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Anti-dsDNA Mouse ELISA

  • Regulatory status:RUO
  • Type:Direct ELISA, HRP-labelled antibody
  • Species:Mouse
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RSHAKRDD061R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Direct ELISA, HRP-labelled antibody

Applications

Serum, Plasma-EDTA, Plasma-Citrate

Sample Requirements

1 µl/well

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

15.6–1000 mU/ml

Limit of Detection

0.78 mU/ml

Intra-assay (Within-Run)

n = 30; CV = 4.2%

Inter-assay (Run-to-Run)

n = 30; CV = 4.7%

Summary

Research topic

Animal studies

Summary

Autoantibodies against DNA are IgG type or IgM type reacting with natural double stranded DNA (dsDNA), single-stranded DNA (ssDNA), or both types. In human SLE (systemic lupus erythematosus), there found anti-dsDNA-IgG with high incidence. In SLE blood anti-dsDNA titer closely related to DNA-anti-DNA complex and low complement level, and serves as an important marker for the activity of the disease.
Experimental model animals with natural incidence of autoimmune diseases similar to those in human , and animals artificially induced inflammation have been used for elucidation of the mechanism of autoimmune diseases and also in searching for new drugs.
A representative model animal of spontaneous autoimmune diseases is MRL/lpr mouse. As MRL/lpr shows high incidence of lymph node tumor, nephritis, angitis, and arthritis, this animal strain is useful for studies on incidence mechanism of human autoimmune diseases including rheumatoid arthritis. Autoantibodies found in MRL/lpr serum are IgG type rheumatoid factor, IgM type rheumatoid factor, anti-ssDNA antibodies, anti-dsDNA antibodies, and anti-Sm antibody, etc.

This kit enables quantification and comparison of IgG type anti-dsDNA autoantibody with a calibration curve using standard antibody preparation.

References to Product

References

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  • Kawane K, Ohtani M, Miwa K, Kizawa T, Kanbara Y, Yoshioka Y, Yoshikawa H, Nagata S. Chronic polyarthritis caused by mammalian DNA that escapes from degradation in macrophages. Nature. 2006 Oct 26;443 (7114):998-1002
  • Kikukawa T, Kojima M, Abe C. A novel assay kits for autoantibodies rate on spontaneous autoimmune model mice. Jap J Inflammation. 2000;20:697-701
  • Kumanogoh A, Shikina T, Watanabe C, Takegahara N, Suzuki K, Yamamoto M, Takamatsu H, Prasad DV, Mizui M, Toyofuku T, Tamura M, Watanabe D, Parnes JR, Kikutani H. Requirement for CD100-CD72 interactions in fine-tuning of B-cell antigen receptor signaling and homeostatic maintenance of the B-cell compartment. Int Immunol. 2005 Oct;17 (10):1277-82
  • Sadanaga A, Nakashima H, Masutani K, Miyake K, Shimizu S, Igawa T, Sugiyama N, Niiro H, Hirakata H, Harada M. Amelioration of autoimmune nephritis by imatinib in MRL/lpr mice. Arthritis Rheum. 2005 Dec;52 (12):3987-96
  • Shimizu S, Sugiyama N, Masutani K, Sadanaga A, Miyazaki Y, Inoue Y, Akahoshi M, Katafuchi R, Hirakata H, Harada M, Hamano S, Nakashima H, Yoshida H. Membranous glomerulonephritis development with Th2-type immune deviations in MRL/lpr mice deficient for IL-27 receptor (WSX-1). J Immunol. 2005 Dec 1;175 (11):7185-92
  • Sung YY, Lee YS, Jung WH, Kim HY, Cheon HG, Yang SD, Rhee SD. Glucose intolerance in young TallyHo mice is induced by leptin-mediated inhibition of insulin secretion. Biochem Biophys Res Commun. 2005 Dec 30;338 (4):1779-87
  • Takeda Y, Takeno M, Iwasaki M, Kobayashi H, Kirino Y, Ueda A, Nagahama K, Aoki I, Ishigatsubo Y. Chemical induction of HO-1 suppresses lupus nephritis by reducing local iNOS expression and synthesis of anti-dsDNA antibody. Clin Exp Immunol. 2004 Nov;138 (2):237-44
  • Tsukuba T, Okamoto K, Okamoto Y, Yanagawa M, Kohmura K, Yasuda Y, Uchi H, Nakahara T, Furue M, Nakayama K, Kadowaki T, Yamamoto K, Nakayama KI. Association of cathepsin E deficiency with development of atopic dermatitis. J Biochem. 2003 Dec;134 (6):893-902
  • Yajima K, Nakamura A, Sugahara A, Takai T. FcgammaRIIB deficiency with Fas mutation is sufficient for the development of systemic autoimmune disease. Eur J Immunol. 2003 Apr;33 (4):1020-9
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