Abstract
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-beta. 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-beta 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-beta in UV-sensitive CS and XP cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
