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IFI16 senses and protects stalled replication forks
Gamble et al. demonstrate that detection of stalled replication forks by the innate immune sensor IFI16 induces an early STING-dependent pro-inflammatory cytokine response independently of cGAS and DNA damage. Furthermore, IFI16 exhibits dual functionality during replication stress by protecting stalled, remodeled replication forks from nucleolytic degradation.
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