Sphingomyelin breakdown and cell fate.
A growing number of cell-surface receptors are now being shown to generate signals that trigger the hydrolysis of sphingomyelin to release diffusible ceramides. Ceramides have been implicated as key mediators in signaling pathways, with outcomes as diverse as cell proliferation, differentiation, growth arrest and apoptosis. The response depends on cell type, whether the signal is integrated with other signals originating from the same receptor and on the subcellular location of sphingomyelin hydrolysis and ceramide release.
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Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Italy. tesrob@flashnet.it
D000818:Animals; D016923:Cell Death / Q000502:physiology*; D002518:Ceramides / Q000378:metabolism*; D004789:Enzyme Activation; D005544:Forecasting; D006801:Humans; D006868:Hydrolysis; D008954:Models, Biological; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D013108:Sphingomyelin Phosphodiesterase / Q000378:metabolism; D013109:Sphingomyelins / Q000378:metabolism / Q000502:physiology*; D019014:fas Receptor / Q000378:metabolism
D002518:Ceramides; D018124:Receptors, Tumor Necrosis Factor; D013109:Sphingomyelins; D019014:fas Receptor; D011494:Protein Kinases; D010744:Phosphoric Monoester Hydrolases; D013108:Sphingomyelin Phosphodiesterase