Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1).
Exposure to ultraviolet light (UV) can induce apoptosis in mammalian cells. The mechanism by which UV radiation engages the suicide apparatus is unclear. Here we demonstrate that UV radiation can activate the Fas pathway via receptor aggregation and subsequent recruitment of the death adaptor molecule FADD/MORT1. UV radiation-induced apoptosis was inhibited by both a dominant negative version of FADD (FADD-DN) and the caspase inhibitor CrmA. Thus, activation of the Fas pathway represents a physiologic mechanism by which UV-damaged cells are eliminated.
Rehemtulla
A
A
Department of Radiation Oncology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
Hamilton
C A
CA
Chinnaiyan
A M
AM
Dixit
V M
VM
D048868:Adaptor Proteins, Signal Transducing; D017209:Apoptosis / Q000528:radiation effects*; D002352:Carrier Proteins / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein; D019085:Fluorescent Antibody Technique, Direct; D006801:Humans; D015843:Serpins / Q000378:metabolism; D014407:Tumor Cells, Cultured; D014466:Ultraviolet Rays; D014764:Viral Proteins; D019014:fas Receptor / Q000378:metabolism* / Q000528:radiation effects
D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; C505533:FADD protein, human; D053200:Fas-Associated Death Domain Protein; D015843:Serpins; D014764:Viral Proteins; D019014:fas Receptor; C074641:interleukin-1beta-converting enzyme inhibitor