Thomas McQuade
University of Massachusetts Medical School
8 Papers
1 Citations
Thomas McQuade is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Necroptosis & RIPK1. The author has an hindex of 6, co-authored 7 publications.
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Papers
The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis
Jixi Li,Thomas McQuade,Ansgar B. Siemer,Johanna Napetschnig,Kenta Moriwaki,Yu-Shan Hsiao,Ermelinda Damko,David Moquin,Thomas Walz,Thomas Walz,Ann E. McDermott,Francis Ka-Ming Chan,Hao Wu +12 more
TL;DR: Insight is provided into the structural changes that occur when RIP kinases are triggered to execute different signaling outcomes and the realm of amyloids is expanded to complex formation and signaling.
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Functional complementation between FADD and RIP1 in embryos and lymphocytes
Haibing Zhang,Xiaohui Zhou,Xiaohui Zhou,Thomas McQuade,Jinghe Li,Francis Ka-Ming Chan,Jianke Zhang +6 more
TL;DR: It is shown that Fadd−/− embryos contain raised levels of RIP1 and exhibit massive necrosis, and an unexpected cell-type-specific interplay between FADD and RIP1 is critical for the regulation of apoptosis and necrosis during embryogenesis and lymphocyte function.
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CYLD deubiquitinates RIP1 in the TNFα-induced necrosome to facilitate kinase activation and programmed necrosis.
TL;DR: The results suggest that CYLD controls RIP1 kinase activity during necrosome assembly, which could lead to reduced requirement for CYLD to remove ubiquitin chains from RIP1 in the TNFR-1 signaling complex.
The Necroptosis Adaptor RIPK3 Promotes Injury-Induced Cytokine Expression and Tissue Repair
Kenta Moriwaki,Sakthi Balaji,Thomas McQuade,Nidhi Malhotra,Joonsoo Kang,Francis Ka-Ming Chan +5 more
TL;DR: An unexpected function of RIPK3 is revealed in NF-κB activation, DC biology, innate inflammatory-cytokine expression, and injury-induced tissue repair.
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RIP1-dependent and independent effects of necrostatin-1 in necrosis and T cell activation.
TL;DR: The results reveal that besides RIP1, Nec-1 also targets other factors crucial for necrosis induction in L929 cells, and high doses of Nec- 1 inhibit other signal transduction pathways such as that for T cell receptor activation.