When Shu entered senior high school, he failed the chemistry exam, and did not know any English.
[5] In 1990, Shu went to the United States and worked as a research assistant at the University of Michigan Medical Center.
[6] In 1999 Shu became a Changjiang scholar and part-time professor at Peking University School of Life Sciences.
[11] In 2000, he and his colleagues showed that FADD, Casper (caspase-8-related protein), and caspase-8 play important roles in NF-kappaB activation pathways.
[12] 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.
[17] 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;[18] that RBCK1, a ubiquitin ligase, negatively regulates TNF and IL-1 triggered inflammatory signaling;[19] that DAK, a dihydroacetone kinase, can inhibit MDA5;[20] and that ISG56 (IFN-stimulated gene 56) is related to VSV replication, and negatively mediates virus-triggered induction of type I IFNs.