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The cellular stress response which can be elicited by a variety of physical or chemical stressors challenges the homeostatic mechanisms of the cells. Two stressors may interact such that, for example, in the presence of a defined thermal stress ("costress") a second weak stressor like electromagnetic fields (50 MHz, 100 microT) produces strong biological effects. Based on the apparent interaction of these stressors a concept is suggested that explains the observed effects and defines the limits of cellular homeostasis in general terms. The homeostatic potential of a cell and hence the ability to cope with stressors can be altered by eliciting or depressing the heat shock response. This manipulation has several promising medical applications.  相似文献   

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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 stress-mediated activation of mitogen-activated 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.  相似文献   

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Gene expression and the thiol redox state   总被引:13,自引:0,他引:13  
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Reactive oxygen signaling and abiotic stress   总被引:11,自引:0,他引:11  
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