Shu Hongbing

Shu Hongbing
Native name 舒红兵
Born January 1967
Rongchang County, Chongqing, China
Residence Wuhan, China
Nationality Chinese
Fields Immunology, Cell Biology
Institutions Peking University; Wuhan University
Alma mater Lanzhou University; Emory University
Doctoral advisor Gary J. Nabel
Other academic advisors David Goeddel
Notable awards Changjiang (Yangtze River) Scholar Award, Chinese Ministry of Education (1999)
Second prize, Chinese State Natural Science Award (2010)
Member of Chinese Academy of Sciences (2011) [1]
This is a Chinese name; the family name is Shu.

Shu Hongbing (Chinese: 舒红兵; born 1967) is a Chinese cytologist and immunologist. He became a member of the Chinese Academy of Sciences in 2011 and TWAS in 2012. Shu is mainly known for his work on cell signal transduction related to immunity.[2]

Life

Shu Hongbing was born to a poor rural family in Rongchang County, Chongqing. His mother died when he was 9 years old. When Shu entered senior high school, he failed the chemistry exam, and did not know any English.[3] He had to go to school barefoot because he could not afford to buy shoes.[3] However, by the time he finished high school with a national stipend in 1983, he was accepted by Lanzhou University with the highest National Matriculation Examination score in his class.[3] After graduating in 1987, Shu entered the Chinese Academy of Medical Sciences Basic Medical Institute Cell Laboratory, where he obtained his master's degree three years later.[4]

In 1990 Shu went to the United States and worked as a research assistant at the University of Michigan Medical Center. In 1992 he became a postgraduate student at Emory University, where he earned his Ph.D. within 3 years.[3] In 1995, he entered David Goeddel's laboratory at Tularik. In 1998 he became an assistant professor at the Department of Immunology of the National Jewish Medical and Research Center; he was promoted to associate professor in 2003.[5] In 1999 Shu became a Changjiang scholar and part-time professor at Peking University School of Life Sciences. At the end of 2004, Wuhan University College of Life Sciences employed him as the dean. In December 2011, he was elected as a member of the Chinese Academy of Sciences. In September 2013, he was appointed as a vice-president of Wuhan University.[6]

Research

In 1999, Shu's team studied downstream signaling by TRAIL receptors. They discovered that a signaling cascade can mediate TRAIL-induced NF-κB activation, and TRAIL-induced apoptosis cannot be blocked by it.[7] In 2000, he and his colleagues showed that FADD, Casper, and caspase-8 play important roles in NF-kappaB activation pathways.[8] In 2002 they used two-hybrid screening to identify BAFF-R-associated downstream proteins, showing that TRAF3 can inhibit BAFF-R-mediated NF-kappaB activation and IL-10 production.[9] They also cloned and identified a novel AIF-homologous molecule called AMID, which can lead the way to caspase-independent apoptosis.[10]

In 2005, his team identified a novel molecule that serves as a signal transfer station. Previously in 2003, a Japanese team had already demonstrated several genes involved in NF-kappaB activation. Shu's team discovered that over-expression of one of these genes had a strong effect on IRF3 activation. Through a series of experiments, they discovered that the product of this gene greatly influences TLR3-independent IFN-β signaling. It was named VISA (virus-induced signaling adaptor). It can also interact with TRIF and TRAF6, and plays an essential role in virus-triggered TLR3-independent and TLR3-mediated antiviral IFN signaling.[11] In 2008 they discovered another adaptor protein, MITA, through expression cloning. MITA is related to VISA, and has the ability to mediate virus-triggered IRF3 activation and IFN expression.[12] Their later studies showed that by ubiquitination and degradation of MITA, E3 ubiquitin ligase RNF5 can negatively regulate cellular antiviral signaling.[13]

In Shu's lab they also showed that SIKE, a physiological suppressor of IKK epsilon and TBK1, can inhibit virus and TLR3-triggered IRF-3 activation;[14] that RBCK1, a ubiquitin ligase, negatively regulates TNF and IL-1 triggered inflammatory signaling;[15] that DAK, a dihydroacetone kinase, can inhibit MDA5;[16] and that ISG56 (IFN-stimulated gene 56) is related to VSV replication, and negatively mediates virus-triggered induction of type I IFNs.[17]

References

  1. ↑ "舒红兵任武汉大学副校长 曾获自然科学奖二等奖". 长江网. Retrieved 20 September 2014.
  2. ↑ "Shu Hongbing". Wuhan University. Retrieved 14 September 2014.
  3. 1 2 3 4 凤栖 (8 November 2013). "舒红兵　从海外揽回的生命科学"少帅"". 中华儿女报刊社. Retrieved 14 September 2014.
  4. ↑ 别鸣 (13 June 2013). "舒红兵院士的生命情怀". Hubei Daily. Retrieved 15 September 2014.
  5. ↑ "舒红兵". 武汉大学病毒学国家重点实验室. 27 April 2013. Retrieved 5 October 2014.
  6. ↑ 夸克 (20 December 2013). "荣昌偏远农家 走出中科院"最年轻"院士". 都市快报. Retrieved 18 September 2014.
  7. ↑ Hu WH, Johnson H, Shu HB (October 1999). "Tumor necrosis factor-related apoptosis-inducing ligand receptors signal NF-kappaB and JNK activation and apoptosis through distinct pathways". J. Biol. Chem. 274 (43): 30603–10. doi:10.1074/jbc.274.43.30603. PMID 10521444.
  8. ↑ Hu WH, Johnson H, Shu HB (April 2000). "Activation of NF-kappaB by FADD, Casper, and caspase-8". J. Biol. Chem. 275 (15): 10838–44. doi:10.1074/jbc.275.15.10838. PMID 10753878.
  9. ↑ Xu LG, Shu HB (December 2002). "TNFR-associated factor-3 is associated with BAFF-R and negatively regulates BAFF-R-mediated NF-kappa B activation and IL-10 production". J. Immunol. 169 (12): 6883–9. doi:10.4049/jimmunol.169.12.6883. PMID 12471121.
  10. ↑ Wu M, Xu LG, Li X, Zhai Z, Shu HB (July 2002). "AMID, an apoptosis-inducing factor-homologous mitochondrion-associated protein, induces caspase-independent apoptosis". J. Biol. Chem. 277 (28): 25617–23. doi:10.1074/jbc.M202285200. PMID 11980907.
  11. ↑ Xu LG, Wang YY, Han KJ, Li LY, Zhai Z, Shu HB (September 2005). "VISA is an adapter protein required for virus-triggered IFN-beta signaling". Mol. Cell 19 (6): 727–40. doi:10.1016/j.molcel.2005.08.014. PMID 16153868.
  12. ↑ Zhong B, Yang Y, Li S, et al. (October 2008). "The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation". Immunity 29 (4): 538–50. doi:10.1016/j.immuni.2008.09.003. PMID 18818105.
  13. ↑ Zhong B, Zhang L, Lei C, et al. (March 2009). "The ubiquitin ligase RNF5 regulates antiviral responses by mediating degradation of the adaptor protein MITA". Immunity 30 (3): 397–407. doi:10.1016/j.immuni.2009.01.008. PMID 19285439.
  14. ↑ Huang J, Liu T, Xu LG, Chen D, Zhai Z, Shu HB (December 2005). "SIKE is an IKK epsilon/TBK1-associated suppressor of TLR3- and virus-triggered IRF-3 activation pathways". EMBO J. 24 (23): 4018–28. doi:10.1038/sj.emboj.7600863. PMC 1356304. PMID 16281057.
  15. ↑ Tian Y, Zhang Y, Zhong B, et al. (June 2007). "RBCK1 negatively regulates tumor necrosis factor- and interleukin-1-triggered NF-kappaB activation by targeting TAB2/3 for degradation". J. Biol. Chem. 282 (23): 16776–82. doi:10.1074/jbc.M701913200. PMID 17449468.
  16. ↑ Diao F, Li S, Tian Y, et al. (July 2007). "Negative regulation of MDA5- but not RIG-I-mediated innate antiviral signaling by the dihydroxyacetone kinase". Proc. Natl. Acad. Sci. U.S.A. 104 (28): 11706–11. doi:10.1073/pnas.0700544104. PMC 1913852. PMID 17600090.
  17. ↑ Li Y, Li C, Xue P, et al. (May 2009). "ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response". Proc. Natl. Acad. Sci. U.S.A. 106 (19): 7945–50. doi:10.1073/pnas.0900818106. PMC 2683125. PMID 19416887.
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