Lunenfeld-Tanenbaum Research Institute

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 Woodgett Lab 

 

Stresses

 
 

As the name implies, the SAPK and p38 MAPK pathways are potently activated by a wide variety of stresses and cellular insults. These include:

  • heat shock
  • UV irradiation
  • inflammatory cytokines (such as TNF and IL-1)
  • tunicamycin
  • chemotherapeutic drugs (e.g. cisplatinum)
  • anisomycin
  • sorbitol/hyperosmolarity
  • gamma irradiation
  • sodium arsenite

The kinases are also induced by ischaemia (p38) or reperfusion following ischaemia (SAPK: Pombo CM, Bonventre JV, Woodgett JR, Kyriakis, JM and Force T (1994) The stress-activated protein kinases (SAPKs) are major c-Jun amino terminal kinases activated by ischemia and reperfusion. J. Biol. Chem. 269, 26546-26550).

Although SAPK and p38 share many agonists, their differential induction by ishaemia or reperfusion clearly indicates that the pathways can be independently regulated by distinct upstream components.
 

 

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