The molecular mechanisms of neuronal apoptosis.
During the past year, apoptosis has been recognized as a process that is perpetually poised to be initiated--often from the cytoplasm rather than from the nucleus--unless it is suppressed by survival factors. Suspected mediators of apoptosis that have recently been investigated include the cysteine protease interleukin-1 beta-converting enzyme, free radicals and cell cycle kinases. Known inhibitors of programmed cell death, such as Bcl-2 and its homologues, have been further studied, and the results suggest that cell death may be regulated by multiple pathways. With the recent identification of the Drosophila gene reaper, which appears to play a role in the initiation of apoptosis, another genetic system for studying cell death has become available.
Eisai London Laboratories, University College London, UK.
L L
LL
Rubin
C L
CL
Gatchalian
G
G
Rimon
S F
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Brooks
D000818:Animals; D017209:Apoptosis; D020170:Caspase 1; D002453:Cell Cycle; D016923:Cell Death; D003546:Cysteine Endopeptidases / Q000502:physiology; D004330:Drosophila / Q000235:genetics; D006801:Humans; D009410:Nerve Degeneration; D009422:Nervous System Diseases / Q000473:pathology; D009474:Neurons / Q000502:physiology*; D011518:Proto-Oncogene Proteins / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D003546:Cysteine Endopeptidases; D020170:Caspase 1