James E. Vince focuses on Programmed cell death, Cell biology, Inflammasome, Necroptosis and Caspase 8. Pyroptosis is the focus of his Programmed cell death research. His Cell biology study incorporates themes from Inhibitor of apoptosis, Macrophage and Virulence.
His Inflammasome study is mostly concerned with Caspase 1 and AIM2. The various areas that James E. Vince examines in his Necroptosis study include Inflammation and Signal transducing adaptor protein. In his research, Systemic inflammation, Receptor, Baculoviral IAP repeat-containing protein 3, Caspase and Ripoptosome is intimately related to Cancer research, which falls under the overarching field of Caspase 8.
Cell biology, Programmed cell death, Necroptosis, Inflammasome and Caspase 8 are his primary areas of study. His biological study spans a wide range of topics, including Inhibitor of apoptosis, Innate immune system and Caspase 1. His Programmed cell death research is multidisciplinary, relying on both Tumor necrosis factor alpha and Effector.
His work on RIPK1 as part of general Necroptosis study is frequently connected to Lytic cycle, therefore bridging the gap between diverse disciplines of science and establishing a new relationship between them. His Inflammasome research incorporates elements of Oxidative stress, Secretion and Mitochondrion. In Caspase 8, James E. Vince works on issues like Molecular biology, which are connected to Cycloheximide, Protein family, Bcl-2-associated X protein and Myeloid cells.
James E. Vince mostly deals with Cell biology, Programmed cell death, Inflammasome, Necroptosis and Pyroptosis. His work carried out in the field of Cell biology brings together such families of science as Inhibitor of apoptosis, Caspase 1, Bcl-2 Homologous Antagonist-Killer Protein and Intrinsic apoptosis. His Programmed cell death study is focused on Apoptosis in general.
His Inflammasome study combines topics from a wide range of disciplines, such as Oxidative stress, Cell type, Cytokine and Effector. His research integrates issues of Signal transduction and Intracellular in his study of Necroptosis. The study incorporates disciplines such as Cancer research and Interferon type I in addition to Pyroptosis.
James E. Vince mainly investigates Programmed cell death, Inflammasome, Cell biology, Necroptosis and Inflammation. His research on Programmed cell death focuses in particular on Pyroptosis. He has included themes like Cancer research and Priming in his Pyroptosis study.
His Inflammasome study combines topics in areas such as Secretion, Insulin resistance, Innate immune system, Cell type and Type 2 Diabetes Mellitus. His Cell biology research is multidisciplinary, incorporating elements of Inhibitor of apoptosis, XIAP, Caspase, Caspase 8 and Caspase 1. His work deals with themes such as Diabetes mellitus, Oxidative stress, Disease and Bioinformatics, which intersect with Inflammation.
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IAP Antagonists Target cIAP1 to Induce TNFα-Dependent Apoptosis
James E. Vince;W. Wei-Lynn Wong;Nufail Khan;Rebecca Feltham.
Recruitment of the Linear Ubiquitin Chain Assembly Complex Stabilizes the TNF-R1 Signaling Complex and Is Required for TNF-Mediated Gene Induction
Tobias L. Haas;Christoph H. Emmerich;Christoph H. Emmerich;Bjã¶rn Gerlach;Bjã¶rn Gerlach;Anna C. Schmukle.
Molecular Cell (2009)
Inhibitor of Apoptosis Proteins Limit RIP3 Kinase-Dependent Interleukin-1 Activation
James E. Vince;W. Wei Lynn Wong;W. Wei Lynn Wong;Ian Gentle;Kate E. Lawlor;Kate E. Lawlor.
RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis.
James A Rickard;James A Rickard;Joanne A O'Donnell;Joanne A O'Donnell;Joseph M Evans;Joseph M Evans;Najoua Lalaoui;Najoua Lalaoui.
RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL
Kate E. Lawlor;Nufail Khan;Alison Mildenhall;Motti Gerlic.
Nature Communications (2015)
AIM2 and NLRP3 inflammasomes activate both apoptotic and pyroptotic death pathways via ASC
V Sagulenko;S J Thygesen;D P Sester;A Idris.
Cell Death & Differentiation (2013)
The NLRP3 inflammasome in health and disease: the good, the bad and the ugly
P Menu;J E Vince.
Clinical and Experimental Immunology (2011)
TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNFα
James E. Vince;Diep Chau;Bernard Callus;W. Wei-Lynn Wong.
Journal of Cell Biology (2008)
TRAF2 Must Bind to Cellular Inhibitors of Apoptosis for Tumor Necrosis Factor (TNF) to Efficiently Activate NF-κB and to Prevent TNF-induced Apoptosis
James E. Vince;Delara Pantaki;Rebecca Feltham;Peter D. Mace.
Journal of Biological Chemistry (2009)
Pyroptosis versus necroptosis: similarities, differences, and crosstalk
Daniel Frank;Daniel Frank;James E. Vince;James E. Vince.
Cell Death & Differentiation (2019)
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