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Biology and Biochemistry

D-Index
57
Citations
23911
World Ranking
13523
National Ranking
5736

Overview

Kim Newton is a researcher affiliated with Genentech in the United States, whose work primarily spans the fields of Biochemistry, Genetics and Molecular Biology, as well as Immunology and Microbiology. Their research focuses on molecular biology and immunology, with specific attention to pulmonary and respiratory medicine, epidemiology, and hematology.

Newton's scholarly output includes a notable concentration on inflammasome and immune disorders, cell death mechanisms and regulation, immune response and inflammation, interferon and immune responses, heme oxygenase-1 and carbon monoxide, ubiquitin and proteasome pathways, and autoimmune and inflammatory disorders research.

Key recent publications by Newton include:

  • "Cell death," 2024, published in Cell
  • "Dying cells fan the flames of inflammation," 2021, published in Science
  • "Shigella ubiquitin ligase IpaH7.8 targets gasdermin D for degradation to prevent pyroptosis and enable infection," 2021, published in Cell Host & Microbe
  • "Ubiquitin Ligase COP1 Suppresses Neuroinflammation by Degrading c/EBPβ in Microglia," 2020, published in Cell
  • "Selective activation of PFKL suppresses the phagocytic oxidative burst," 2021, published in Cell

Newton frequently collaborates with scholars such as Vishva M. Dixit, Joshua D. Webster, Nobuhiko Kayagaki, Rohit Reja, and Debra L. Dugger. These coauthors have contributed with various joint publications, with collaboration counts ranging from eight to twenty papers per coauthor.

Their research has been presented in several prestigious scientific venues, most notably:

  • Nature (7 publications)
  • Cell (4 publications)
  • Cell Death and Differentiation (4 publications)
  • bioRxiv (Cold Spring Harbor Laboratory) (3 publications)
  • Science (1 publication)

Best Publications

  • Cryopyrin activates the inflammasome in response to toxins and ATP

    Sanjeev Mariathasan;David S. Weiss;Kim Newton;Jacqueline McBride

  • Non-canonical inflammasome activation targets caspase-11

    Nobuhiko Kayagaki;Søren Warming;Mohamed Lamkanfi;Lieselotte Vande Walle

  • Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf.

    Sanjeev Mariathasan;Kim Newton;Denise M. Monack;Domagoj Vucic

  • Signaling in Innate Immunity and Inflammation

    Kim Newton;Vishva M. Dixit

  • Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis.

    Kim Newton;Debra L. Dugger;Katherine E. Wickliffe;Neeraj Kapoor

  • Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella

    Petr Broz;Kim Newton;Mohamed Lamkanfi;Sanjeev Mariathasan

  • Ubiquitin Chain Editing Revealed by Polyubiquitin Linkage-Specific Antibodies

    Kim Newton;Marissa L. Matsumoto;Ingrid E. Wertz;Donald S. Kirkpatrick

  • Kinase RIP3 Is Dispensable for Normal NF-κBs, Signaling by the B-Cell and T-Cell Receptors, Tumor Necrosis Factor Receptor 1, and Toll-Like Receptors 2 and 4

    Kim Newton;Xiaoqing Sun;Vishva M. Dixit

  • Absent in melanoma 2 is required for innate immune recognition of Francisella tularensis

    Jonathan W. Jones;Nobuhiko Kayagaki;Petr Broz;Thomas Henry

  • A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes

    Kim Newton;Alan W. Harris;Mary L. Bath;Kenneth G.C. Smith

  • RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury.

    K Newton;D L Dugger;A Maltzman;J M Greve

  • Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation

    Anwesha Dey;Dhaya Seshasayee;Rajkumar Noubade;Dorothy M. French

  • Pannexin-1 Is Required for ATP Release during Apoptosis but Not for Inflammasome Activation

    Yan Qu;Shahram Misaghi;Kim Newton;Laurie L. Gilmour

  • Cleavage of RIPK1 by caspase-8 is crucial for limiting apoptosis and necroptosis

    Kim Newton;Katherine E Wickliffe;Debra L Dugger;Allie Maltzman

  • Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-xL

    David C. S. Huang;Michael Hahne;Michael Schroeter;Karl Frei

  • RIPK1 and RIPK3: critical regulators of inflammation and cell death.

    Kim Newton

  • Necroptosis and Inflammation

    Kim Newton;Gerard Manning

  • Phosphorylation of NLRC4 is critical for inflammasome activation

    Yan Qu;Shahram Misaghi;Anita Izrael-Tomasevic;Kim Newton

  • RIPK1 inhibits ZBP1-driven necroptosis during development.

    Kim Newton;Katherine E. Wickliffe;Allie Maltzman;Debra L. Dugger

  • Activity of caspase-8 determines plasticity between cell death pathways.

    Kim Newton;Katherine E. Wickliffe;Allie Maltzman;Debra L. Dugger

Frequent Co-Authors

Domagoj Vucic
Domagoj Vucic Genentech
Wyne P. Lee
Wyne P. Lee Genentech
Jinfeng Liu
Jinfeng Liu Genentech
Andreas Strasser
Andreas Strasser Walter and Eliza Hall Institute of Medical Research
Zora Modrusan
Zora Modrusan Genentech
Lorraine A. O'Reilly
Lorraine A. O'Reilly Walter and Eliza Hall Institute of Medical Research
Denise M. Monack
Denise M. Monack Stanford University
Mohamed Lamkanfi
Mohamed Lamkanfi Ghent University

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