Browse > Article
http://dx.doi.org/10.7314/APJCP.2013.14.12.7069

Connections Between Various Trigger Factors and the RIP1/RIP3 Signaling Pathway Involved in Necroptosis  

Zhang, Yuan-Yuan (Faculty of Pharmacy, Bengbu Medical College)
Liu, Hao (Faculty of Pharmacy, Bengbu Medical College)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.14, no.12, 2013 , pp. 7069-7074 More about this Journal
Abstract
Programmed cell death is a basic cellular process that is critical to maintaining tissue homeostasis. In contrast to apoptosis, necrosis was previously regarded as an unregulated and uncontrollable process. However, as research has progressed, necrosis, also known as necroptosis or programmed necrosis, is drawing increasing attention, not least becasu of its possible impications for cancer research. Necroptosis exhibits a unique signaling pathway that requires the involvement of receptor interaction protein kinases 1 and 3 (RIP1 and RIP3), mixed lineage kinase domain-like (MLKL), and phosphoglycerate mutase 5 (PGAM5) and can be specifically inhibited by necrostatins. Not only does necroptosis serve as a backup cell death program when apoptosis is inhibited, but it is now recognized to play a pivotal role in regulating various physiological processes and the pathogenesis of a variety of human diseases such as ischemic brain injury, immune system disorders and cancer. The control of necroptosis by various defined trigger factors and signaling pathways now offers the opportunity to target this cellular process for therapeutic purposes. The purpose of this paper is to review current findings concerning the connections between various trigger factors and the RIP1/RIP3 signaling pathway as it relates to necroptosis.
Keywords
Necroptosis; TNFR; Fas; TRAILR; RIP1-RIP3 necrosome; MLKL complex;
Citations & Related Records
연도 인용수 순위
  • Reference
1 Alexopoulou L, Holt AC, Medzhitov R, et al (2001). Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3. Nature, 413, 732-8.   DOI   ScienceOn
2 Andera L (2009). Signaling activated by the death receptors of the TNFR family. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub, 153, 173-80.   DOI
3 Bao L, Li Y, Deng SX, et al (2006). Sitosterol-containing lipoproteins trigger free sterol-induced caspase-independent death in ACAT-competent macrophages. J Biol Chem, 281, 33635-49.   DOI   ScienceOn
4 Budd RC, Yeh WCTschopp J (2006). cFLIP regulation of lymphocyte activation and development. Nat Rev Immunol, 6, 196-204.   DOI   ScienceOn
5 Chan FKBaehrecke EH (2012). RIP3 finds partners in crime. Cell, 148, 17-8.   DOI   ScienceOn
6 Chan FK, Shisler J, Bixby JG, et al (2003). A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses. J Biol Chem, 278, 51613-21.   DOI   ScienceOn
7 Cho YS, Challa S, Moquin D, et al (2009). Phosphorylationdriven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell, 137, 1112-23.   DOI   ScienceOn
8 Degterev A, Huang Z, Boyce M, et al (2005). Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat Chem Biol, 1, 112-9.   DOI   ScienceOn
9 Feoktistova M, Geserick P, Kellert B, et al (2011). cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms. Mol Cell, 43, 449-63.   DOI   ScienceOn
10 Festjens N, Vanden Berghe T, Cornelis S, et al (2007). RIP1, a kinase on the crossroads of a cell's decision to live or die. Cell Death Differ, 14, 400-10.   DOI   ScienceOn
11 Fricker N, Beaudouin J, Richter P, et al (2010). Model-based dissection of CD95 signaling dynamics reveals both a proand antiapoptotic role of c-FLIPL. J Cell Biol, 190, 377-89.   DOI   ScienceOn
12 Galluzzi L, Vanden Berghe T, Vanlangenakker N, et al (2011). Programmed necrosis from molecules to health and disease. Int Rev Cell Mol Biol, 289, 1-35.   DOI   ScienceOn
13 Golks A, Brenner D, Fritsch C, et al (2005). c-FLIPR, a new regulator of death receptor-induced apoptosis. J Biol Chem, 280, 14507-13.   DOI   ScienceOn
14 Han W, Li L, Qiu S, et al (2007). Shikonin circumvents cancer drug resistance by induction of a necroptotic death. Mol Cancer Ther, 6, 1641-9.   DOI   ScienceOn
15 Holen I, Croucher PI, Hamdy FC, et al (2002). Osteoprotegerin (OPG) is a survival factor for human prostate cancer cells. Cancer Res, 62, 1619-23.
16 He S, Liang Y, Shao F, et al (2011). Toll-like receptors activate programmed necrosis in macrophages through a receptorinteracting kinase-3-mediated pathway. Proc Natl Acad Sci U S A, 108, 20054-9.   DOI
17 He S, Wang L, Miao L, et al (2009). Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. Cell, 137, 1100-11.   DOI   ScienceOn
18 Hitomi J, Christofferson DE, Ng A, et al (2008). Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway. Cell, 135, 1311-23.   DOI   ScienceOn
19 Holler N, Zaru R, Micheau O, et al (2000). Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nat Immunol, 1, 489-95.   DOI   ScienceOn
20 Hoshino K, Takeuchi O, Kawai T, et al (1999). Cutting edge: Tolllike receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. J Immunol, 162, 3749-52.
21 Hsu TS, Yang PM, Tsai JS, et al (2009). Attenuation of cadmiuminduced necrotic cell death by necrostatin-1: potential necrostatin-1 acting sites. Toxicol Appl Pharmacol, 235, 153-62.   DOI   ScienceOn
22 Hymowitz SG, Christinger HW, Fuh G, et al (1999). Triggering cell death: the crystal structure of Apo2L/TRAIL in a complex with death receptor 5. Mol Cell, 4, 563-71.   DOI   ScienceOn
23 Kim JW, Choi EJJoe CO (2000). Activation of death-inducing signaling complex (DISC) by pro-apoptotic C-terminal fragment of RIP. Oncogene, 19, 4491-9.   DOI   ScienceOn
24 Jain MV, Paczulla AM, Klonisch T, et al (2013). Interconnections between apoptotic, autophagic and necrotic pathways: implications for cancer therapy development. J Cell Mol Med, 17, 12-29.   DOI   ScienceOn
25 Kaiser WJ, Sridharan H, Huang C, et al (2013). Toll-like Receptor 3-mediated necrosis via TRIF, RIP3 and MLKL. J Biol Chem.
26 Kemp TJ, Kim JS, Crist SA, et al (2003). Induction of necrotic tumor cell death by TRAIL/Apo-2L. Apoptosis, 8, 587-99.   DOI   ScienceOn
27 Kim S, Dayani L, Rosenberg PA, et al (2010). RIP1 kinase mediates arachidonic acid-induced oxidative death of oligodendrocyte precursors. Int J Physiol Pathophysiol Pharmacol, 2, 137-47.
28 Krammer PH (2000). CD95's deadly mission in the immune system. Nature, 407, 789-95.   DOI   ScienceOn
29 Krueger A, Schmitz I, Baumann S, et al (2001). Cellular FLICEinhibitory protein splice variants inhibit different steps of caspase-8 activation at the CD95 death-inducing signaling complex. J Biol Chem, 276, 20633-40.   DOI   ScienceOn
30 Kumar H, Kawai TAkira S (2011). Pathogen recognition by the innate immune system. Int Rev Immunol, 30, 16-34.   DOI   ScienceOn
31 Laird MD, Wakade C, Alleyne CH, Jr., et al (2008). Hemininduced necroptosis involves glutathione depletion in mouse astrocytes. Free Radic Biol Med, 45, 1103-14.   DOI   ScienceOn
32 Laster SM, Wood JGGooding LR (1988). Tumor necrosis factor can induce both apoptic and necrotic forms of cell lysis. J Immunol, 141, 2629-34.
33 Lin Y, Choksi S, Shen HM, et al (2004). Tumor necrosis factor-induced nonapoptotic cell death requires receptorinteracting protein-mediated cellular reactive oxygen species accumulation. J Biol Chem, 279, 10822-8.   DOI   ScienceOn
34 Lavrik INKrammer PH (2012). Regulation of CD95/Fas signaling at the DISC. Cell Death Differ, 19, 36-41.   DOI   ScienceOn
35 Li J, McQuade T, Siemer AB, et al (2012). The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis. Cell, 150, 339-50.   DOI   ScienceOn
36 Li Y, Yang X, Ma C, et al (2008). Necroptosis contributes to the NMDA-induced excitotoxicity in rat's cultured cortical neurons. Neurosci Lett, 447, 120-3.   DOI   ScienceOn
37 Ma Y, Temkin V, Liu H, et al (2005). NF-kappaB protects macrophages from lipopolysaccharide-induced cell death: the role of caspase 8 and receptor-interacting protein. J Biol Chem, 280, 41827-34.   DOI   ScienceOn
38 Mahalingam D, Szegezdi E, Keane M, et al (2009). TRAIL receptor signalling and modulation: Are we on the right TRAIL? Cancer Treat Rev, 35, 280-8.   DOI   ScienceOn
39 Marsters SA, Sheridan JP, Pitti RM, et al (1997). A novel receptor for Apo2L/TRAIL contains a truncated death domain. Curr Biol, 7, 1003-6.   DOI   ScienceOn
40 Meurette O, Huc L, Rebillard A, et al (2005). TRAIL (TNFrelated apoptosis-inducing ligand) induces necrosis-like cell death in tumor cells at acidic extracellular pH. Ann N Y Acad Sci, 1056, 379-87.   DOI
41 Meurette O, Rebillard A, Huc L, et al (2007). TRAIL induces receptor-interacting protein 1-dependent and caspasedependent necrosis-like cell death under acidic extracellular conditions. Cancer Res, 67, 218-26.   DOI   ScienceOn
42 O'Donnell MA, Perez-Jimenez E, Oberst A, et al (2011). Caspase 8 inhibits programmed necrosis by processing CYLD. Nat Cell Biol, 13, 1437-42.   DOI   ScienceOn
43 Micheau OTschopp J (2003). Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes. Cell, 114, 181-90.   DOI   ScienceOn
44 Moquin DChan FK (2010). The molecular regulation of programmed necrotic cell injury. Trends Biochem Sci, 35, 434-41.   DOI   ScienceOn
45 O'Donnell MA, Legarda-Addison D, Skountzos P, et al (2007). Ubiquitination of RIP1 regulates an NF-kappaB-independent cell-death switch in TNF signaling. Curr Biol, 17, 418-24.   DOI   ScienceOn
46 Oberst A, Dillon CP, Weinlich R, et al (2011). Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3- dependent necrosis. Nature, 471, 363-7.   DOI   ScienceOn
47 Oettgen HF, Carswell EA, Kassel RL, et al (1980). Endotoxininduced tumor necrosis factor. Recent Results Cancer Res, 75, 207-12.   DOI
48 Pan G, Ni J, Wei YF, et al (1997a). An antagonist decoy receptor and a death domain-containing receptor for TRAIL. Science, 277, 815-8.   DOI   ScienceOn
49 Pan G, O'Rourke K, Chinnaiyan AM, et al (1997b). The receptor for the cytotoxic ligand TRAIL. Science, 276, 111-3.   DOI
50 Poltorak A, He X, Smirnova I, et al (1998). Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. Science, 282, 2085-8.   DOI   ScienceOn
51 Sheridan JP, Marsters SA, Pitti RM, et al (1997). Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors. Science, 277, 818-21.   DOI   ScienceOn
52 Van Herreweghe F, Festjens N, Declercq W, et al (2010). Tumor necrosis factor-mediated cell death: to break or to burst, that's the question. Cell Mol Life Sci, 67, 1567-79.   DOI   ScienceOn
53 Sun L, Wang H, Wang Z, et al (2012). Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. Cell, 148, 213-27.   DOI   ScienceOn
54 Tenev T, Bianchi K, Darding M, et al (2011). The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. Mol Cell, 43, 432-48.   DOI   ScienceOn
55 Upton JW, Kaiser WJMocarski ES (2010). Virus inhibition of RIP3-dependent necrosis. Cell Host Microbe, 7, 302-13.   DOI   ScienceOn
56 Vandenabeele P, Galluzzi L, Vanden Berghe T, et al (2010). Molecular mechanisms of necroptosis: an ordered cellular explosion. Nat Rev Mol Cell Biol, 11, 700-14.   DOI   ScienceOn
57 Vanlangenakker N, Vanden Berghe T, Bogaert P, et al (2011). cIAP1 and TAK1 protect cells from TNF-induced necrosis by preventing RIP1/RIP3-dependent reactive oxygen species production. Cell Death Differ, 18, 656-65.   DOI   ScienceOn
58 Vercammen D, Brouckaert G, Denecker G, et al (1998). Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways. J Exp Med, 188, 919-30.   DOI   ScienceOn
59 Vercammen D, Vandenabeele P, Beyaert R, et al (1997). Tumour necrosis factor-induced necrosis versus anti-Fas-induced apoptosis in L929 cells. Cytokine, 9, 801-8.   DOI   ScienceOn
60 Wang L, Du FWang X (2008). TNF-alpha induces two distinct caspase-8 activation pathways. Cell, 133, 693-703.   DOI   ScienceOn
61 Xu X, Chua CC, Kong J, et al (2007). Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells. J Neurochem, 103, 2004-14.   DOI   ScienceOn
62 Wang Z, Jiang H, Chen S, et al (2012). The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways. Cell, 148, 228-43.   DOI   ScienceOn
63 Wu W, Liu PLi J (2012). Necroptosis: an emerging form of programmed cell death. Crit Rev Oncol Hematol, 82, 249-58.   DOI   ScienceOn
64 Wyllie AH, Kerr JFCurrie AR (1980). Cell death: the significance of apoptosis. Int Rev Cytol, 68, 251-306.   DOI
65 Zhang QL, Niu Q, Ji XL, et al (2008). Is necroptosis a death pathway in aluminum-induced neuroblastoma cell demise? Int J Immunopathol Pharmacol, 21, 787-96.   DOI