
<ArticleTitle>Studies on <prot>p53</prot> and <prot>Bax</prot> protein expression in Cockayne syndrome cells after UV irradiation and <prot>interferon-beta</prot> treatment.</ArticleTitle>
<AbstractText>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 <prot>p53</prot> in normal human fibroblast cells, and this accumulation was suppressed by treatment with <prot>HuIFN-beta</prot>. On the other hand, a large amount of <prot>p53</prot> 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 <prot>HuIFN-beta</prot> reduced the level of pro-apoptotic <prot>Bax</prot> protein without suppression of nuclear accumulation of <prot>p53</prot> in the CS cells but not in the XP cells. These findings suggest that there are different mechanisms of UV-refractoriness caused by <prot>HuIFN-beta</prot> in UV-sensitive CS and XP cells.</AbstractText>
