http://www.pnas.org/content/111/42/E4458.short
There's a wealth of stuff in this paper and it's all pretty cool. The idea is to examine the finding that inhibiting mitochondrial respiration extends lifespan. These guys pick apart a feedback mechanism involving HIF-1 and AMPK that responds to, and balances, ROS levels. They find that HIF-1 and AMPK cross-repress and regulate ROS levels in different directions, potentially allowing for fine control over ROS levels. The feedback system is coupled to free iron homeostasis (free iron can lead to the production of ROS) and intriguingly seems to modulate resistance to bacterial pathogens (suggesting that mitochondrial ROS lowers rates of infection).
(By the way, they're using ROS probes DCF-DA and Amplex Red -- not cpYFP, which we have issues with)
There's a wealth of stuff in this paper and it's all pretty cool. The idea is to examine the finding that inhibiting mitochondrial respiration extends lifespan. These guys pick apart a feedback mechanism involving HIF-1 and AMPK that responds to, and balances, ROS levels. They find that HIF-1 and AMPK cross-repress and regulate ROS levels in different directions, potentially allowing for fine control over ROS levels. The feedback system is coupled to free iron homeostasis (free iron can lead to the production of ROS) and intriguingly seems to modulate resistance to bacterial pathogens (suggesting that mitochondrial ROS lowers rates of infection).
(By the way, they're using ROS probes DCF-DA and Amplex Red -- not cpYFP, which we have issues with)
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