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杰出青年
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全所PI名录 >

 
侯法建
研究员,研究组长,博士生导师
E-mail: fhou@@sibcb.ac.cn


个人简介

1995年毕业于武汉大学,获学士学位;2001年毕业于中科院上海生化所,获博士学位。2001年11月至2012年1月于美国德州大学西南医学中心从事博士后研究。2012年2月起,在中科院上海生物化学与细胞生物学研究所任研究员,研究组长。


研究方向

天然免疫与炎症的生化细胞机理及相关疾病


研究工作
当病原体入侵高等有机体时,会引发免疫反应,包括天然免疫和适应性免疫。天然免疫反应起始于宿主细胞的受体分子对病原体上的特异分子或者其它“异己”成分的识别,随后激活特定的信号通路,诱导相应基因表达,防御病原体侵染。譬如当病毒感染细胞时,病毒相关的核酸分子会被细胞内的受体分子识别而激活相应的信号通路,诱导抗病毒的干扰素产生。天然免疫反应能够为有机体提供及时的保护,但是其信号异常也可能导致自身免疫疾病等后果。肿瘤发生过程中产生的危险信号分子也可以激活天然免疫反应,诱导炎症。我们近期聚焦RIG-I-MAVS信号通路,利用生物化学和分子生物学方法在细胞和动物水平上来解析其中的分子细胞机制,研究该信号通路与自身免疫疾病发生的相关性及其在肿瘤治疗中的功能作用。


代表性论文

  1. Zhu W#, Li J#, Zhang R, Cai Y, Wang C, Qi S, Chen S, Liang X, Qi N*, Hou F* (2019) TRAF3IP3 mediates the recruitment of TRAF3 to MAVS for antiviral innate immunity. EMBO J, doi: 10.15252/embj.2019102075
  2. Cadena C, Ahmad S, Xavier A, Willemsen J, Park S, Park J, Oh S, Fujita T, Hou F, Binder M, Hur S* (2019) Ubiquitin-Dependent and -Independent Roles of E3 Ligase RIPLET in Innate Immunity. Cell, 177, 1-14
  3. Zhou P, Ding X, Wan X, Liu L, Yuan X, Zhang W, Hui X, Meng G, Xiao H, Li B, Zhong J, Hou F, Deng L, Zhang Y* (2018) MLL5 suppresses antiviral innate immune response by facilitating STUB1-mediated RIG-I degradation. Nat Commun, |9:1243|DOI: 10.1038/s41467-018-03563-8
  4. Li X, Gadzinsky A, Gong L, Tong H, Calderon V, Li Y, Kitamura D, Klein U, Langdon WY, Hou F, Zou YR, Gu H* (2018) Cbl Ubiquitin Ligases Control B Cell Exit from the Germinal-Center Reaction. Immunity, 48, 530-541
  5. Qi N#, Shi Y#, Zhang R, Zhu W, Yuan B, Li X, Wang C, Zhang X, Hou F* (2017) Multiple truncated isoforms of MAVS prevent its spontaneous aggregation in antiviral innate immune signalling. Nat Commun, |8:15676|DOI: 10.1038/ncomms15676
  6. Shi Y#, Yuan B#, Zhu W#, Zhang R, Li L, Hao X, Chen S, Hou F* (2017) Ube2D3 and Ube2N are essential for RIG-I-mediated MAVS aggregation in antiviral innate immunity. Nat Commun, |8:15138| DOI:10.1038/ncomms 15138
  7. Shi Y#, Yuan B#, Qi N#, Zhu W, Su J, Li X, Qi P, Zhang D, Hou F* (2015) An autoinhibitory mechanism modulates MAVS activity in antiviral innate immune response. Nat Commun, |6:78111|DOI: 10.1038/ncomms8811
  8. Xu H, He X, Zheng H, Huang L, Hou F, Yu Z, Cruz MJ, Borkowski B, Zhang X*, Chen ZJ*, Jiang Q-X* (2014) Structural basis for the prion-like MAVS filaments in antiviral innate immunity. ELife, 3, e01489
  9. Hou F, Sun L, Zheng H, Skaug B, Jiang QX, and Chen ZJ* (2011) MAVS Forms Functional Prion-like Aggregates to Activate and Propagate Antiviral Innate Immune Response. Cell, 146, 448-461
  10. Chu CW, Hou F, Zhang J, Phu L, Loktev AV, Kirkpatrick DS. Jackson PK, Zhao Y, and Zou H* (2011) A novel acetylation of beta-tubulin by San modulates microtubule polymerization via down-regulating tubulin incorporation. Mol Biol Cell, 22, 448-456
  11. Zeng W, Sun L, Jiang X, Chen X, Hou F, Adhikari A, Xu M, and Chen ZJ* (2010) Reconstitution of the RIG-I pathway reveals a signaling role of unanchored polyubiquitin chains in innate immunity. Cell, 141, 315-330
  12. Gordillo M, Vega H, Trainer AH, Hou F, Sakai N, Luque R, Kayserili H, Basaran S, Skovby F, Hennekam RC, Uzielli ML, Schnur RE, Manouvrier S, Chang S, Blair E, Hurst JA, Forzano F, Meins M, Simola KO, Raas-Rothschild A, Schultz RA, McDaniel LD, Ozono K, Inui K, Zou H and Jabs EW* (2008) The molecular mechanism underlying Roberts syndrome involves loss of ESCO2 acetyltransferase activity. Hum Mol Genet, 17(14), 2172-80
  13. Hou F, Chu CW, Kong X, Yokomori K, and Zou H* (2007) The acetyltransferase activity of San stabilizes the mitotic cohesin at the centromeres in a shugoshin-independent manner. J Cell Biol, 177, 587-597
  14. Hou F, and Zou H* (2005) Two human orthologues of Eco1/Ctf7 acetyltransferases are both required for proper sister-chromatid cohesion. Mol Biol Cell, 16, 3908-3918
  15. Jia J, Zhang L, Zhang Q, Tong C, Wang B, Hou F, Amanai K, and Jiang J* (2005) Phosphorylation by double-time/CKIepsilon and CKIalpha targets cubitus interruptus for Slimb/beta-TRCP-mediated proteolytic processing. Dev Cell, 9, 819-830

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