James M. Murphy focuses on Cell biology, Necroptosis, Signal transduction, Programmed cell death and Kinase. His Cell biology research includes themes of Proinflammatory cytokine, Biochemistry and Cytokine. His Necroptosis study combines topics in areas such as Tumor necrosis factor alpha, Cancer research, Protein kinase A and Effector.
His study in Programmed cell death is interdisciplinary in nature, drawing from both Enzyme, Cell type and Fatty acid metabolism. James M. Murphy has researched Kinase in several fields, including Molecular biology and Peptide sequence. His studies deal with areas such as FADD, Caspase 8 and Phosphorylation as well as RIPK1.
Cell biology, Necroptosis, Programmed cell death, Kinase and Signal transduction are his primary areas of study. His studies in Cell biology integrate themes in fields like Protein structure, Receptor and Biochemistry. His Necroptosis study combines topics from a wide range of disciplines, such as Tumor necrosis factor alpha, Cancer research, Cell membrane and Protein kinase A.
His Programmed cell death research is multidisciplinary, incorporating perspectives in Inflammation and Heterozygote advantage. His study in the fields of Kinase activity under the domain of Kinase overlaps with other disciplines such as Lytic cycle. His study in Signal transduction is interdisciplinary in nature, drawing from both Innate immune system and Protein kinase domain.
His primary scientific interests are in Cell biology, Necroptosis, Phosphorylation, Kinase and Effector. His Cell biology research incorporates elements of Ubiquitin and Allosteric regulation. His Necroptosis research is under the purview of Programmed cell death.
His study looks at the intersection of Phosphorylation and topics like Cell membrane with Transport protein and DNA-binding protein. Kinase activity, Signal transduction, HEK 293 cells, Xenopus and Janus kinase is closely connected to Protein structure in his research, which is encompassed under the umbrella topic of Kinase. As part of one scientific family, he deals mainly with the area of Effector, narrowing it down to issues related to the Regulator, and often Platelet activation, Platelet, Muscular dystrophy and N-terminus.
His primary areas of study are Cell biology, Necroptosis, Programmed cell death, Phosphorylation and Effector. His work deals with themes such as Receptor and Immune system, which intersect with Cell biology. The study incorporates disciplines such as Heterozygote advantage and Phenotype, Compound heterozygosity in addition to Necroptosis.
The various areas that James M. Murphy examines in his Programmed cell death study include Inflammation, Mutation, Missense mutation and Cancer research. His Phosphorylation research integrates issues from Transport protein and Cell membrane. James M. Murphy has researched Effector in several fields, including Xenopus, HEK 293 cells, Signal transduction, Regulator and Protein structure.
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The Pseudokinase MLKL Mediates Necroptosis via a Molecular Switch Mechanism
James M. Murphy;Peter E. Czabotar;Peter E. Czabotar;Joanne M. Hildebrand;Joanne M. Hildebrand;Isabelle S. Lucet.
Immunity (2013)
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.
Cell (2014)
Monocyte chemotactic protein-1 secreted by primary breast tumors stimulates migration of mesenchymal stem cells.
R.M. Dwyer;S.M. Potter-Beirne;K.A. Harrington;A.J. Lowery.
Clinical Cancer Research (2007)
Activation of the pseudokinase MLKL unleashes the four-helix bundle domain to induce membrane localization and necroptotic cell death
Joanne M. Hildebrand;Maria C. Tanzer;Isabelle S. Lucet;Isabelle S. Lucet;Samuel N. Young.
Proceedings of the National Academy of Sciences of the United States of America (2014)
Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner.
Stephanie A. Conos;Stephanie A. Conos;Kaiwen W Chen;Dominic De Nardo;Dominic De Nardo;Hideki Hara.
Proceedings of the National Academy of Sciences of the United States of America (2017)
Suppression of Cytokine Signaling by SOCS3: Characterization of the Mode of Inhibition and the Basis of Its Specificity
Jeffrey J Babon;Nadia J Kershaw;Nadia J Kershaw;James M Murphy;James M Murphy;Leila N Varghese;Leila N Varghese.
Immunity (2012)
The molecular regulation of Janus kinase (JAK) activation.
Jeffrey J. Babon;Jeffrey J. Babon;Isabelle S. Lucet;Isabelle S. Lucet;James M. Murphy;James M. Murphy;Nicos A. Nicola;Nicos A. Nicola.
Biochemical Journal (2014)
SOCS3 binds specific receptor–JAK complexes to control cytokine signaling by direct kinase inhibition
Nadia J Kershaw;James M Murphy;James M Murphy;Nicholas P D Liau;Nicholas P D Liau;Leila N Varghese;Leila N Varghese.
Nature Structural & Molecular Biology (2013)
A robust methodology to subclassify pseudokinases based on their nucleotide-binding properties.
James M. Murphy;James M. Murphy;Qingwei Zhang;Samuel N. Young;Michael L. Reese.
Biochemical Journal (2014)
TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice
James A Rickard;Holly Anderton;Nima Etemadi;Ueli Nachbur.
eLife (2014)
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