Li Jiang
Indiana University
12 Papers
27 Citations
Li Jiang is an academic researcher from Indiana University. The author has contributed to research in topics: Biology & eIF2. The author has an hindex of 6, co-authored 8 publications.
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Papers
Phosphorylation of eIF2 directs ATF5 translational control in response to diverse stress conditions.
TL;DR: It is shown that the expression of the basic zipper transcriptional regulator ATF5 is induced in response to many different stresses, including endoplasmic reticulum stress, arsenite exposure, and proteasome inhibition, by a mechanism requiring eIF2 phosphorylation.
310
Genome-wide Analysis of tRNA Charging and Activation of the eIF2 Kinase Gcn2p
John M. Zaborske,Jana Narasimhan,Li Jiang,Sheree A. Wek,Kimberly A. Dittmar,Florien Freimoser,Tao Pan,Ronald C. Wek +7 more
TL;DR: A microarray technology is applied to analyze genome-wide changes in tRNA charging in yeast upon activation of Gcn2p in response to amino acid starvation and high salinity, showing a complex cellular relationship between tRNAs charging, amino acid availability, and non-nutrient stress.
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The roles of stress-activated Sty1 and Gcn2 kinases and of the protooncoprotein homologue Int6/eIF3e in responses to endogenous oxidative stress during histidine starvation.
Naoki Nemoto,Tsuyoshi Udagawa,Takahiro Ohira,Li Jiang,Kouji Hirota,Caroline Wilkinson,Jürg Bähler,Nic Jones,Kunihiro Ohta,Ronald C. Wek,Katsura Asano +10 more
TL;DR: It is shown that mutants lacking sty1(+) or gcn2(+) display reduced viabilities during histidine depletion stress in a manner suppressible by the antioxidant N-acetyl cysteine, suggesting that these protein kinases function to alleviate endogenous oxidative damage generated during nutrient starvation.
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c-Fms Signaling Mediates Neurofibromatosis Type-1 Osteoclast Gain-In-Functions
Yongzheng He,Steven D. Rhodes,Shi Chen,Xiaohua Wu,Jin Yuan,Xianlin Yang,Li Jiang,Xianqi Li,Naoyuki Takahashi,Mingjiang Xu,Khalid S. Mohammad,Theresa A. Guise,Feng Chun Yang +12 more
TL;DR: It is found that PLX3397 prevented bone loss in Nf1+/−-OVX mice by reducing osteoclast differentiation and bone resorptive activity in vivo, implicate the M-CSF/c-Fms signaling axis as a critical pathway underlying the aberrant functioning of N f1 haploinsufficient osteoclasts and may provide a potential therapeutic target for treating NF1 associated osteoporosis and osteopenia.
Genetic disruption of the small GTPase RAC1 prevents plexiform neurofibroma formation in mice with neurofibromatosis type 17.
Julie A. Mund,Su Jung Park,Abbi Smith,Yongzheng He,Li Jiang,Eric T. Hawley,Michelle J. Roberson,Dana Mitchell,Mohannad Abu-Sultanah,Jin Yuan,Waylan K. Bessler,George E. Sandusky,Shi Chen,Chi Zhang,Steven D. Rhodes,D. Wade Clapp +15 more
TL;DR: It is concluded that the RAC1-GTPase is a key downstream node of RAS and that genetic disruption of the Rac1 allele completely prevents PN tumor formation in vivo in mice.
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