Jo-1, Recombinant, Human (Histidyl t-RNA Synthetase)

Recombinant Human Histidyl tRNA synthetase (JO-1) is a single, non-glycosylated, polypeptide chain having a molecular mass of 55kD.\n\nDimers and Aggregates:\n(same/less than) 1% as determined by silver-stained SDS-PAGE gel analysis.\n\nEndotoxin:\n(same/less than) 0.1ng/ug (IEU/ug) of Human Histidyl tRNA synthetase .\n\nProtein Content:\nProtein quantitation was carried out by:\n1. 0.25-2.0 mg/ml Bradford assay vs. BSA.\n\nApplications:\nWestern Blot: Strongly reactive with human anti JO-1antisera.\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. For long-term storage, store at -20 degrees C. Aliquots are stable for at least 6 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

J4998-12

Size

50ug

Form

Supplied as a liquid in 6M Urea, 500mM sodium chloride, 10mM Tris, pH 8.0.

Purity

(same/more than) 95% by RP-HPLC, FPLC, or reducing/non-reducing SDS-PAGE Silver Stain. Chromatographically purified.

References

1. Intracellular localization of histidyl-tRNA synthetase/Jo-1 antigen in T24 cells and some other cells. Kamei H, J Autoimmun 2004 May;22(3):201-10 2. Jo-1 syndrome with associated poorly differentiated adenocarcinoma. Watkins J, Farzaneh-Far R, Wykes F, Rheumatology (Oxford) 2004 Mar;43(3):389-90 3. A woman with anti-histidyl-aminoacyl-tRNA synthetase (Jo-1 antibodies), myositis, hyperglycemia, interstitial lung disease, and morbilliform rashes. Tsai CY, Tsai YY, Chou CT, Rheumatol Int 2004 Feb 10; 4. G-1:C73 recognition by an arginine cluster in the active site of Escherichia coli histidyl-tRNA synthetase. Connolly SA, Rosen AE, Francklyn CS, Biochemistry 2004 Feb 3;43(4):962-9 5. Recognition of G-1:C73 atomic groups by Escherichia coli histidyl-tRNA synthetase. Rosen AE, Musier-Forsyth K, J Am Chem Soc 2004 Jan 14;126(1):64-5 6. The role of Jo-1 in the immunopathogenesis of polymyositis: current hypotheses. Ascherman DP, Curr Rheumatol Rep 2003 Dec;5(6):425-30.