D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Molecular Biology D-index 57 Citations 11,119 187 World Ranking 1472 National Ranking 41

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • DNA

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.

His most cited work include:

  • The Pseudokinase MLKL Mediates Necroptosis via a Molecular Switch Mechanism (643 citations)
  • RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis. (356 citations)
  • RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis. (356 citations)

What are the main themes of his work throughout his whole career to date?

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.

He most often published in these fields:

  • Cell biology (106.04%)
  • Necroptosis (69.06%)
  • Programmed cell death (58.49%)

What were the highlights of his more recent work (between 2019-2021)?

  • Cell biology (106.04%)
  • Necroptosis (69.06%)
  • Phosphorylation (35.47%)

In recent papers he was focusing on the following fields of study:

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.

Between 2019 and 2021, his most popular works were:

  • MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis (32 citations)
  • MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis (32 citations)
  • A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction. (20 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • DNA

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.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

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)

939 Citations

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)

508 Citations

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)

491 Citations

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)

445 Citations

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)

269 Citations

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)

267 Citations

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)

263 Citations

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)

251 Citations

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)

245 Citations

TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice

James A Rickard;Holly Anderton;Nima Etemadi;Ueli Nachbur.
eLife (2014)

230 Citations

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