TNNI3 Human Native
Human heart tissue.
Troponin I cardiac muscle, Cardiac troponin I, TNNI3, TNNC1, CMH7, RCM1, cTnI, CMD2A, MGC116817.
Sterile Filtered White lyophilized (freeze-dried) powder.
Greater than 98.0% as determined by SDS-PAGE.
Description
TNNI3 Native produced in Human heart tissue is a full length protein which has an additional amino acid residues on its N terminus that are not present on the skeletal form, making this protein a promising analyte for indicating cardiac specificity.
TNNI3 Native is purified by proprietary chromatographic technique.
Product Specs
Troponin I cardiac muscle, Cardiac troponin I, TNNI3, TNNC1, CMH7, RCM1, cTnI, CMD2A, MGC116817.
Human heart tissue.
Product Science Overview
The discovery of troponin dates back to the early 1970s when researchers identified its role in muscle contraction. Troponin I, specifically, was found to inhibit the interaction between actin and myosin, thereby preventing muscle contraction in the absence of calcium ions . The cardiac-specific isoform of troponin I (cTnI) is unique to cardiac muscle cells and is not found in skeletal muscle, making it a highly specific biomarker for cardiac injury .
Cardiac Troponin-I is a 24 kDa protein that binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. This binding prevents myosin from interacting with actin in relaxed muscle, thereby inhibiting contraction. Upon calcium binding to troponin C, a conformational change occurs, allowing the actin-myosin interaction and subsequent muscle contraction .
The clinical significance of cTnI lies in its role as a biomarker for myocardial infarction (heart attack). Elevated levels of cTnI in the blood are indicative of cardiac muscle damage. This makes cTnI an invaluable tool in the diagnosis and management of acute coronary syndromes (ACS). The development of highly sensitive assays for cTnI has further enhanced its utility in clinical practice .
Cardiac Troponin-I levels are typically very low in healthy individuals, with the 99th percentile being less than a few nanograms per liter of blood. However, in the event of myocardial injury, cTnI levels rise significantly within a few hours, peaking at around 24 hours and remaining elevated for up to two weeks. This rapid and sustained increase in cTnI levels allows for the early detection and monitoring of myocardial infarction .
Recent advancements in assay sensitivity have led to the development of high-sensitivity cardiac troponin (hs-cTn) assays. These assays can detect even minor elevations in cTnI levels, allowing for the identification of subclinical myocardial injury. However, this increased sensitivity also means that cTnI can be elevated in conditions other than myocardial infarction, such as chronic kidney disease, heart failure, and extreme physical exertion .
