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The Human Troponin I (TNNI3) ELISA quantitates Hu TNNI3 in human serum, plasma, or cell culture medium. The assay will exclusively recognize both natural and recombinant Hu TNNI3. Principle of the method The Human TNNI3 solid-phase sandwich ELISA (enzyme-linked immunosorbent assay) is designed to measure the amount of the target bound between a matched antibody pair. A target-specific antibody has been pre-coated in the wells of the supplied microplate. Samples, standards, or controls are then added into these wells and bind to the immobilized (capture) antibody. The sandwich is formed by the addition of the second (detector) antibody, a substrate solution is added that reacts with the enzyme-antibody-target complex to produce measurable signal. The intensity of this signal is directly proportional to the concentration of target present in the original specimen. Rigorous validation Each manufactured lot of this ELISA kit is quality tested for criteria such as sensitivity, specificity, precision, and lot-to-lot consistency. See manual for more information on validation.Cardiac Troponin I (Cardiac-specific troponin I, TnI, Troponin I) is an integral inhibitory protein in cardiac muscle that exists as part of a complex with troponin C (TnC) and troponin T (TnT). The TnT subunit of troponin binds to tropomyosin-t form, a troponin-tropomyosin complex, anchored in place by the binding of TnI to actin, within muscle thin filaments. Structural change resulting from the binding of calcium to specific sites on the regulatory TnC subunit, releases the inhibitory region of TnI from actin, anabling the attachment of the molecular motor protein myosin, allowing for muscle contraction and hence movement. The measurements of blood TnI and TnT levels is an important diagnostics indicator of heart muscle damage, and can be used to differentiate between angina and myocardial infarction in patients with chest pains. Cardiac Troponin I has also been shown to inhibit angiogenesis in vivo and in vitro. Mutations in the Cardiac Troponin I gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM).
