W
W. Wei-Lynn Wong
Researcher at University of Zurich
Publications - 55
Citations - 7210
W. Wei-Lynn Wong is an academic researcher from University of Zurich. The author has contributed to research in topics: Programmed cell death & Tumor necrosis factor alpha. The author has an hindex of 30, co-authored 53 publications receiving 6416 citations. Previous affiliations of W. Wei-Lynn Wong include University Health Network & University of Melbourne.
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Journal ArticleDOI
IAP Antagonists Target cIAP1 to Induce TNFα-Dependent Apoptosis
James E Vince,W. Wei-Lynn Wong,Nufail Khan,Rebecca Feltham,Diep Chau,Afsar U. Ahmed,Christopher A. Benetatos,Srinivas K. Chunduru,Stephen M. Condon,Mark A. McKinlay,Robert Brink,Martin Leverkus,Vinay Tergaonkar,Pascal Schneider,Bernard A. Callus,Frank Koentgen,David L. Vaux,John Silke +17 more
TL;DR: It is shown that apoptosis caused by an IAC is blocked by the caspase 8 inhibitor crmA and that IAP antagonists activate NF-κB signaling via inhibtion of cIAP1.
Journal ArticleDOI
Linear ubiquitination prevents inflammation and regulates immune signalling
Björn Gerlach,Stefanie M. Cordier,Anna C. Schmukle,Christoph H. Emmerich,Christoph H. Emmerich,Eva Rieser,Tobias L. Haas,Andrew I. Webb,James A Rickard,Holly Anderton,W. Wei-Lynn Wong,Ueli Nachbur,Lahiru Gangoda,Uwe Warnken,Anthony W. Purcell,John Silke,Henning Walczak,Henning Walczak +17 more
TL;DR: It is concluded that by enabling linear ubiquitination in the TNF receptor signalling complex, SHARPIN interferes with TNF-induced cell death and, thereby, prevents inflammation.
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HMG-CoA reductase inhibitors and the malignant cell: the statin family of drugs as triggers of tumor-specific apoptosis
W. Wei-Lynn Wong,Jim Dimitroulakos,Mark D. Minden,Mark D. Minden,Linda Z. Penn,Linda Z. Penn +5 more
TL;DR: Clinical trials are warranted to further assess the safety and efficacy of statins as novel and immediately available anti-cancer agents and the experimental evidence supporting a role for the statin family of drugs to this new application will be reviewed.
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RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL
Kate E. Lawlor,Nufail Khan,Alison L Mildenhall,Motti Gerlic,Ben A. Croker,Akshay A. D’Cruz,Cathrine Hall,Sukhdeep Kaur. Spall,Holly Anderton,Seth L. Masters,Maryam Rashidi,Ian P. Wicks,Warren S. Alexander,Yasuhiro Mitsuuchi,Christopher A. Benetatos,Stephen M. Condon,W. Wei-Lynn Wong,John Silke,David L. Vaux,James E Vince +19 more
TL;DR: It is shown that following LPS treatment, or LPS-induced necroptosis, the TLR adaptor protein TRIF and inhibitor of apoptosis proteins (IAPs: X-linked IAP, cellular IAP1 and IAP2) regulate RIPK3 and MLKL ubiquitylation, and RIPK 3 can promote NLRP3 inflammasome and IL-1β inflammatory responses independent ofMLKL and necroPTotic cell death.
Journal ArticleDOI
Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.
James E Vince,W. Wei-Lynn Wong,W. Wei-Lynn Wong,Ian E Gentle,Kate E. Lawlor,Kate E. Lawlor,Ramanjaneyulu Allam,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Kylie D. Mason,Kylie D. Mason,Olaf Gross,Stephen B. Ma,Stephen B. Ma,Greta Guarda,Holly Anderton,Holly Anderton,Rosa Castillo,Georg Häcker,John Silke,John Silke,Jürg Tschopp +21 more
TL;DR: It is demonstrated that activation of the cell death-inducing ripoptosome platform and RIP3 can generate bioactive IL-1β and implicate them as additional targets for the treatment of pathological IL- 1-driven inflammatory responses.