Epitope regions on U1 small nuclear RNA recognized by anti-U1RNA-specific autoantibodies.

Hoet, Rene; Weerd, P De; Gunnewiek, Jacqueline Klein; Koornneef, I.; Venrooij, W.J. van

doi:10.1172/jci116049

Cited by 25 publications

(24 citation statements)

References 20 publications

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“…The presence in MCTD patients' sera of autoantibodies directed to ribonucleoprotein antigens is widely documented [3,10,11]. Recently, we reported high titres of antibodies to the constitutive 73-kD heat shock protein in a series of 18 MCTD sera [5].…”

Section: Discussionmentioning

confidence: 98%

Antibodies to small ribonucleoprotein and to 73-kD heat shock protein: two distinct markers of mixed connective tissue disease

Appelboom

Kahn

Mairesse³

1995

Clinical and Experimental Immunology

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SUMMARYWe set out to discover whether antibodies to small ribonucleoprotein antigens (RNP) and to 73-kD heat shock protein (hsp 73) which have been proposed as markers of mixed connective tissue disease (MCTD) recognize different epitopes. MCTD serum was itnmunoadsorbed on hsp 73-coupled Sepharose and the affinity retained, and non-retained fractions were checked by immunobtotting for recognition of either purified bovine hsp 73 or calf thymus extract RNPs. The hsp 73 atfinity-bound serum fraction recognized hsp 73 but not RNP antigens, the reverse being true for the non-retained fraction. We conclude that anti-hsp 73 and anti-RNPs are distinct markers of MCTD.

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Section: Discussionmentioning

confidence: 98%

Antibodies to small ribonucleoprotein and to 73-kD heat shock protein: two distinct markers of mixed connective tissue disease

Appelboom

Kahn

Mairesse³

1995

Clinical and Experimental Immunology

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“…16 Still others recognize the U1 small nuclear RNA molecule ( Figure 3). 17,18 More recently, it has been found that the C-terminal arginine -glycine dipeptide repeats of the Sm D1 and D3 proteins contain symmetrical dimethylarginine residues, which form a major epitope recognized by anti-Sm antibodies. 19 It was found that 10 of 12 human anti-Sm antisera as well as Lerner and Steitz's anti-Sm monoclonal antibody Y12 recognized a C-terminal peptide of the D1 protein containing symmetrical dimethylarginines, but not the same peptide without this modi cation or containing a single asymmetrical dimethylarginine.…”

Section: Chapter 4: Return To Immunologymentioning

confidence: 99%

Henry Kunkel, Stephanie Smith, clinical immunology, and split genes

Reeves

Narain

Satoh

2003

Lupus

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The York Avenue (New York) 'ecosystem' from the 1940s through the 1980s enabled Henry Kunkel to apply new scientific methodology to understanding human disease. Stephanie Smith, a young woman with lupus, was treated at the Rockefeller University Hospital in the 1960s. Studies of her antinuclear antibodies by Kunkel and Eng Tan led to the discovery of a precipitin line specific for lupus, and the responsible antigen was designated Sm (for 'Smith'). This review outlines the history of Sm antigen from an interesting precipitin line to the identification of small nuclear RNA molecules and small nuclear ribonucleoproteins, and subsequently the discovery of RNA splicing. The story illustrates Henry Kunkel's approach to science, emphasizing how 'accidental' clinical observations, in the hands of skilled investigators, can have unexpected and potentially momentous implications.

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“…71 The U1 snRNA molecule itself is a major target of autoimmunity in SLE-overlap syndromes, 72 and it has been shown that changes in the titer of anti-U1 snRNA autoantibodies may correlate with the severity of the disease. 73 The most immunodominant epitopes of the autoantigenic U1 snRNA molecule are located in stemloop II (nts 49 ± 65 and 76 ± 90) and stemloop IV (nts 150 ± 153), 74 and were recently characterized in more detail using several recombinant human monoclonal antibodies (scFvs). 75,76 Figure 3 Modification of the 28S rRNA molecule during apoptosis.…”

Section: Modi®cations Of Small Structural Rnasmentioning

confidence: 99%

Caspase-dependent cleavage of nucleic acids

et al. 2000

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Autoimmune diseases are frequently characterized by the presence of autoantibodies directed against nucleic acidprotein complexes present in the nucleus of the cell. The mechanisms by which these autoantigenic molecules escape immunological tolerance are largely unknown, although a number of recent observations suggest that modified selfproteins generated during apoptosis may play an important role in the development of autoimmunity. It has been hypothesized that the recognition of these modified selfproteins by the immune system may promote autoantibody production. While apoptosis is specifically characterized by posttranslational modification of proteins, recent findings also show that nucleic acids are modified. This review summarizes the specific cleavages of some of these key nucleic acids, i.e. chromosomal DNA, ribosomal RNA and small structural RNAs (U1 snRNA, Y RNA), in apoptotic cells.

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Epitope regions on U1 small nuclear RNA recognized by anti-U1RNA-specific autoantibodies.

Cited by 25 publications

References 20 publications

Antibodies to small ribonucleoprotein and to 73-kD heat shock protein: two distinct markers of mixed connective tissue disease

Antibodies to small ribonucleoprotein and to 73-kD heat shock protein: two distinct markers of mixed connective tissue disease

Henry Kunkel, Stephanie Smith, clinical immunology, and split genes

Caspase-dependent cleavage of nucleic acids

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