Is SIRT2 required for necroptosis?

Kim Newton, Joanne M. Hildebrand, Zhirong Shen, Diego Rodriguez, Silvia Alvarez-Diaz, Sean Petersen, Saumil Shah, Debra L. Dugger, Chunzi Huang, Johan Auwerx, Peter Vandenabeele, Douglas R. Green, Avi Ashkenazi, Vishva M. Dixit, William J. Kaiser, Andreas Strasser, Alexei Degterev and John Silke ()
Additional contact information
Kim Newton: Genentech, Inc.
Joanne M. Hildebrand: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
Zhirong Shen: National Institute of Biological Sciences, Zhongguancun Life Science Park
Diego Rodriguez: St Jude Children’s Research Hospital
Silvia Alvarez-Diaz: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
Sean Petersen: Genentech, Inc.
Saumil Shah: Tufts University
Debra L. Dugger: Genentech, Inc.
Chunzi Huang: Emory Vaccine Center, Emory University School of Medicine
Johan Auwerx: Laboratory of Integrative and Systems Physiology, EPFL, CH-1015 Lausanne, Switzerland
Peter Vandenabeele: Molecular Signaling and Cell Death Unit, Inflammation Research Center, VIB, 9052 Gent, Belgium
Douglas R. Green: St Jude Children’s Research Hospital
Avi Ashkenazi: Genentech, Inc.
Vishva M. Dixit: Genentech, Inc.
William J. Kaiser: Emory Vaccine Center, Emory University School of Medicine
Andreas Strasser: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
Alexei Degterev: Tufts University
John Silke: The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia

Nature, 2014, vol. 506, issue 7489, E4-E6

Abstract: Abstract Arising from N. Narayan et al. Nature 492, 199–204 (2012)10.1038/nature11700 Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments to regulate many cellular processes1,2; recently, Narayan et al.3 reported that SIRT2 was required for necroptosis on the basis of their findings that SIRT2 inhibition, knockdown or knockout prevented necroptosis. We sought to confirm and explore the role of SIRT2 in necroptosis and tested four different sources of the SIRT2 inhibitor AGK2, three independent short interfering RNAs (siRNAs) against Sirt2, and cells from two independently generated Sirt2−/− mouse strains; however, we were unable to show that inhibiting or depleting SIRT2 protected cells from necroptosis. Furthermore, Sirt2−/− mice succumbed to tumour-necrosis factor (TNF)-induced systemic inflammatory response syndrome (SIRS) more rapidly than wild-type mice, whereas Ripk3−/− mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.

Date: 2014
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DOI: 10.1038/nature13024

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