ArticleClinical and experimental immunology2001
Treatment of MRL/lpr mice, a genetic autoimmune model, with the Ras inhibitor, farnesylthiosalicylate (FTS).
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 46 citations in OpenAlex.
- Network-based machine learning to identify biomarkers for systemic lupus erythematosus.BMC biology · 2026Article
- Upregulation of RAF and RalGDS gene expression by TGF-β in systemic sclerosis dermal fibroblasts: a controlled in vitro study.Clinical rheumatology · 2026Article
- The role of endothelin and RAS/ERK signaling in immunopathogenesis-related fibrosis in patients with systemic sclerosis: an updated review with therapeutic implications.Arthritis research & therapy · 2022Review
- Immunosuppressants Tacrolimus and Sirolimus revert the cardiac antifibrotic properties of p38-MAPK inhibition in 3D-multicellular human iPSC-heart organoids.Frontiers in cell and developmental biology · 2022Article
- Polygenic autoimmune disease risk alleles impacting B cell tolerance act in concert across shared molecular networks in mouse and in humans.Frontiers in immunology · 2022Review
- Small GTPase RAS in multiple sclerosis - exploring the role of RAS GTPase in the etiology of multiple sclerosis.Small GTPases · 2020Review
- Inhibition of Ras GTPases prevents Collagen-Induced Arthritis by Reducing the Generation of Pathogenic CD4ACR open rheumatology · 2020Article
- Brain Protease Activated Receptor 1 Pathway: A Therapeutic Target in the Superoxide Dismutase 1 (SOD1) Mouse Model of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020Article
- Ras Signaling Inhibitors Attenuate Disease in Adjuvant-Induced ArthritisFrontiers in immunology · 2017Article
- Innate inflammation induced by the 8-oxoguanine DNA glycosylase-1-KRAS-NF-κB pathway.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- An increase in tolerogenic dendritic cell and natural regulatory T cell numbers during experimental autoimmune encephalomyelitis in Rras-/- mice results in attenuated disease.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Therapeutic effect of farnesylthiosalicylic acid on adjuvant-induced arthritis through suppressed release of inflammatory cytokines.Clinical and experimental immunology · 2014Article
- Prevention of induced colitis in mice by the ras antagonist farnesylthiosalicylic acid.Digestive diseases and sciences · 2012Article
- Ras inhibition by FTS attenuates brain tumor growth in mice by direct antitumor activity and enhanced reactivity of cytotoxic lymphocytes.Oncotarget · 2012Article
- Signal transduction pathways in chronic inflammatory autoimmune disease: small GTPases.The open rheumatology journal · 2012Article
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- Ras inhibition induces insulin sensitivity and glucose uptake.PloS one · 2011 · on this mapArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation and proliferation of lymphocytes requires the active signal transducer Ras. Activation of lymphocytes, associated with autoimmunity, may therefore be modified by S-farnesylthiosalicylic acid (FTS), a synthetic substance that detaches Ras from the inner cell membrane and induces its rapid degradation. The MRL/lpr mouse is a genetic model of a generalized autoimmune disease sharing many features and organ pathology with systemic lupus erythematosus (SLE) and the primary antiphospholipid syndrome (APS). The objective of the present study was to examine the effect of FTS on laboratory and clinical pathology in the MRL/lpr mouse. Female MRL/lpr (n = 50) and MRL/++ control (n = 35) mice were treated intraperitoneally with either FTS (5 mg/kg/day) or saline between 6 and 18 weeks of age. The mice were weighed, tested for proteinuria and lymphadenopathy, lymphocyte proliferation, antibodies, grip strength and behaviour in an open field. FTS treatment resulted in a 50% decrease in splenocyte proliferation to ConA, LPS and a disease specific antigen, beta(2)-glycoprotein-I, and in a significant decrease in serum antibody levels against cardiolipin and dsDNA. Proteinuria and grip strength were normalized and lymphadenopathy and postmortem lymph node and spleen weights were significantly reduced in FTS treated MRL/lpr mice. These findings indicate that modulation of Ras activation has a significant impact on the MRL/lpr model and may represent a new therapeutic approach for the treatment of systemic autoimmune diseases such as SLE and APS.
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