RNP-68K (Sm-Free)

Product Information

Anti-RNP antibodies were found in the sera of mixed connective tissue disease (MCTD) patients, and when these antibodies occur at high titre and in the absence of Sm, they are a good marker for MCTD. Such autoantibodies are also known to occur in the sera of patients with a range of other rheumatic diseases including progressive systemic sclerosis, rheumatoid arthritis, discoid lupus erythematosus, Sjögren's syndrome and various overlapping conditions.

The snRNPs are a group of nuclear particles comprised of several polypeptides associated with a small nuclear RNA molecule.  The most abundant snRNPs are involved in pre-mRNA-splicing. At least 13 different snRNAs have been identified in mammalian cells. Whereas autoantibodies directed against Sm are able to precipitate a wide range of snRNAs, RNP autoantibodies are only able to precipitate one particular type, referred to as U1snRNA. Anti-RNP antibodies react with the U1 snRNP-specific polypeptides (68K, A and C antigens) whereas anti-Sm antibodies react with polypeptides associated with U1, U2, U5 and U4/U6 snRNAs (B,B', D, E, F and G antigens).

Current methods for the detection of autoantibodies to RNP often require the simultaneous determination of reactivity to both RNP/Sm and Sm antigens. The reactivity with Sm is then subtracted from that with RNP/Sm, the difference being considered to be due to RNP-specific autoantibodies. The availability of RNP antigen in the absence of Sm would avoid the necessity for a dual assay to detect anti-RNP antibodies and assays have been reported using isolated U1-RNP specific subunits.

Since the 68K U1-RNP polypeptide constitutes the major MCTD RNP autoantigen, efforts to produce a recombinant RNP antigen have focussed on this subunit, and not the U1-RNP specific subunits A and C which are known to share sequence homology and cross-reactivity with the Sm antigen B/B.

Clinical Indications

Mixed connective tissue diseases
Systemic Lupus Erythematosus

Certificate of Analysis

Please log in to view certificates of analysis for this item

MSDS

References

1. Tan, E.M. & Kunkel, H.G. (1966) J. Immunol. 96, 464
2. Mattioli, M. & Reichlin, M. (1971) J. Immunol. 107, 1281
3. Sharp, G.C. et al. (1972) Am. J. Med. 52, 148
4. Sharp, G.C. et al. (1976) New Engl. J. Med. 295, 1149
5. Notman, D.D. et al. (1975) Ann. Intern. Med. 83, 464
6. Tan, E.M. et al. (1988) Clin. Immunol. Pathol. 47, 121
7. Tan, E.M. (1989) Adv. Immunol. 44, 93
8. van Venrooij, W.J. & Pruijn, G.J.M. (1995) Curr. OpinionImmunol. 7, 819
9. Guldner, H.H. (1986) Clin. Immunol. Immunopathol. 40, 532
10. Williams, D.G. et al. (1988) J. Immunol. Meth. 113, 25
11. Luhrmann, R. et al. (1990) Biochim. Biophys. Acta 1087, 265
12. Petersson, I. et al. (1984) J. Biol. Chem. 259, 5907
13. Reuter, R. et al. (1990) Eur. J. Immunol. 20, 437
14. Takeda, Y. et al. (1989) Clin. Immunol. Immunopathol. 50, 213
15. Williams, D.G. et al. (1988) J. Immunol. Meth. 113, 25
16. Combe, B. et al. (1989) Clin. Exp. Immunol. 75, 18
17. Francoeur, A.M. (1989) J. Clin. Immunol. 9, 256
18. Nyman, U. et al. (1990) Clin. Exp. Immunol. 81, 52
19. Ter-Borg, E.J. et al. (1991) J. Rheumatol. 18, 363
20. Frorath, B. et al. (1991) BioTechniques 11, 364
21. Habets, W.J. et al. (1989) Proc. Natl. Acad. Sci. USA 86, 4674
22. Theissen, H. et al. (1986) EMBO J. 5, 3209
23. Kawai, J. et al. (2001) Nature 409, 685