Schlafen family member 11

Definition:

Inhibitor of DNA replication that promotes cell death in response to DNA damage. Acts as a guardian of the genome by killing cells with defective replication. Persistently blocks stressed replication forks by opening chromatin across replication initiation sites at stressed replication forks, possibly leading to unwind DNA ahead of the MCM helicase and block fork progression, ultimately leading to cell death. Acts independently of ATR. Also acts as an interferon (IFN)-induced antiviral protein which acts as an inhibitor of retrovirus protein synthesis. Specifically abrogates the production of retroviruses such as human immunodeficiency virus 1 (HIV-1) by acting as a specific inhibitor of the synthesis of retroviruses encoded proteins in a codon-usage-dependent manner. Binds to tRNAs and exploits the unique viral codon bias towards A/T nucleotides. The exact inhibition mechanism is unclear: may either sequester tRNAs, prevent their maturation via post-transcriptional processing or may accelerate their deacylation. Does not inhibit reverse transcription, integration or production and nuclear export of viral RNA.

References:

[1]. Junko Murai, et al. SLFN11 Blocks Stressed Replication Forks Independently of ATR. Mol Cell. 2018 Feb 1;69(3):371-384.e6. [Content Brief]

[2]. Yanhua Mu, et al. SLFN11 inhibits checkpoint maintenance and homologous recombination repair. EMBO Rep. 2016 Jan;17(1):94-109. [Content Brief]

[3]. Manqing Li, et al. Codon-usage-based inhibition of HIV protein synthesis by human schlafen 11. Nature. 2012 Nov 1;491(7422):125-8. [Content Brief]

[4]. Gabriele Zoppoli, et al. Putative DNA/RNA helicase Schlafen-11 (SLFN11) sensitizes cancer cells to DNA-damaging agents. Proc Natl Acad Sci U S A. 2012 Sep 11;109(37):15030-5. [Content Brief]

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