Publications by authors named "A Haimovici"

Cellular senescence is a response to many stressful insults. DNA damage is a consistent feature of senescent cells, but in many cases its source remains unknown. Here, we identify the cellular endonuclease caspase-activated DNase (CAD) as a critical factor in the initiation of senescence.

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Article Synopsis
  • - Mitochondria respond to infections with signals that can trigger inflammation, but the full understanding of how this works is still being explored.
  • - The study reveals that the enzyme caspase-activated DNase (CAD) plays a key role in activating mitochondrial pro-inflammatory responses, aiding the body's defense against viral infections.
  • - In experiments, cells and mice lacking CAD showed weakened immune responses to viral infections, indicating that CAD is crucial for linking mitochondrial activity to inflammation and overall immune defense.
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One of the tasks of mitochondria is the rule over life and death: when the outer membrane is permeabilized, the release of intermembrane space proteins causes cell death by apoptosis. For a long time, this mitochondrial outer membrane permeabilization (MOMP) has been accepted as the famous step from which no cell returns. Recent results have however shown that this quite plainly does not have to be the case.

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The bacterium Helicobacter pylori induces gastric inflammation and predisposes to cancer. H. pylori-infected epithelial cells secrete cytokines and chemokines and undergo DNA-damage.

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