Treatment of MRL/lpr mice, a genetic autoimmune model, with the ras inhibitor, farnesylthiosalicylate (FTS)

Clinical and Experimental Immunology

Volumn 126, Issue 3, 2001, Pages 570-577

  Katzav, A ^a   Kloog, Y ^b   Korczyn, A D ^a,b   Niv, H ^b   Karussis, D M ^d   Wang, N ^a   Rabinowitz, R ^a   Blank, M ^b,c   Shoenfeld, Y ^b,c   Chapman, J ^a,b  

^a Department of Physiology and Pharmacology ^*  (Israel)

^b TEL AVIV UNIVERSITY   (Israel)

^c SHEBA MEDICAL CENTER   (Israel)

^d HADASSAH HEBREW UNIVERSITY MEDICAL CENTER   (Israel)

Author keywords

Antiphospholipid syndrome; Lymphocyte activation; MRL lpr; Ras

Indexed keywords

ANTIBODY; ANTIGEN; BETA2 GLYCOPROTEIN 1; CARDIOLIPIN; CONCANAVALIN A; DNA; FARNESYLTHIOSALICYLIC ACID; LIPOPOLYSACCHARIDE; RAS PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANTIBODY BLOOD LEVEL; ARTICLE; AUTOIMMUNE DISEASE; BEHAVIOR; CONTROLLED STUDY; DISEASE MODEL; DRUG EFFECT; DRUG MECHANISM; FEMALE; GRIP STRENGTH; LYMPH NODE; LYMPHADENOPATHY; LYMPHOCYTE PROLIFERATION; MOUSE; NONHUMAN; OPEN FIELD TEST; PRIORITY JOURNAL; PROTEINURIA; SPLEEN CELL; SPLEEN WEIGHT;

ANIMALS; ANTIPHOSPHOLIPID SYNDROME; AUTOANTIBODIES; AUTOIMMUNE DISEASES; FARNESOL; FEMALE; LUPUS ERYTHEMATOSUS, SYSTEMIC; LYMPHATIC DISEASES; LYMPHOCYTE ACTIVATION; LYMPHOCYTES; MICE; MICE, INBRED MRL LPR; RAS PROTEINS; SALICYLIC ACIDS;

EID: 0035652626     PISSN: 00099104     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1365-2249.2001.01674.x     Document Type: Article

References (44)

1. Lymphocyte activation in health and disease
2. Signal transduction by lymphocyte antigen receptors
3. Signal transduction in T cells
4. Stimulation of p21ras upon T-cell activation
5. GTPases in antigen receptor signalling
6. The regulation and function of p21ras during T-cell activation and growth
7. Function and regulation of Ras
8. p21ras is modified by a farnesyl isoprenoid
9. Specific isoprenoid modification is required for function of normal, but not oncogenic, Ras protein
10. Isoprenoid addition to Ras protein is the critical modification for its membrane association and transforming activity
11. Dislodgment and accelerated degradation of Ras
12. Membrane interactions of a constitutively active GFP-Ki-Ras 4B and their role in signaling. Evidence from lateral mobility studies
13. The Ras antagonist S-farnesylthiosalicylic acid induces inhibition of MAPK activation
14. Stringent structural requirements for anti-Ras activity of S-prenyl analogues
15. Growth inhibition of ras-dependent tumors in nude mice by a potent ras-dislodging antagonist
16. Farnesyl derivatives of rigid carboxylic acids-inhibitors of ras-dependent cell growth
17. Immunopharmacology: Immunomodulation and immunotherapy
18. Experimental models for antiphospholipid studies
19. Experimental and induced animal models of systemic lupus erythematosus and Sjogren's syndrome
20. Animal models for nervous system disease in systemic lupus erythematosus
21. Protooncogenes autoimmunity
22. Down-regulation of autoantibody levels of cyclosporine and bromocriptine treatment in patients with uveitis
23. Differential effects of anti-beta2-glycoprotein I antibodies on endothelial cells and on the manifestations of experimental antiphospholipid syndrome
24. Anti-intercellular adhesion molecule-1 (ICAM-1) antibody treatment prevents central and peripheral nervous system disease in autoimmune-prone mice
25. Delineation of two defects responsible for T-cell hyporesponsiveness to concanavalin A in MRL congenic mice
26. Comparison of in vitro and in vivo mitogenic and polyclonal antibody and autoantibody responses to peptidoglycan, LPS, protein A, PWN, PHA and Con A in normal and autoimmune mice
27. Serum glomerular binding activity is highly correlated with renal disease in MRL/lpr mice
28. Modulation of glomerular structure and function in murine lupus nephritis by methylprednisolone and cyclophosphamide
29. + T cells, cyto-kine gene expression and disease activity in MRL/MpJ-lpr/lpr mice
30. Rapamycin prolongs survival and arrests pathophysiologic changes in murine systemic lupus erythema-tosus
31. Reduction of mortality and lymphadenopathy in MRL-lpr/lpr mice treated with nonmitogenic anti-CD3 monoclonal antibody
32. - double negative T cells and of the autoimmune syndrome in MRL-lpr/lpr mice
33. Lympho-proliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
34. The lpr gene causes an intrinsic T cell abnormality that is required for hyperproliferation
35. Expression of heterozygous lpr gene in MRL mice. I. Defective T-cell reactivity and polyclonal B-cell activation
36. - T lymphocytes from MRL lpr mice
37. Cyclophosphamide-induced changes in the MRL-lpr/lpr mouse: Effects upon cellular composition, immune function, and disease
38. Inhibition of the Ras-pathway of cell activation with s-trans-trans-farnesyl-thiosalicylic acid (FTS); in vivo suppression of experimental autoimmune encephalo-myelitis (EAE) and differential in vitro effects on lymphocytes and astrocytes
39. Treatment of experimental auto-immune neuritis by a Ras inhibitor s-farnesylthiosalicylic acid (FTS)
40. The complexity of signaling pathways activated by the BCR
41. Selective inhibition of Ras-dependent cell growth by farnesylthiosalisylic acid
42. A new functional Ras antagonist inhibits human pancreatic tumor growth in nude mice
43. Novel Ras antagonist blocks human melanoma growth
44. The Ras antagonist, farnesylthiosalicylic acid (FTS), inhibits experimentally-induced liver cirrhosis in rats