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Showing 1–10 of 10 results
Advanced filters: Author: Lori Broderick Clear advanced filters

  • Here, the authors perform large trans-ancestry fine-mapping analyses identifying large numbers of association signals and putative target genes for colorectal cancer risk, advancing our understanding of the genetic and biological basis of this cancer.

    • Zhishan Chen
    • Xingyi Guo
    • Wei Zheng
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-17

  • Topoisomerases are required to release topological stress on DNA during replication and transcription. Here, Broderick et al. report genetic variants in TOP2B that cause a syndromic B cell immunodeficiency associated with reduced TOP2B function, defects in B cell development and B cell activation.

    • Lori Broderick
    • Shawn Yost
    • Hal M. Hoffman
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-15

  • Interleukin-18 (IL-18), a pyroptosis-related cytokine linking immunity and metabolism, regulates appetite, body weight and glucose homeostasis. IL-18 has paradoxical roles: its deficiency leads to obesity, whereas chronic signalling promotes liver fibrosis. Elevated in obesity and diabetes mellitus, IL-18 remains a compelling therapeutic target, with IL-18 binding protein showing anti-fibrotic potential in preclinical and early clinical studies.

    • Christian Stoess
    • Janset Onyuru
    • Ariel E. Feldstein
    Comments & Opinion
    Nature Reviews Endocrinology
    Volume: 22, P: 3-4

  • A multi-ancestry genome-wide association study meta-analysis, combined with transcriptome- and methylome-wide association analyses, identifies risk loci associated with colorectal cancer. Credible effector genes and their target tissues are also highlighted, showing that over a third probably act outside the colonic mucosa.

    • Ceres Fernandez-Rozadilla
    • Maria Timofeeva
    • Ulrike Peters
    Research
    Nature Genetics
    Volume: 55, P: 89-99

  • Inflammasome-driven inflammation extends into the extracellular space and to neighboring cells through the passive release of specks consisting of the adaptor ASC; this perpetuates the innate immune response and adds a dimension beyond interleukin 1 to autoinflammation.

    • Lori Broderick
    • Hal M Hoffman
    News & Views
    Nature Immunology
    Volume: 15, P: 698-700

  • Leucine-rich repeat (LRR) domains are commonly present in immune regulatory proteins. Here the authors show that LRR exonic modularity and alternative splicing of an LRR-containing protein, NLRP3, modulate the ratio of functional/afunctional NLRP3 isoforms to instill a stochastic regulation of NLRP3-mediated inflammation and innate immunity.

    • Florian Hoss
    • James L. Mueller
    • Eicke Latz
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-13

  • Here, the authors summarize new insights into the pathogenesis of NAFLD and NASH, in particular the mechanisms responsible for liver injury and fibrosis. They highlight how a complex interplay between the environment (especially diet), host genetics and the gut microflora is crucial for the development and progression of NAFLD.

    • Alexander Wree
    • Lori Broderick
    • Ariel E. Feldstein
    Reviews
    Nature Reviews Gastroenterology & Hepatology
    Volume: 10, P: 627-636

  • In this Review, the authors summarize the pathophysiological mechanisms of IL-1-mediated autoinflammation. They describe the epidemiological and clinical features of autoinflammatory diseases, challenges associated with diagnostics and disease management, and current and future therapies for targeting the IL-1 pathway.

    • Lori Broderick
    • Hal M. Hoffman
    Reviews
    Nature Reviews Rheumatology
    Volume: 18, P: 448-463