Stress signaling of apoptosis via ceramide and c-jun kinase Academic Article uri icon


MeSH Major

  • Clindamycin
  • Erythromycin
  • Penicillins
  • Syphilis, Cutaneous
  • Treponema pallidum


  • Mammalian systems respond to environmental stress by either adapting for survival or undergoing programmed cell death (apoptosis). While it is generally believed that the caspase family of proteases are essential effectors of the apoptotic response, much less is clear about the signaling machinery required to activate the caspase system in response to stress stimuli. In the past few years, increasing evidence has linked the sphingomyelin and c-jun kinase (JNK) pathways to the death response in various cellular systems. Both signaling pathways are evolutionarily conserved through yeast. Since yeast does not undergo apoptosis, these pathways appear evolutionarily older than the caspase-mediated death programs. This paper reviews the role of sphingomyelin/ceramide and the JNK pathways in co-ordinating the signaling events leading to apoptosis. © W. S. Maney & Son Ltd.

publication date

  • December 1999



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1177/09680519990050041001

Additional Document Info

start page

  • 216

end page

  • 221


  • 5


  • 4