W
Wi S. Lai
Researcher at National Institutes of Health
Publications - 50
Citations - 6900
Wi S. Lai is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Tristetraprolin & Zinc finger. The author has an hindex of 31, co-authored 49 publications receiving 6402 citations. Previous affiliations of Wi S. Lai include Howard Hughes Medical Institute & Research Triangle Park.
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Journal ArticleDOI
Feedback Inhibition of Macrophage Tumor Necrosis Factor-α Production by Tristetraprolin
TL;DR: Findings identify TTP as a component of a negative feedback loop that interferes with TNF-α production by destabilizing its messenger RNA, which represents a potential target for anti-TNF- α therapies.
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A pathogenetic role for TNFα in the syndrome of cachexia, arthritis, and autoimmunity resulting from tristetraprolin (TTP) deficiency
Gregory A. Taylor,Ester Carballo,David M. Lee,Wi S. Lai,Michael J. Thompson,Dhavalkumar D. Patel,Daniel I. Schenkman,Gary S. Gilkeson,Hal E. Broxmeyer,Barton F. Haynes,Perry J. Blackshear +10 more
TL;DR: Treatment of young TTP-deficient mice with antibodies to tumor necrosis factor alpha (TNF alpha) prevented the development of essentially all aspects of the phenotype, indicating a role for TTP in regulating TNF alpha synthesis, secretion, turnover, or action.
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Evidence that tristetraprolin binds to AU-rich elements and promotes the deadenylation and destabilization of tumor necrosis factor alpha mRNA.
Wi S. Lai,Ester Carballo,Julie R. Strum,Elizabeth A. Kennington,Ruth S. Phillips,Perry J. Blackshear,Perry J. Blackshear +6 more
TL;DR: It is shown here that TTP binding to the TNF-α ARE is dependent upon the integrity of both zinc fingers, since mutation of a single cysteine residue in either zinc finger to arginine severely attenuated the binding of TTP to theTNF- α ARE.
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Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stability.
TL;DR: It is shown that TTP deficiency also results in increased cellular production of granulocyte-macrophage colony-stimulating factor (GM-CSF) and increased stability of its mRNA, apparently secondary to decreased deadenylation.
Journal ArticleDOI
Oncogenic RAS Signaling Promotes Tumor Immunoresistance by Stabilizing PD-L1 mRNA
Matthew A. Coelho,Sophie de Carné Trécesson,Sareena Rana,Davide Zecchin,Christopher I. Moore,Miriam Molina-Arcas,Philip East,Bradley Spencer-Dene,Emma Nye,Karin Barnouin,Ambrosius P. Snijders,Wi S. Lai,Perry J. Blackshear,Perry J. Blackshear,Julian Downward,Julian Downward +15 more
TL;DR: It is demonstrated that RAS can drive cell‐intrinsic PD‐L1 expression, thus presenting therapeutic opportunities to reverse the innately immunoresistant phenotype of RAS mutant cancers and a post‐transcriptional mechanism whereby oncogenic RAS signaling increases PD‐l1 expression.