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Articles by P Shi
Total Records ( 2 ) for P Shi
  Y. Y Shen , P Shi , Y. B Sun and Y. P. Zhang

The evolution of flight is the most important feature of birds, and this ability has helped them become one of the most successful groups of vertebrates. However, some species have independently lost their ability to fly. The degeneration of flight ability is a long process, and some species remain transitional locomotive models. Most of the energy required for locomotion is supplied by mitochondria via oxidative phosphorylation. Thus, rapidly flying birds should require a more energy efficient metabolism than weakly flying or flightless species. Therefore, we speculated that evolutionary constraints acted on the mtDNA of birds with different locomotive abilities. To test this hypothesis, we compared 76 complete avian mitochondrial genomes. Weakly flying and flightless birds, compared to rapidly flying birds, accumulated more nonsynonymous nucleotide substitutions relative to synonymous substitutions. Even after controlling for mutation rate, this trend remained significant. This finding was further tested for its generality by examining 214 complete mammalian mitochondrial genomes. The same as birds, a negative correlation was also found for the Ka/Ks ratio and locomotive speed. Our results demonstrated that, in addition to the previously described role for effective population size, functional constraints due to locomotion play an important role in the evolution of mtDNA.

  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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