T
Tuo Li
Researcher at University of Texas Southwestern Medical Center
Publications - 21
Citations - 6491
Tuo Li is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Stimulator of interferon genes & Gene. The author has an hindex of 17, co-authored 20 publications receiving 4640 citations. Previous affiliations of Tuo Li include Princeton University & University of Washington.
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Journal ArticleDOI
The CRAPome: a contaminant repository for affinity purification–mass spectrometry data
Dattatreya Mellacheruvu,Zachary Wright,Amber L. Couzens,Jean-Philippe Lambert,Nicole St-Denis,Tuo Li,Yana Miteva,Simon Hauri,Mihaela E. Sardiu,Teck Yew Low,Vincentius A. Halim,Vincentius A. Halim,Richard D. Bagshaw,Nina C. Hubner,Abdallah Al-Hakim,Annie Bouchard,Denis Faubert,Damian Fermin,Wade H. Dunham,Marilyn Goudreault,Zhen Yuan Lin,Beatriz Gonzalez Badillo,Tony Pawson,Daniel Durocher,Benoit Coulombe,Ruedi Aebersold,Ruedi Aebersold,Giulio Superti-Furga,Jacques Colinge,Albert J. R. Heck,Hyungwon Choi,Matthias Gstaiger,Shabaz Mohammed,Ileana M. Cristea,Keiryn L. Bennett,Michael P. Washburn,Michael P. Washburn,Brian Raught,Rob M. Ewing,Rob M. Ewing,Anne-Claude Gingras,Alexey I. Nesvizhskii +41 more
TL;DR: The contaminant repository for affinity purification (the CRAPome) is presented and its use for scoring protein-protein interactions is described and aggregating negative controls from multiple AP-MS studies can increase coverage and improve the characterization of background associated with a given experimental protocol.
Journal ArticleDOI
Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation
Siqi Liu,Xin Cai,Jiaxi Wu,Qian Cong,Xiang Chen,Tuo Li,Fenghe Du,Junyao Ren,You Tong Wu,Nick V. Grishin,Zhijian J. Chen +10 more
TL;DR: A common signaling mechanism used by all three types of innate immune receptor-adaptor protein pairs to activate IRF3 and generate IFNs is reported, which is important because cells must regulate their IFN production carefully to avoid inflammation and autoimmunity.
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The cGAS-cGAMP-STING pathway connects DNA damage to inflammation, senescence, and cancer.
TL;DR: This review summarizes recent findings on how genomic instability leads to cGAS activation and how this pathway critically connects DNA damage to autoinflammatory diseases, cellular senescence, and cancer.
Journal ArticleDOI
Apoptotic Caspases Prevent the Induction of Type I Interferons by Mitochondrial DNA
Anthony Rongvaux,Ruaidhri Jackson,Christian C. D. Harman,Tuo Li,A. Phillip West,Marcel R. de Zoete,Marcel R. de Zoete,Youtong Wu,Brian Yordy,Saquib A. Lakhani,Chia-Yi Kuan,Tadatsugu Taniguchi,Gerald S. Shadel,Zhijian J. Chen,Zhijian J. Chen,Akiko Iwasaki,Akiko Iwasaki,Richard A. Flavell,Richard A. Flavell +18 more
TL;DR: The results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response and to inactivate this response in a caspase-dependent manner, which provides a dual control, which determines whether mitochondria initiate an immunologically silent or a proinflammatory type of cell death.
Journal ArticleDOI
Autophagy induction via STING trafficking is a primordial function of the cGAS pathway.
TL;DR: It is reported that cGAMP-induced autophagy is important for the clearance of DNA and viruses in the cytosol and Interestingly, STING from the sea anemone Nematostella vectensis inducesAutophagy but not interferons in response to stimulation by cGamp, which suggests that induction of autophileagy is a primordial function of the cGAS–STING pathway.