36 research outputs found
Nitric Oxide Induces Cell Death by Regulating Anti-Apoptotic BCL-2 Family Members
Nitric oxide (NO) activates the intrinsic apoptotic pathway to induce cell death. However, the mechanism by which this pathway is activated in cells exposed to NO is not known. Here we report that BAX and BAK are activated by NO and that cytochrome c is released from the mitochondria. Cells deficient in Bax and Bak or Caspase-9 are completely protected from NO-induced cell death. The individual loss of the BH3-only proteins, Bim, Bid, Puma, Bad or Noxa, or Bid knockdown in Bim−/−/Puma−/− MEFs, does not prevent NO-induced cell death. Our data show that the anti-apoptotic protein MCL-1 undergoes ASK1-JNK1 mediated degradation upon exposure to NO, and that cells deficient in either Ask1 or Jnk1 are protected against NO-induced cell death. NO can inhibit the mitochondrial electron transport chain resulting in an increase in superoxide generation and peroxynitrite formation. However, scavengers of ROS or peroxynitrite do not prevent NO-induced cell death. Collectively, these data indicate that NO degrades MCL-1 through the ASK1-JNK1 axis to induce BAX/BAK-dependent cell death
A multi-item multi-objective inventory model in exponential fuzzy environment using chance-operator techniques
Effect of reliability on multi-item inventory system with shortages and partial backlog incorporating time dependent demand and deterioration
An integrated economic disposal and lot-sizing problem for perishable inventories with batch production and corrupt stock-dependent holding cost
Microbial diversity in innovative mesophilic/thermophilic temperature-phased anaerobic digestion of sludge
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