Troponin C-I-T Complex
Human cardiac tissue.
Troponin I cardiac muscle, Cardiac troponin I, TNNI3, TNNC1, CMH7, RCM1, cTnI, CMD2A, MGC116817, Troponin C slow skeletal and cardiac muscles, TN-C, TNNC1, TNNC, TNC, CMD1Z
Sterile Filtered brown solution.
Description
Human Cardiac Troponin C-I-T Complex Protein produced in Human heart tissue having a molecular mass of approximately 75kDa.
Product Specs
The Troponin Complex is a protein complex crucial for regulating muscle contraction in skeletal and cardiac muscles. Composed of three subunits—Troponin I, Troponin T, and Troponin C—each subunit contributes uniquely to the complex's function. For instance, Troponin I acts as an inhibitor of actomyosin ATPase activity. Notably, the forms of Troponin T and Troponin I present in cardiac muscles differ from those found in skeletal muscles. Purified subunits of rcTnI, rcTnC, and rcTnT are recombined in vitro under specific conditions to form the complex.
This product consists of Human Cardiac Troponin C-I-T Complex Protein. It is produced in human heart tissue and has a molecular mass of approximately 75kDa.
This product appears as a sterile filtered solution that is brown in color.
The Troponin C-I-T Complex solution (0.2µm filtered) is supplied in a buffer containing 25mM TRIS, 0.15M NaCl, and 0.09% sodium azide, at pH 7.5.
For short-term storage (up to 2-4 weeks), the product can be stored at 4°C. For extended storage, it is recommended to store the product frozen at -20°C. The addition of a carrier protein (0.1% HSA or BSA) is advised for long-term storage. It is important to avoid repeated freezing and thawing of the product.
The donor of the starting material for this product has undergone testing and received certification confirming negative results for antibodies against HIV-1, HIV-2, HCV, HBSAG, Syphilis, and HIV/HBV/HCV.
Troponin I cardiac muscle, Cardiac troponin I, TNNI3, TNNC1, CMH7, RCM1, cTnI, CMD2A, MGC116817, Troponin C slow skeletal and cardiac muscles, TN-C, TNNC1, TNNC, TNC, CMD1Z
Human cardiac tissue.
Product Science Overview
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Troponin C (TnC):
- Function: TnC binds calcium ions, which is essential for the initiation of muscle contraction. It has two distinct domains: the N-terminal domain, which binds calcium ions, and the C-terminal domain, which binds to the other troponin subunits and to tropomyosin.
- Role in Contraction: Upon binding calcium, TnC undergoes a conformational change that allows it to interact with TnI, leading to the displacement of tropomyosin from the actin binding sites, thereby facilitating the interaction between actin and myosin and resulting in muscle contraction.
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Troponin I (TnI):
- Function: TnI is the inhibitory subunit of the complex. It binds to actin and inhibits the ATPase activity of actomyosin, preventing muscle contraction in the absence of calcium.
- Role in Contraction: When calcium binds to TnC, the inhibitory effect of TnI is relieved, allowing muscle contraction to proceed.
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Troponin T (TnT):
- Function: TnT binds to tropomyosin, anchoring the troponin complex to the thin filament of the muscle fiber.
- Role in Contraction: TnT ensures the proper positioning of the troponin complex on the thin filament, which is crucial for the regulation of muscle contraction.
The cardiac-specific isoforms of troponin I (cTnI) and troponin T (cTnT) are highly specific biomarkers for cardiac muscle injury. They are released into the bloodstream when cardiac muscle cells are damaged, making them invaluable in the diagnosis of acute myocardial infarction (AMI) and other cardiac conditions .
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Diagnostic Use:
- Acute Myocardial Infarction (AMI): Elevated levels of cTnI and cTnT in the blood are indicative of myocardial injury and are used to diagnose AMI. These biomarkers are considered the gold standard for the detection of myocardial necrosis .
- Chronic Conditions: Elevated troponin levels can also be observed in chronic conditions such as heart failure, chronic kidney disease, and other non-acute cardiac conditions. The presence of elevated troponin in these conditions is associated with a worse prognosis .
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Mechanisms of Release:
- Necrosis: Traditionally, the release of troponins into the bloodstream has been attributed to the necrosis of cardiac muscle cells.
- Non-Necrotic Release: Recent studies suggest that troponin release can occur without cardiomyocyte necrosis, such as during extreme physical exercise or in chronic diseases .
Despite extensive research, many aspects of the troponin complex’s function and regulation remain incompletely understood. Ongoing studies aim to elucidate the precise mechanisms of troponin regulation and release, as well as to develop more sensitive and specific assays for the detection of cardiac injury .
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Mutations and Cardiomyopathies:
- Genetic Mutations: Mutations in the genes encoding the troponin subunits have been linked to various cardiomyopathies, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Understanding these mutations can provide insights into the pathophysiology of these diseases and inform the development of targeted therapies .
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Therapeutic Targets:
