The kinase p38α is activated by many stresses, but the intensity and duration of the signal depends on the stimuli.
the p38α-signaling output in response to stress is modulated by the expression levels of the downstream kinase MK2.
MK2 reexpression and binding to p38α is critical for cell viability in response to stress and illustrate how particular p38α-activation patterns induced by different signals shape the stress-induced cell fate.
This mechanism relies on the ability of p38α to bind to and stabilize MK2, which is required to recover cell homeostasis. The inability to reassemble the p38–MK2 complex in response to strong or sustained stress may function as a sensor of irreversible damage leading to cell death.
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