17 Papers
35 Citations
Yi Shi is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Transfer RNA & Biology. The author has an hindex of 10, co-authored 14 publications. Previous affiliations of Yi Shi include Chinese Academy of Sciences.
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Papers
CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase
Weiwei He,Ge Bai,Huihao Zhou,Na Wei,Nicholas M. White,Janelle L. Lauer,Huaqing Liu,Yi Shi,Calin Dan Dumitru,Karen Lettieri,Veronica I. Shubayev,Albena Jordanova,Velina Guergueltcheva,Patrick R. Griffin,Robert W. Burgess,Samuel L. Pfaff,Xiang-Lei Yang +16 more
TL;DR: This work reports that GlyRSCMT2D acquires a neomorphic binding activity that directly antagonizes an essential signalling pathway for motor neuron survival, and indicates that the VEGF–Nrp1 signalling axis is an actionable target for treating CMT2d.
tRNA synthetase counteracts c-Myc to develop functional vasculature
Yi Shi,Xiaoling Xu,Qian Zhang,Guangsen Fu,Zhongying Mo,George S Wang,Shuji Kishi,Xiang-Lei Yang +7 more
TL;DR: It is shown here that SerRS intervenes by antagonizing c-Myc, the major transcription factor promoting VEGFA expression, through a tandem mechanism, and an anti-angiogenic activity for SIRT2 is discovered.
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Oxidative Stress Diverts tRNA Synthetase to Nucleus for Protection against DNA Damage
Na Wei,Yi Shi,Lan N. Truong,Kathleen M. Fisch,Tao Xu,Elisabeth Gardiner,Guangsen Fu,Yun-Shiuan Olivia Hsu,Shuji Kishi,Andrew I. Su,Xiaohua Wu,Xiang-Lei Yang +11 more
TL;DR: It is found that oxidative stress induces TyrRS to rapidly translocate from the cytosol to the nucleus to protect against DNA damage, and angiogenin mediates or potentiates this stress-induced translocalization.
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Neddylation requires glycyl-tRNA synthetase to protect activated E2
Zhongying Mo,Qian Zhang,Ze Liu,Janelle L. Lauer,Yi Shi,Litao Sun,Patrick R. Griffin,Xiang-Lei Yang +7 more
TL;DR: It is reported that glycyl-tRNA synthetase (GlyRS), an essential enzyme in protein synthesis, also plays a critical role in neddylation, and this function is probably conserved in all eukaryotic GlyRS enzymes.
Glucocorticoid-induced apoptosis requires FOXO3A activity.
TL;DR: It is concluded that DEX might maintain FOXO3A in its unphosphorylated, active form, which may explain, in part, their resistance to apoptosis and may be a potential target for cancer therapy.
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