Is SIRT2 required for necroptosis?

Arising from N. Narayan et al. Nature492, 199–204 (2012)10.1038/nature11700 Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments to regulate many cellular processes 1 , 2 ; recently, Narayan et al. 3 reported that SIRT2 was required for necroptosis on the...

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Published inNature (London) Vol. 506; no. 7489; pp. E4 - E6
Main Authors Newton, Kim, Hildebrand, Joanne M., Shen, Zhirong, Rodriguez, Diego, Alvarez-Diaz, Silvia, Petersen, Sean, Shah, Saumil, Dugger, Debra L., Huang, Chunzi, Auwerx, Johan, Vandenabeele, Peter, Green, Douglas R., Ashkenazi, Avi, Dixit, Vishva M., Kaiser, William J., Strasser, Andreas, Degterev, Alexei, Silke, John
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 27.02.2014
Nature Publishing Group
Subjects
631/80/82/2344
Animals
Apoptosis
Body temperature
brief-communications-arising
Cell death
Cell physiology
Cell research
Enzymes
Experiments
Female
Humanities and Social Sciences
Humans
Male
multidisciplinary
Necrosis - enzymology
Regulation
Rodents
Science
Sirtuin 2 - genetics
Sirtuin 2 - metabolism
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Abstract Arising from N. Narayan et al. Nature492, 199–204 (2012)10.1038/nature11700 Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments to regulate many cellular processes 1 , 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.
AbstractList Arising from N. Narayan et al. Nature492, 199–204 (2012)10.1038/nature11700 Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments to regulate many cellular processes 1 , 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.
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.
Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes 1 , 2 . Recently Narayan et al ., reported that SIRT2 was required for necroptosis based on their findings that SIRT2 inhibition, knock-down or knock-out 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 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 TNF induced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3 −/− mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.
Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes¹,². Recently Narayan et al., reported that SIRT2 was required for necroptosis based on their findings that SIRT2 inhibition, knock-down or knock-out 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 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 TNF induced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3−/− mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.
Audience Academic
Author Strasser, Andreas
Shen, Zhirong
Rodriguez, Diego
Huang, Chunzi
Degterev, Alexei
Dixit, Vishva M.
Newton, Kim
Petersen, Sean
Dugger, Debra L.
Auwerx, Johan
Ashkenazi, Avi
Hildebrand, Joanne M.
Green, Douglas R.
Shah, Saumil
Kaiser, William J.
Vandenabeele, Peter
Silke, John
Alvarez-Diaz, Silvia
AuthorAffiliation 10 Department of Biomedical Molecular Biology, Ghent University, 9052 Gent, Belgium
8 Laboratory of Integrative and Systems Physiology, EPFL, CH-1015 Lausanne, Switzerland
9 Molecular Signaling and Cell Death Unit, Inflammation Research Center, VIB, 9052 Gent, Belgium
1 Genentech, Inc., South San Francisco, CA 94080, USA
5 Department of Biochemistry, Tufts University, Boston, Massachusetts 02111, USA
6 Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322, USA
3 Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia
2 The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
7 Department of Immunology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA
4 National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China
11 Methusalem BOF09/01M00709, Ghent University, 9052 Gent, Belgium
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/24572428$$D View this record in MEDLINE/PubMed
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Duprez (CR8) 2011; 35
Günther (CR9) 2011; 477
Outeiro (CR7) 2007; 317
Beirowski (CR12) 2011; 108
Houtkooper, Pirinen, Auwerx (CR1) 2012; 13
He (CR5) 2009; 137
Piao (CR10) 2012; 5
Murphy (CR14) 2013; 39
Welz (CR11) 2011; 477
Bobrowska, Donmez, Weiss, Guarente, Bates (CR13) 2012; 7
Sebastian, Satterstrom, Haigis, Mostoslavsky (CR2) 2012; 287
Cho (CR4) 2009; 137
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PS Welz (BFnature13024_CR11) 2011; 477
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Snippet Arising from N. Narayan et al. Nature492, 199–204 (2012)10.1038/nature11700 Sirtuins can promote deacetylation of a wide range of substrates in diverse...
Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes¹,². Recently Narayan et...
Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments to regulate many cellular processes1,2; recently, Narayan et...
Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes 1 , 2 . Recently Narayan...
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Animals
Apoptosis
Body temperature
brief-communications-arising
Cell death
Cell physiology
Cell research
Enzymes
Experiments
Female
Humanities and Social Sciences
Humans
Male
multidisciplinary
Necrosis - enzymology
Regulation
Rodents
Science
Sirtuin 2 - genetics
Sirtuin 2 - metabolism
Title Is SIRT2 required for necroptosis?
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