D-Index & Metrics Best Publications

D-Index & Metrics

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
Immunology D-index 53 Citations 15,313 110 World Ranking 2418 National Ranking 116

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Cytokine
  • Immune system

Seth L. Masters spends much of his time researching Inflammasome, Immunology, Inflammation, Cell biology and Innate immune system. His biological study spans a wide range of topics, including mir-223, microRNA and Cellular differentiation. His research in Immunology intersects with topics in Adipose tissue, Internal medicine and Endocrinology.

His Inflammation study incorporates themes from Interleukin 33, Cancer research, Transcription factor and Haematopoiesis. His work in Cell biology addresses issues such as Programmed cell death, which are connected to fields such as Proinflammatory cytokine. Seth L. Masters interconnects Pyrin domain, Glycolysis, Lipopolysaccharide and Immunity in the investigation of issues within Innate immune system.

His most cited work include:

  • Succinate is an inflammatory signal that induces IL-1β through HIF-1α (1591 citations)
  • A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases (1061 citations)
  • Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes (896 citations)

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

Seth L. Masters mainly focuses on Cell biology, Immunology, Inflammasome, Innate immune system and Inflammation. Seth L. Masters has included themes like Protein structure and Programmed cell death in his Cell biology study. His study explores the link between Immunology and topics such as Inflammatory bowel disease that cross with problems in Colitis.

His work investigates the relationship between Inflammasome and topics such as Mutation that intersect with problems in Aicardi–Goutières syndrome and Regulator. His Innate immune system research includes elements of Immunity and TLR4. His Inflammation research is multidisciplinary, relying on both Tumor necrosis factor alpha, Cancer research and mir-223.

He most often published in these fields:

  • Cell biology (69.27%)
  • Immunology (51.83%)
  • Inflammasome (55.05%)

What were the highlights of his more recent work (between 2018-2021)?

  • Cell biology (69.27%)
  • Innate immune system (43.12%)
  • Inflammasome (55.05%)

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

His primary scientific interests are in Cell biology, Innate immune system, Inflammasome, Cancer research and Inflammation. The concepts of his Cell biology study are interwoven with issues in Interferon, Macrophage and Stimulator of interferon genes. His work in the fields of Innate immune system, such as Pattern recognition receptor, overlaps with other areas such as Membrane transport protein.

His Inflammasome study contributes to a more complete understanding of Immunology. His Immunology research is multidisciplinary, incorporating perspectives in Gastrointestinal tract and Deubiquitination. The Cancer research study combines topics in areas such as Tumor necrosis factor alpha, Medical microbiology, Compound heterozygosity, Monocyte and Efferocytosis.

Between 2018 and 2021, his most popular works were:

  • Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease (53 citations)
  • Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease (53 citations)
  • RIPLET, and not TRIM25, is required for endogenous RIG-I-dependent antiviral responses. (36 citations)

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

  • Gene
  • Cytokine
  • Immune system

Seth L. Masters mainly focuses on Cell biology, Innate immune system, Programmed cell death, Necroptosis and Signal transduction. His Cell biology study combines topics from a wide range of disciplines, such as Interferon, Influenza A virus and TRIM25. Innate immune system is a primary field of his research addressed under Immune system.

His work carried out in the field of Immune system brings together such families of science as Pyroptosis, Inflammasome, NLRC4 and Type three secretion system. His Programmed cell death study integrates concerns from other disciplines, such as Phenotype, Missense mutation, Mutation, Cancer research and Heterozygote advantage. His Necroptosis research is multidisciplinary, incorporating elements of Caspase 3, Inflammation, Compound heterozygosity and Periodic fever syndrome.

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

Succinate is an inflammatory signal that induces IL-1β through HIF-1α

G. M. Tannahill;A. M. Curtis;J. Adamik;E. M. Palsson-McDermott.
Nature (2013)

1950 Citations

STAT4 and the Risk of Rheumatoid Arthritis and Systemic Lupus Erythematosus

Elaine F. Remmers;Robert M. Plenge;Annette T. Lee;Robert R. Graham;Robert R. Graham.
The New England Journal of Medicine (2007)

1174 Citations

Horror Autoinflammaticus: The Molecular Pathophysiology of Autoinflammatory Disease

Seth L. Masters;Anna Simon;Ivona Aksentijevich;Daniel L. Kastner.
Annual Review of Immunology (2009)

1100 Citations

A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases

Rebecca C Coll;Avril A B Robertson;Jae Jin Chae;Sarah C Higgins.
Nature Medicine (2015)

1046 Citations

Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes

Seth L Masters;Aisling Dunne;Shoba L Subramanian;Rebecca L Hull.
Nature Immunology (2010)

1036 Citations

An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist

Ivona Aksentijevich;Seth L. Masters;Polly J. Ferguson;Paul Dancey.
The New England Journal of Medicine (2009)

826 Citations

The B30.2 domain of pyrin, the familial Mediterranean fever protein, interacts directly with caspase-1 to modulate IL-1beta production.

Jae Jin Chae;Geryl Wood;Seth L. Masters;Katharina Richard.
Proceedings of the National Academy of Sciences of the United States of America (2006)

574 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)

422 Citations

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)

363 Citations

Cutting Edge: miR-223 and EBV miR-BART15 Regulate the NLRP3 Inflammasome and IL-1β Production

Moritz Haneklaus;Motti Gerlic;Mariola Kurowska-Stolarska;Ashleigh-Ann Rainey.
Journal of Immunology (2012)

357 Citations

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