, we show that nuclear PrxV associates with coilin‐containing bodies suggesting possible interaction of this protein with transcription complexes. We also studied etoposide‐induced phosphorylation of histone H2AX (γ‐H2AX) in human cells in which PrxV activity was downregulated (knockdown, KD‐clones) or compromised by overexpression of redox‐negative (RD) protein. In KD clones, but not in RD‐clones, formation of etoposide‐induced γ‐H2AX was increased, indicating that PrxV inhibits conversion of topoisomerase II cleavage complexes into double‐strand DNA breaks but this inhibition is not caused by its antioxidant activity.