{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T01:52:13Z","timestamp":1760061133032,"version":"build-2065373602"},"reference-count":20,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2001,5,18]],"date-time":"2001-05-18T00:00:00Z","timestamp":990144000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2001,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human interferon (HuIFN) has a protective effect against ultraviolet (UV)\u2010induced 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\u2010\u03b2. On the other hand, a large amount of p53 was found in both nuclear and cytoplasmic fractions of one SV40\u2010transformed XP and two SV40\u2010transformed CS cell strains irrespective of UV irradiation. Treatment with HuIFN\u2010\u03b2 reduced the level of pro\u2010apoptotic 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\u2010refractoriness caused by HuIFN\u2010\u03b2 in UV\u2010sensitive CS and XP cells. 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