TY - JOUR
T1 - Fas ligand
T2 - A sensor for DNA damage critical in skin cancer etiology
AU - Hill, Laurie L.
AU - Ouhtit, Allal
AU - Loughlin, Susan M.
AU - Kripke, Margaret L.
AU - Ananthaswamy, Honnavara N.
AU - Owen-Schaub, Laurie B.
PY - 1999/8/6
Y1 - 1999/8/6
N2 - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.
AB - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.
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U2 - 10.1126/science.285.5429.898
DO - 10.1126/science.285.5429.898
M3 - Article
C2 - 10436160
AN - SCOPUS:0033529581
SN - 0036-8075
VL - 285
SP - 898
EP - 900
JO - Science
JF - Science
IS - 5429
ER -