USP15生物学功能的研究进展
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摘要
去泛素化酶(DUBs)是体内分解蛋白泛素链的一类蛋白酶体系,对蛋白泛素化降解过程起校正作用。泛素特异性蛋白酶(USP)家族是DUBs中最大的家族,通过多种途径参与免疫应答,且与一些疾病和肿瘤的发生具有明显相关性。USP15是USP家族的重要组成部分,参与调节转化生长因子β、p53、核因子κB等重要的信号转导通路,与一些肿瘤的发生发展相关。USP15也可通过调节I型干扰素产生和T细胞活化参与免疫反应,并具有多种重要生物学功能,包括维持基因稳定性、调节转录因子及抗病毒等重要的细胞活动。
Deubiquitinases( DUBs) are a class of enzyme protein systems that decompose protein ubiquitin chains in vivo,correcting the process of protein ubiquitination and degradation. The ubiquitin-specific protease( USP) family is the largest family in DUBs,which is involved in the immune response through a variety of pathways and has a significant correlation with the occurrence of some diseases and tumors. USP15 is an important component of the USP family,participating in regulating important signal transduction pathways of transforming growth factor-β,p53 and nuclear factor-κB,associated with the development of some tumors. USP15 also participates in immune responses by regulating type I interferon production and T cell activation,and has a variety of important biological functions,including maintaining gene stability,regulating transcription factors,and antiviral activity,and other important cellular activities.
Deubiquitinases( DUBs) are a class of enzyme protein systems that decompose protein ubiquitin chains in vivo,correcting the process of protein ubiquitination and degradation. The ubiquitin-specific protease( USP) family is the largest family in DUBs,which is involved in the immune response through a variety of pathways and has a significant correlation with the occurrence of some diseases and tumors. USP15 is an important component of the USP family,participating in regulating important signal transduction pathways of transforming growth factor-β,p53 and nuclear factor-κB,associated with the development of some tumors. USP15 also participates in immune responses by regulating type I interferon production and T cell activation,and has a variety of important biological functions,including maintaining gene stability,regulating transcription factors,and antiviral activity,and other important cellular activities.
引文
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[32]Zhang L,Zhou F,García de Vinuesa A,et al.TRAF4 promotes TGF-beta receptor signaling and drives breast cancer metastasis[J].Mol Cell,2013,51(5):559-572.
[33]Schweitzer K,Bozko PM,Dubiel W,et al.CSN controls NF-kappaB by deubiquitinylation of IkappaBalpha[J].EMBO J,2007,26(6):1532-1541.
[34]Meek DW.Regulation of the p53 response and its relationship to cancer[J].Biochem J,2015,469(3):325-346.
[35]Wade M,Li YC,Wahl GM.MDM2,MDMX and p53 in oncogenesis and cancer therapy[J].Nat Rev Cancer,2013,13(2):83-96.
[2]Zou Q,Jin J,Hu H,et al.USP15 stabilizes MDM2 to mediate cancer-cell survival and inhibit antitumor T cell responses[J].Nat Immunol,2014,15(6):562-570.
[3]Xu K,Pei H,Zhang Z,et al.Ubiquitin-specific protease 15 promotes tumor cell invasion and proliferation in glioblastoma[J].Oncol Lett,2018,15(3):3846-3851.
[4]吕莹,胡勇.去泛素化酶的研究进展[J].临床医药实践,2018,27(2):128-131.
[5]Chou CK,Chang YT,Korinek M,et al.The Regulations of Deubiquitinase USP15 and Its Pathophysiological Mechanisms in Diseases[J].Int J Mol Sci,2017,18(3).pii:E902.
[6]Harper S,Besong TM,Emsley J,et al.Structure of the USP15N-terminal domains:A beta-hairpin mediates close association between the DUSP and UBL domains[J].Biochemistry,2011,50(37):7995-8004.
[7]Vlasschaert C,Xia X,Coulombe J,et al.Evolution of the highly networked deubiquitinating enzymes USP4,USP15,and USP11[J].BMC Evol Biol,2015,15:230.
[8]吴静静,顾文莉.泛素特异蛋白酶4研究进展[J].生命的化学,2014,34(6):823-828.
[9]Long L,Thelen JP,Furgason M,et al.The U4/U6 recycling factor SART3 has histone chaperone activity and associates with USP15to regulate H2B deubiquitination[J].J Biol Chem,2014,289(13):8916-8930.
[10]Fukagai K,Waku T,Chowdhury A,et al.USP15 stabilizes the transcription factor Nrf1 in the nucleus,promoting the proteasome gene expression[J].Biochem Biophys Res Commun,2016,478(1):363-370.
[11]Fielding AB,Concannon M,Darling S,et al.The deubiquitylase USP15 regulates topoisomeraseⅡalpha to maintain genome integrity[J].Oncogene,2018,37(17):2326-2342.
[12]Faronato M,Patel V,Darling S,et al.The deubiquitylase USP15stabilizes newly synthesized REST and rescues its expression at mitotic exit[J].Cell Cycle,2013,12(12):1964-1977.
[13]Takeuchi O,Akira S.MDA5/RIG-I and virus recognition[J].Curr Opin Immunol,2008,20(1):17-22.
[14]Fujita T,Onoguchi K,Onomoto K,et al.Triggering antiviral response by RIG-I-related RNA helicases[J].Biochimie,2007,89(6/7):754-760.
[15]Zhang H,Wang D,Zhong H,et al.Ubiquitin-specific protease 15negatively regulates virus-induced typeⅠinterferon signaling via catalytically-dependent and independent mechanisms[J].Sci Rep,2015,5:11220.
[16]Pauli EK,Chan YK,Davis ME,et al.The ubiquitin-specific protease USP15 promotes RIG-I-mediated antiviral signaling by deubiquitylating TRIM25[J].Sci Signal,2014,7(307):ra3.
[17]Bhoj VG,Chen ZJ.Ubiquitylation in innate and adaptive immunity[J].Nature,2009,458(7237):430-437.
[18]Zou Q,Jin J,Xiao Y,et al.T cell intrinsic USP15 deficiency promotes excessive IFN-gamma production and an immunosuppressive tumor microenvironment in MCA-induced fibrosarcoma[J].Cell Rep,2015,13(11):2470-2479.
[19]Su ZJ,Cao JS,Wu YF,et al.Deubiquitylation of hepatitis B virus X protein(HBx)by ubiquitin-specific peptidase 15(USP15)increases HBx stability and its transactivation activity[J].Sci Rep,2017,7:40246.
[20]吴燕芳.泛素特异性肽酶15与乙型肝炎病毒X蛋白的相互作用及对其功能影响[D].福州:福建医科大学,2016.
[21]Martinez-Zapien D,Ruiz FX,Poirson J,et al.Structure of the E6/E6AP/p53 complex required for HPV-mediated degradation of p53[J].Nature,2016,529(7587):541-545.
[22]Vos RM,Altreuter J,White EA,et al.The ubiquitin-specific peptidase USP15 regulates human papillomavirus type 16 E6 protein stability[J].J Virol,2009,83(17):8885-8892.
[23]Chiang C,Pauli EK,Biryukov J,et al.The Human Papillomavirus E6 Oncoprotein Targets USP15 and TRIM25 To Suppress RIG-ⅠMediated Innate Immune Signaling[J].J Virol,2018,92(6).pii:e01737-17.
[24]时静,张险峰,郑永辉.HIV-1 Nef蛋白最新功能及其增强病毒感染性分子机理的研究进展[J].病毒学报,2018,34(1):113-120.
[25]Pyeon D,Timani KA,Gulraiz F,et al.Function of ubiquitin(Ub)specific protease 15(USP15)in HIV-1 replication and viral protein degradation[J].Virus Res,2016,223:161-169.
[26]Zhang J,Zhang X,Xie F,et al.The regulation of TGF-beta/SMAD signaling by protein deubiquitination[J].Protein Cell,2014,5(7):503-517.
[27]王路凡.E3泛素连接酶TRIM21正调控TGFβ信号通路功能及其机制的研究[D].上海:华东师范大学,2015.
[28]周芳芳,李芳,谢枫,等.TRAF4介导TGF-β信号通路的激活并可作为乳腺癌发生的生物学检测指标[J].中国科学(生命科学),2014,44(6):537-542.
[29]Heldin CH,Landstrom M,Moustakas A.Mechanism of TGF-beta signaling to growth arrest,apoptosis,and epithelial-mesenchymal transition[J].Curr Opin Cell Biol,2009,21(2):166-176.
[30]Massague J,Seoane J,Wotton D.Smad transcription factors[J].Genes Dev,2005,19(23):2783-2810.
[31]Eichhorn PJ,Rodon L,Gonzalez-Junca A,et al.USP15 stabilizes TGF-beta receptorⅠand promotes oncogenesis through the activation of TGF-beta signaling in glioblastoma[J].Nat Med,2012,18(3):429-435.
[32]Zhang L,Zhou F,García de Vinuesa A,et al.TRAF4 promotes TGF-beta receptor signaling and drives breast cancer metastasis[J].Mol Cell,2013,51(5):559-572.
[33]Schweitzer K,Bozko PM,Dubiel W,et al.CSN controls NF-kappaB by deubiquitinylation of IkappaBalpha[J].EMBO J,2007,26(6):1532-1541.
[34]Meek DW.Regulation of the p53 response and its relationship to cancer[J].Biochem J,2015,469(3):325-346.
[35]Wade M,Li YC,Wahl GM.MDM2,MDMX and p53 in oncogenesis and cancer therapy[J].Nat Rev Cancer,2013,13(2):83-96.