A cytosolic heat shock protein 90 and cochaperone CDC37 complex is required for RIP3 activation during necroptosis

Proceedings of the National Academy of Sciences of the United States of America

Volumn 112, Issue 16, 2015, Pages 5017-5022

  Li, Dianrong ^a,b   Xu, Tao ^b   Cao, Yang ^b   Wang, Huayi ^b   Li, Lin ^b   Chen, She ^b   Wang, Xiaodong ^b,c   Shen, Zhirong ^b,c  

^a BEIJING NORMAL UNIVERSITY   (China)

^b NATIONAL INSTITUTE OF BIOLOGICAL SCIENCES   (China)

^c SHANGHAI JIAO TONG UNIVERSITY SCHOOL OF MEDICINE   (China)

Author keywords

CDC37; HSP90; Kinase; Necrosis; RIP3

Indexed keywords

CELL CYCLE PROTEIN 37; HEAT SHOCK PROTEIN 90; HEAT SHOCK PROTEIN 90 INHIBITOR; MIXED LINEAGE KINASE; RECEPTOR INTERACTING PROTEIN KINASE 3; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; CDC37 PROTEIN, HUMAN; CELL CYCLE PROTEIN; CHAPERONIN; MLKL PROTEIN, HUMAN; PROTEIN BINDING; PROTEIN KINASE; RECEPTOR INTERACTING PROTEIN SERINE THREONINE KINASE; RIPK3 PROTEIN, HUMAN;

ANIMAL CELL; ARTICLE; CELL SURVIVAL; CONTROLLED STUDY; CYTOSOL; ENZYME ACTIVATION; GENE SILENCING; IN VIVO STUDY; MOUSE; NECROPTOSIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION; ANIMAL; ANTAGONISTS AND INHIBITORS; APOPTOSIS; CELL LINE; HUMAN; MACROPHAGE; METABOLISM; NECROSIS; RAT;

MAMMALIA; RATTUS;

ANIMALS; APOPTOSIS; CELL CYCLE PROTEINS; CELL LINE; CHAPERONINS; CYTOSOL; HSP90 HEAT-SHOCK PROTEINS; HUMANS; MACROPHAGES; MICE; NECROSIS; PROTEIN BINDING; PROTEIN KINASES; RATS; RECEPTOR-INTERACTING PROTEIN SERINE-THREONINE KINASES;

EID: 84928128217     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1505244112     Document Type: Article

References (27)

1. Cho YS, et al. (2009) Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell 137(6): 1112-1123.
2. He S, et al. (2009) Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. Cell 137(6):1100-1111.
3. Zhang DW, et al. (2009) RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science 325(5938):332-336.
4. He S, Liang Y, Shao F, Wang X (2011) Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway. Proc Natl Acad Sci USA 108(50):20054-20059.
5. Kaiser WJ, et al. (2013) Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. J Biol Chem 288(43):31268-31279.
6. Li J, et al. (2012) The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis. Cell 150(2):339-350.
7. Sun L, et al. (2012) Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. Cell 148(1-2):213-227.
8. Murphy JM, et al. (2013) The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism. Immunity 39(3):443-453.
9. Hildebrand JM, et al. (2014) Activation of the pseudokinase MLKL unleashes the fourhelix bundle domain to induce membrane localization and necroptotic cell death. Proc Natl Acad Sci USA 111(42):15072-15077.
10. Wang H, et al. (2014) Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3. Mol Cell 54(1):133-146.
11. Chen X, et al. (2014) Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death. Cell Res 24(1):105-121.
12. Cai Z, et al. (2014) Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis. Nat Cell Biol 16(1):55-65.
13. Dondelinger Y, et al. (2014) MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. Cell Reports 7(4):971-981.
14. Kaiser WJ, Upton JW, Mocarski ES (2013) Viral modulation of programmed necrosis. Curr Opin Virol 3(3):296-306.
15. Wang X, et al. (2014) Direct activation of RIP3/MLKL-dependent necrosis by herpes simplex virus 1 (HSV-1) protein ICP6 triggers host antiviral defense. Proc Natl Acad Sci USA 111(43):15438-15443.
16. Duprez L, et al. (2011) RIP kinase-dependent necrosis drives lethal systemic inflammatory response syndrome. Immunity 35(6):908-918.
17. Taipale M, Jarosz DF, Lindquist S (2010) HSP90 at the hub of protein homeostasis: Emerging mechanistic insights. Nat Rev Mol Cell Biol 11(7):515-528.
18. Trepel J, Mollapour M, Giaccone G, Neckers L (2010) Targeting the dynamic HSP90 complex in cancer. Nat Rev Cancer 10(8):537-549.
19. Degterev A, et al. (2008) Identification of RIP1 kinase as a specific cellular target of necrostatins. Nat Chem Biol 4(5):313-321.
20. Kummar S, et al. (2010) Phase I trial of 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), a heat shock protein inhibitor, administered twice weekly in patients with advanced malignancies. Eur J Cancer 46(2):340-347.
21. Ramanathan RK, et al. (2005) Phase I pharmacokinetic-pharmacodynamic study of 17-(allylamino)-17-demethoxygeldanamycin (17AAG, NSC 330507), a novel inhibitor of heat shock protein 90, in patients with refractory advanced cancers. Clin Cancer Res 11(9):3385-3391.
22. Vanden Berghe T, Kalai M, van Loo G, Declercq W, Vandenabeele P (2003) Disruption of HSP90 function reverts tumor necrosis factor-induced necrosis to apoptosis. J Biol Chem 278(8):5622-5629.
23. Chen W, et al. (2013) Diverse sequence determinants control human and mouse receptor interacting protein 3 (RIP3) and mixed lineage kinase domain-like (MLKL) interaction in necroptotic signaling. J Biol Chem 288(23):16247-16261.
24. Zhou W, Yuan J (2014) Necroptosis in health and diseases. Semin Cell Dev Biol 35:14-23.
25. Maki JL, Tres Brazell J, Teng X, Cuny GD, Degterev A (2013) Expression and purification of active receptor interacting protein 1 kinase using a baculovirus system. Protein Expr Purif 89(2):156-161.
26. Bai L, et al. (2011) Blocking NF-kappaB and Akt by Hsp90 inhibition sensitizes Smac mimetic compound 3-induced extrinsic apoptosis pathway and results in synergistic cancer cell death. Apoptosis 16(1):45-54.
27. Wang L, Du F, Wang X (2008) TNF-alpha induces two distinct caspase-8 activation pathways. Cell 133(4):693-703.