## Abstract The fate of cells arrested in mitosis by antimitotic compounds is complex but is influenced by competition between pathways promoting cell death and pathways promoting mitotic exit. As components of both of these pathways are regulated by Cdc20βdependent degradation, I hypothesize that
Integrated activation of MAP3Ks balances cell fate in response to stress
β Scribed by Ann M. Winter-Vann; Gary L. Johnson
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 368 KB
- Volume
- 102
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
In vivo, tissues and organs are exposed to numerous stressors that require cells to respond appropriately for viability and homeostasis. Cells respond to these stressors, which range from UV irradiation, heat shock, chemicals, and changes in osmolality, to oxidative stress and inflammatory cytokines, by activating pathways that protect cells from damage. If the stress is too great, cells commit to undergo apoptosis. Such cell fate decisions involve the stressβmediated activation of mitogenβactivated protein kinase (MAPK) networks, ultimately under the control of MAPK kinase kinases, or MAP3Ks. It is the MAP3Ks that coordinate the localization, duration and magnitude of MAPK activation in response to cell stress. A single stressor may activate several MAP3Ks, each of which impacts the balance between survival and apoptotic signaling. In this prospect article, we review the specific MAP3Ks that integrate the physiological response to cell stressors. The interrelationships among different stressors are discussed, with an emphasis on how the balance of signaling through MAP3Ks controls the MAPK response to determine cell fate. J. Cell. Biochem. 102: 848β858, 2007. Β© 2007 WileyβLiss, Inc.
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