Fas ligand, death gene.
The concept of death genes goes back to the early days of programmed cell death, when a researcher's model system was required to be dependent on transcription of the dying cell in order to qualify as apoptosis. In 1987 Andrew Wyllie,1 one of the pioneers of cell death research, outlined four 'cardinal elements' of apoptosis: one of which was a requirement for macromolecular synthesis. In the following years the complexity of the apoptotic process has become evident and while it is now clear that apoptosis does not have to rely on gene expression, the idea of death genes remains. Induction of an apoptotic cascade via activation of caspases, selective release of mitochondrial proteins and further activation of caspases, can be stimulated by engagement of the Fas surface molecule via membrane bound or soluble forms of Fas ligand (FasL). The FasL gene, which is often transcriptionally inactive, becomes activated in many forms of transcription/translation dependent apoptosis. Here we will discuss FasL as a candidate death gene.
Pinkoski
M J
MJ
Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, California, CA 92121, USA. michael@liai.org
Green
D R
DR
D017209:Apoptosis / Q000235:genetics*; D017637:Clonal Deletion; D053222:Fas Ligand Protein; D005786:Gene Expression Regulation; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000378:metabolism; D018448:Models, Immunological; D013601:T-Lymphocytes / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics* / Q000378:metabolism
D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor