David L Boyle

Summary

Affiliation: University of California
Country: USA

Publications

  1. Boyle D, Kavanaugh A. The pathobiology of psoriatic synovium. Curr Opin Rheumatol. 2008;20:404-7 pubmed publisher
    ..The role of synovia remains unclear, but we now have a better understanding of the pathology of innate and adaptive immunity and are reminded that psoriatic arthritis is a systemic disease. ..
  2. Hammaker D, Boyle D, Inoue T, Firestein G. Regulation of the JNK pathway by TGF-beta activated kinase 1 in rheumatoid arthritis synoviocytes. Arthritis Res Ther. 2007;9:R57 pubmed
    ..The data identify TAK1 as a pivotal upstream kinase and potential therapeutic target to modulate synoviocyte activation in RA. ..
  3. Gong W, Kolker S, USACHEV Y, Walder R, Boyle D, Firestein G, et al. Acid-sensing ion channel 3 decreases phosphorylation of extracellular signal-regulated kinases and induces synoviocyte cell death by increasing intracellular calcium. Arthritis Res Ther. 2014;16:R121 pubmed publisher
    ..Thus, activation of ASIC3 on FLS by acidic pH from an inflamed joint could limit synovial proliferation resulting in reduced accumulation of inflammatory mediators and subsequent joint damage. ..
  4. Lee S, Boyle D, Berdeja A, Firestein G. Regulation of inflammatory arthritis by the upstream kinase mitogen activated protein kinase kinase 7 in the c-Jun N-terminal kinase pathway. Arthritis Res Ther. 2012;14:R38 pubmed publisher
    ..01). MKK7 plays a critical regulatory role in the JNK pathway in a murine model of arthritis. Targeting MKK7 rather than JNK could provide site and event specificity when treating synovitis. ..