S2-16
Ref. 3D-CRB1001195
| 1mg | 271.00 € | ||
| 500µg | 198.00 € |
Product Information
- H-KRKLEGDLKLTQESIMDLENDKQQL-OHKRKLEGDLKLTQESIMDLENDKQQL-acidH-Lys-Arg-Lys-Leu-Glu-Gly-Asp-Leu-Lys-Leu-Thr-Gln-Glu-Ser-Ile-Met-Asp- Leu-Glu-Asn-Asp-Lys-Gln-Gln
Myocarditis is an inflammatory heart disease often associated with a previous viral infection. Evidence has suggested that myocarditis may be due to autoimmune responses directed against cardiac tissue. The inflammatory immune response caused after infection may break tolerance by mechanisms of molecular mimicry, bystander activation, and loss of immune regulation. Experimental autoimmune myocarditis (EAM) is a model of inflammatory heart disease generated by immunizing susceptible rats or mice with cardiac myosin or its myocarditic epitopes. In the EAM model, cellular infiltrates consist primarily of T cells and macrophages, and T lymphocytes responsive to cardiac myosin can transfer disease. Cardiac myosin is a large peptide, which is composed of two H chains and two pairs of L chains. Proteolysis of myosin yields three subfragments including a globular head or subfragment 1 (S1) region, an alpha helical coiled coil rod comprised of subfragment 2 (S2), and light meromyosin (LMM). In the Lewis rat, the S2 subfragment has been shown to produce the most severe myocarditis.
Chemical properties
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