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Studies on p53 and Bax protein expression in Cockayne syndrome cells after UV irradiation and interferon‐β treatment
Author(s) -
Sugita Katsuo,
Chi XiaoJun,
Hiwasa Takaki,
Nobuo Nobuo
Publication year - 2001
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.917
Subject(s) - cockayne syndrome , xeroderma pigmentosum , interferon , fibroblast , irradiation , apoptosis , microbiology and biotechnology , ultraviolet irradiation , cytoplasm , cell , cell culture , chemistry , biology , virology , dna damage , dna , biochemistry , genetics , physics , nuclear physics
Human interferon (HuIFN) has a protective effect against ultraviolet (UV)‐induced killing of Cockayne syndrome (CS) and xeroderma pigmentosum (XP) cells. Irradiation with ultraviolet (UV) resulted in nuclear accumulation of p53 in normal human fibroblast cells, and this accumulation was suppressed by treatment with HuIFN‐β. On the other hand, a large amount of p53 was found in both nuclear and cytoplasmic fractions of one SV40‐transformed XP and two SV40‐transformed CS cell strains irrespective of UV irradiation. Treatment with HuIFN‐β reduced the level of pro‐apoptotic Bax protein without suppression of nuclear accumulation of p53 in the CS cells but not in the XP cells. These findings suggest that there are different mechanisms of UV‐refractoriness caused by HuIFN‐β in UV‐sensitive CS and XP cells. Copyright © 2001 John Wiley & Sons, Ltd.