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Sirtuin‐mediated deacetylation pathway stabilizes Werner syndrome protein

Tomoaki Kahyo, Raúl Mostoslavsky, Makoto Goto, Mitsutoshi Setou

FEBS Letters · 2008 · ▲ 39 citations

Genomic instability Deregulated nutrient-sensing Caloric restriction Rat Mouse

Abstract

Caloric restriction (CR) is known to promote longevity in various species. Sirtuin-mediated deacetylation has been shown to be related to the promotion of longevity in some species. Here, we show that CR of rats led to an increase in the level of Werner syndrome protein (WRN), a recognized DNA repair protein. In addition, CR simultaneously increased the level of SIRT1, a mammalian sirtuin. In HEK293T cells, sirtuin inhibitors decreased the WRN level, and this effect was suppressed by proteasomal inhibitors. Furthermore, we found a decrease in the WRN level in Sirt1-deficient mice. These results indicate that sirtuin-mediated deacetylation stabilizes WRN. STRUCTURED SUMMARY:

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Provenance

Source: OpenAlex
DOI: 10.1016/j.febslet.2008.06.031
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Fetched: 2026-10-22 MST

Cite this

APA

Kahyo, T., Mostoslavsky, R., Goto, M., & Setou, M. (2008). Sirtuin‐mediated deacetylation pathway stabilizes Werner syndrome protein. <em>FEBS Letters</em>. https://doi.org/10.1016/j.febslet.2008.06.031

Vancouver

Kahyo T, Mostoslavsky R, Goto M, Setou M. Sirtuin‐mediated deacetylation pathway stabilizes Werner syndrome protein. FEBS Letters. 2008. doi:10.1016/j.febslet.2008.06.031.

BibTeX

@article{tomoaki2008Sirtui, title = {Sirtuin‐mediated deacetylation pathway stabilizes Werner syndrome protein}, author = {Tomoaki Kahyo and Raúl Mostoslavsky and Makoto Goto and Mitsutoshi Setou}, journal = {FEBS Letters}, year = {2008}, doi = {10.1016/j.febslet.2008.06.031}, }