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Articles by F Zhao
Total Records ( 2 ) for F Zhao
  F Zhao , J Qi and S. C. Schuster
 

The woolly mammoth (Mammuthus primigenius) died out about several thousand years ago, yet recent paleogenomic studies have successfully recovered genetic information from both the mitochondrial and nuclear genomes of this extinct species. Mammoths belong to Afrotheria, a group of mammals exhibiting extreme morphological diversity and large genome sizes. In this study, we found that the mammoth genome contains a larger proportion of interspersed repeats than any other mammalian genome reported so far, in which the proliferation of the RTE family of retrotransposons (covering 12% of the genome) may be the main reason for an increased genome size. Phylogenetic analysis showed that RTEs in mammoth are closely related to the family BovB/RTE. The incongruence of the reconstructed RTE phylogeny indicates that RTEs in mammoth may be acquired through an ancient lateral gene transfer event. A recent proliferation of SINEs was also found in the probocidean lineage, whereas the Afrotherian-wide SINEs in mammoth have undergone a rather flat and stepwise expansion. Comparisons of the transposable elements (TEs) between mammoth and other mammals may shed light on the evolutionary history of TEs in various mammalian lineages.

  S Zhu , W Pan , P Shi , H Gao , F Zhao , X Song , Y Liu , L Zhao , X Li , Y Shi and Y. Qian
 

Interleukin 17 (IL-17) plays critical roles in the pathogenesis of various autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE). How the signals triggered by this powerful inflammatory cytokine are controlled to avoid abnormal inflammatory responses is not well understood. In this study, we report that TRAF3 is a receptor proximal negative regulator of IL-17 receptor (IL-17R) signaling. TRAF3 greatly suppressed IL-17–induced NF-B and mitogen-activated protein kinase activation and subsequent production of inflammatory cytokines and chemokines. Mechanistically, the binding of TRAF3 to IL-17R interfered with the formation of the receptor signaling activation complex IL-17R–Act1–TRAF6, resulting in suppression of downstream signaling. TRAF3 markedly inhibited IL-17–induced expression of inflammatory cytokine and chemokine genes in vivo and consequently delayed the onset and greatly reduced the incidence and severity of EAE. Thus, TRAF3 is a negative regulator of IL-17R proximal signaling.

 
 
 
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