Affiliation: University of California
- Regulation of c-Jun N-terminal kinase by MEKK-2 and mitogen-activated protein kinase kinase kinases in rheumatoid arthritisDeepa R Hammaker
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
J Immunol 172:1612-8. 2004..These data indicate that MEKK2 is a potent activator of the JNK pathway in FLS and that signal complexes including MEKK2, MKK4, MKK7, and/or JNK are potential therapeutic targets in RA...
- Differential roles of MAPK kinases MKK3 and MKK6 in osteoclastogenesis and bone lossDavid L Boyle
Medicine, University of California San Diego, La Jolla, California, United States of America
PLoS ONE 9:e84818. 2014..MKK3 directly mediates osteoclastogenesis while MKK6 likely contributes to pro-inflammatory cytokine production that promotes osteoclast formation. ..
- Synoviocyte innate immune responses: TANK-binding kinase-1 as a potential therapeutic target in rheumatoid arthritisDeepa Hammaker
Division of Rheumatology, Allergy, and Immunology, University of California San Diego, School of Medicine, 9500 Gilman Dr MC0656, La Jolla, USA
Rheumatology (Oxford) 51:610-8. 2012..Since IP-10 is a promising therapeutic target in RA, we evaluated whether blocking TBK1 might be an effective way to modulate IP-10 expression...
- Decreased collagen-induced arthritis severity and adaptive immunity in MKK-6-deficient miceDeepa Hammaker
University of California San Diego at La Jolla, CA 92093, USA
Arthritis Rheum 64:678-87. 2012..However, the role of these kinases in adaptive immunity-dependent models of chronic arthritis is not known. The goal of this study was to evaluate MKK-3 and MKK-6 deficiency in the collagen-induced arthritis (CIA) model...
- PUMA-mediated apoptosis in fibroblast-like synoviocytes does not require p53Xin You
Division of Rheumatology, Allergy and Immunology, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA
Arthritis Res Ther 8:R157. 2006..Therefore, approaches to gene therapy that involve increasing PUMA expression could be an effective inducer of synoviocyte cell death in rheumatoid arthritis regardless of the p53 status in the synovium...
- Regulation of the JNK pathway by TGF-beta activated kinase 1 in rheumatoid arthritis synoviocytesDeepa R Hammaker
Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, Gilman Dr, La Jolla, CA 92093, USA
Arthritis Res Ther 9:R57. 2007..In contrast to other cell lineages, MEKK1, MEKK2, and MEKK3 did not contribute to JNK phosphorylation in FLSs. The data identify TAK1 as a pivotal upstream kinase and potential therapeutic target to modulate synoviocyte activation in RA...
- "Go upstream, young man": lessons learned from the p38 sagaD Hammaker
Division of Rheumatology, Allergy and Immunology, UC San Diego School of Medicine, La Jolla, CA 92093 0656, USA
Ann Rheum Dis 69:i77-82. 2010..Alternative strategies, such as targeting kinases higher in the signalling cascade or using less selective compounds, might be more successful as suggested by the efficacy seen with Syk and JAK inhibitors...
- Assessment of rituximab's immunomodulatory synovial effects (ARISE trial). 1: clinical and synovial biomarker resultsA Kavanaugh
University of California, San Diego, Division of Rheumatology, Allergy, and Immunology, 9500 Gilman Drive, Mail Code 0943, La Jolla, CA 92093 0943, USA
Ann Rheum Dis 67:402-8. 2008..Marked depletion of circulating B cells, seen in almost all patients, does not correlate with efficacy. The potential synovial immunomodulatory effects of rituximab have not been fully defined...
- Signal transduction networks in rheumatoid arthritisD Hammaker
Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, CA 92093, USA
Ann Rheum Dis 62:ii86-9. 2003....