JBC Podcast: A new mechanism for cell death

February 7, 2013 § Leave a comment

 

Listen to the podcast

Listen to the podcast

Heart failure, brain ischemia, and strokes have one thing in common: an intracellular overload of calcium. In a recent Paper of the Week in the Journal of Biological Chemistry, researchers described how this calcium overload comes about and leads to cell death.

The calcium overload is caused by a hyperactivation of acid-sensing ion channels. One class of these channels are the degenerin/epithelial amiloride-sensitive sodium channels (DEG/ENaC) . The hyperactivation of DEG/ENaC channels has been shown to lead to apoptosis in mammalian cells. But the mechanism of how these channels contribute to cell death remains unclear.

A team led by Wei-Xing Zong at Stony Brook University in New York demonstrated that the hyperactivation of DEG/ENaC channels and the calcium overload activated a mechanism of apoptosis mediated by the ubiquitin-binding protein p62 and the autophagy-related protein LC3. These two proteins ultimately led to cell death via the proapoptotic protein caspase-8.

The authors concluded in their paper that the mechanism involving p62 and LC3 was a novel mechanism for caspase-8-mediated apoptosis.

To learn more about the details of this work, listen to this podcast where the public outreach coordinator for the American Society for Biochemistry and Molecular Biology, Geoff Hunt, chats with Zong.

A mutated and hyperactive DEG/ENaC channel promotes interactions between LC3, caspase-8, and p62.

A mutated and hyperactive DEG/ENaC channel promotes interactions between LC3, caspase-8, and p62.

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