Research of 3C Protease Picornaviruses and Its Cleavage Substrates

Abstract

Abstract:

Picornavirus is a big family of animal viruses, viral protein synthesis needs its own proteases’ cleavage to form sructural and functional proteins. 3C protease is one of picornaviruses’ own proteases. 3C can also cleave some host proteins to benifit viral replication. 3C protease’s structural characteristics, active center, cleavage sites and cleavage substrates’ functions are key of further understanding 3C protease mechanism. Here follows the review on these issues.

Key words: Picornavirus, 3C protease, Cleavage substrates

Liu Yan, Li Bingqing, Meng Hong. Research of 3C Protease Picornaviruses and Its Cleavage Substrates[J]. Biotechnology Bulletin, 2014, 0(8): 46-51.

References

［1］Cui S, Wang J, Fan T, et al. Crystal structure of human enterovirus 71 3C protease［J］. J Mol Biol, 2011, 408（3）：449-461.
［2］Qiu J. Enterovirus 71 infection：a new threat to global public health［J］. Lancet Neurol, 2008, 7：868-869.
［3］秦咸蕴, 林霖, 杨燕, 等. EV71 非结构蛋白的结构和功能及其为靶点的药物研究进展［J］. 药学学报, 2011, 46（7）：753-761.
［4］Li ML, Hsu TA, Chen TC, et al. The 3C protease activity of enterovirus 71 induces human neural cell apoptosis［J］. Virology, 2002, 293（2）：386-395.
［6］Wang QM. Protease inhibitors as potential antiviral agents for the treatment of picornaviral infections［M］. Birkh?user Basel：Antiviral Agents， 2001：229-253.
［7］周建华, 丛国正, 高闪电, 等.口蹄疫病毒株OA/583C蛋白酶的结构模拟和功能分析［J］. 华北农学报, 2007, 22（6）：9-13.
［8］Parks GD, Baker JC, Palmenberg AC. Proteolytic cleavage of encephalomyocarditis virus capsid region substrates by precursors to the 3C enzyme［J］. J Virol, 1989, 63（3）：1054-1058.
［9］Lu G, Qi J, Chen Z, et al. Enterovirus 71 and coxsackievirus A16 3C proteases：binding to rupintrivir and their substrates and anti-hand, foot, and mouth disease virus drug design［J］. Journal of Virology, 2011, 85（19）：10319-10331.
［10］Kundu P, Raychaudhuri S, Tsai W, et al. Shutoff of RNA polymerase II transcription by poliovirus involves 3C protease-mediated cleavage of the TATA-binding protein at an alternative site：incomplete shutoff of transcription interferes with efficient viral replication［J］. J Virol, 2005, 79（15）：9702-9713.
［11］Nakajima N, Horikoshi M, Roeder RG. Factors involved in specific transcription by mammalian RNA polymerase II：purification, genetic specificity, and TATA box-promoter interactions of TFIID［J］. Mol Cell Biol, 1988, 8（10）：4028-4040.
［12］Calandria C, Irurzun A, Barco á, et al. Individual expression of poliovirus 2A pro and 3C pro induces activation of caspase-3 and PARP cleavage in HeLa cells［J］. Virus Res, 2004, 104（1）：39-49.
［13］Clark ME, H?mmerle T, Wimmer E, et al. Poliovirus proteinase 3C converts an active form of transcription factor IIIC to an inactive form：a mechanism for inhibition of host cell polymerase III transcription by poliovirus［J］. EMBO J, 1991, 10（10）：2941.
［14］Tesar M, Marquardt O. Foot-and-mouth disease virus protease 3C inhibits cellular transcription and mediates cleavage of histone H3［J］. Virology, 1990, 174（2）：364-374.
［15］Yalamanchili P, Weidman K, Dasgupta A. Cleavage of transcriptio-nal activator Oct-1 by poliovirus encoded protease 3Cpro［J］. Virology, 1997, 239（1）：176-185.
［16］Kliewer S, Muchardt C, Gaynor R, Dasgupta A. Loss of a phosphory-lated form of transcription factor CREB/ATF in poliovirus-infected cells［J］. J Virol, 1990, 64（9）：4507-4515.
［17］Yalamanchili P, Datta U, Dasgupta A. Inhibition of host cell transcription by poliovirus：cleavage of transcription factor CREB by poliovirus-encoded protease 3Cpro［J］. Journal of Virology, 1997, 71（2）：1220-1226.
［18］Weidman MK, Yalamanchili P, Ng B, et al. Poliovirus 3C protease-mediated degradation of transcriptional activator p53 requires a cellular activity［J］. Virology, 2001, 291（2）：260-271.
［19］weng KF, Li ML, Hung CT, et al. Enterovirus 71 3C protease cleaves a novel target CstF-64 and inhibits cellular polyadenylation［J］. PLoS Pathogens, 2009, 5（9）：e1000593.
［20］Lin JY, Li ML, Shih SR. Far upstream element binding protein 2 interacts with enterovirus 1 internal ribosomal entry site and negatively regulates viral translation［J］. Nucleic Acids Res, 2009, 37：47-59.
［21］Chen LL, Kung YA, Weng KF, et al. Enterovirus 71 infection cleaves a negative regulator for viral internal ribosomal entry site-driven translation［J］. J Virol, 2013, 87（7）：3828-3838.
［22］Li W, Ross-Smith N, Proud CG, et al. Cleavage of translation initiation factor 4AI（eIF4AI）but not eIF4AII by foot-and-mouth disease virus 3C protease：identification of the eIF4AI cleavage site［J］. FEBS Letters, 2001, 507（1）：1-5.
［23］Belsham GJ, McInerney GM, Ross-Smith N. Foot-and-mouth disease virus 3C protease induces cleavage of translation initiation factors eIF4A and eIF4G within infected cells［J］. Journal of Virology, 2000, 74（1）：272-280.
［24］Strong R, Belsham GJ. Sequential modification of translation initiation factor eIF4GI by two different foot-and-mouth disease virus proteases within infected baby hamster kidney cells：identification of the 3Cpro cleavage site［J］. Journal of General Virology, 2004, 85（10）：2953-2962.
［25］Breyne S, Bonderoff JM, Chumakov KM, et al. Cleavage of eukaryotic initiation factor eIF5B by enterovirus 3C proteases［J］. Virology, 2008, 378（1）：118-122.
［26］Kuyumcu-Martinez NM, Joachims M, Lloyd RE. Efficient cleavage of ribosome-associated poly（A）-binding protein by enterovirus 3C protease［J］. Journal of Virology, 2002, 76（5）：2062-2074.
［27］Kuyumcu-Martinez M, Belliot G, Sosnovtsev SV, et al. Calicivirus 3C-like proteinase inhibits cellular translation by cleavage of poly（A）-binding protein［J］. J Virol, 2004, 78（15）：8172-8182.
［28］Kuyumcu-Martinez NM, Van Eden ME, Younan P, et al. Cleavage of poly（A）-binding protein by poliovirus 3C protease inhibits host cell translation：a novel mechanism for host translation shutoff［J］. Mol Cell Biol, 2004, 24（4）：1779-1790.
［29］Zhang B, Morace G, Gauss-Muller V, Kusov Y. Poly（A）binding protein, C-terminally truncated by the hepatitis A virus proteinase 3C, inhibits viral translation［J］. Nucleic Acids Res, 2007, 35：5975-5984.
［30］Bonderoff JM, LaRey JL, Lloyd RE. Cleavage of poly（A）-binding protein by poliovirus 3C proteinase inhibits viral internal ribosome entry site-mediated translation［J］. J Virol, 2008, 82：9389-9399.
［31］Kobayashi M, Arias C, Garabedian A, et al. Site-specific cleavage of the host poly（A）binding protein by the encephalomyocarditis virus 3C proteinase stimulates viral replication［J］. J Virol, 2012, 86（19）：10686-10694.
［32］Lei X, Sun Z, Liu X, et al. Cleavage of the adaptor protein TRIF by enterovirus 71 3C inhibits antiviral responses mediated by Toll-like receptor 3［J］. Journal of Virology, 2011, 85（17）：8811-8818.
［33］Wang D, Fang L, Li K, et al. Foot-and-mouth disease virus 3C protease cleaves NEMO to impair innate immune signaling［J］. Journal of Virology, 2012, 86（17）：9311-9322.
［34］Mukherjee A, Morosky SA, Delorme-Axford E, et al. The coxsackie-virus B 3C^pro protease cleaves MAVS and TRIF to attenuate host type I interferon and apoptotic signaling［J］. PLoS Pathogens, 2011, 7（3）：e1001311.
［35］Lei X, Xiao X, Xue Q, et al. Cleavage of interferon regulatory factor 7 by enterovirus 71 3C suppresses cellular responses［J］. Journal of Virology, 2013, 87（3）：1690-1698.
［36］Joachims M, Harris KS, Etchison D. Poliovirus protease 3C mediates cleavage of microtubule-associated protein 4［J］. Virology, 1995, 211（2）：451-461.