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Apoptotic cells let down their guard

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Now, Anathy et al. reveal the counterintuitive process through which ROS promote apoptosis... Stimulation of the receptor sets off a molecular chain of events, including activation of caspases, which eventually triggers apoptosis... Anathy et al. wanted to nail down how ROS influence the Fas pathway... The obvious mechanism—that Fas activation triggers a surge of ROS, amplifying the death pathway—appears to be wrong, the researchers found... The decline in glutaredoxin 1 makes an impact... High levels of ROS can trigger glutathionylation—the addition of a glutathione molecule to cysteine amino acids in a protein... The amount of glutathionylation climbed after Fas stimulation—a rise the researchers could prevent by cranking up glutaredoxin 1 production... So ROS's role in the cell's demise is to spur glutathionylation... But rather than boosting ROS levels to ramp up glutathionylation, cells achieve the same effect by degrading glutaredoxin 1 and dialing down their defenses against oxidation... How glutathionylation promotes cellular suicide isn't clear... But Fas itself is glutathionylated, and the altered receptors bunch up and slip into lipid rafts in the cell membrane, possibly strengthening signaling through the Fas pathway.

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Glutathionylated proteins (green) show up in cells after stimulation of Fas.
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fig1: Glutathionylated proteins (green) show up in cells after stimulation of Fas.


Apoptotic cells let down their guard
Glutathionylated proteins (green) show up in cells after stimulation of Fas.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2654292&req=5

fig1: Glutathionylated proteins (green) show up in cells after stimulation of Fas.

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

Now, Anathy et al. reveal the counterintuitive process through which ROS promote apoptosis... Stimulation of the receptor sets off a molecular chain of events, including activation of caspases, which eventually triggers apoptosis... Anathy et al. wanted to nail down how ROS influence the Fas pathway... The obvious mechanism—that Fas activation triggers a surge of ROS, amplifying the death pathway—appears to be wrong, the researchers found... The decline in glutaredoxin 1 makes an impact... High levels of ROS can trigger glutathionylation—the addition of a glutathione molecule to cysteine amino acids in a protein... The amount of glutathionylation climbed after Fas stimulation—a rise the researchers could prevent by cranking up glutaredoxin 1 production... So ROS's role in the cell's demise is to spur glutathionylation... But rather than boosting ROS levels to ramp up glutathionylation, cells achieve the same effect by degrading glutaredoxin 1 and dialing down their defenses against oxidation... How glutathionylation promotes cellular suicide isn't clear... But Fas itself is glutathionylated, and the altered receptors bunch up and slip into lipid rafts in the cell membrane, possibly strengthening signaling through the Fas pathway.

No MeSH data available.