Troponin I Type 3 (cardiac) Antibody Summary
| Immunogen |
Fusion protein of complete mouse cardiac troponin 1. Accession # P48787.
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| Specificity |
Specific for the ~25k cardiac troponin I protein.
|
| Clonality |
Polyclonal
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| Host |
Rabbit
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| Gene |
TNNI3
|
| Purity |
Unpurified
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Applications/Dilutions
| Dilutions |
|
| Application Notes |
Suggested dilution is 1:2,000 although higher dilutions can sometimes be used as cardiac troponin I expression is quite high in cardiac muscle.
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Packaging, Storage & Formulations
| Storage |
Store at -20C. Avoid freeze-thaw cycles.
|
| Buffer |
Neat whole antisera
|
| Preservative |
No Preservative
|
| Purity |
Unpurified
|
Alternate Names for Troponin I Type 3 (cardiac) Antibody
- Cardiac troponin I
- CMD1FF
- CMD2A
- CMH7MGC116817
- cTnI
- familial hypertrophic cardiomyopathy 7
- RCM1
- TNNC1troponin I, cardiac
- troponin I type 3 (cardiac)
- troponin I, cardiac muscle
Background
Biological Significance: Troponin I (cTnI) is 1 of 3 subunits, along with troponin C (TnC) and troponin T (TnT) of troponin complex found in cardiac muscle. cTnI binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place. Phosphorylation of cardiac isoform of TnI at serines 22,23 in the unique amino-terminal end molecule decreases the calcium sensitivity of the sarcomere, promotes calcium dissociation from troponin C and by extension enhances rates of cross-bridge cycling and diastolic relaxation (Noland, Jr. et al., 1995; Noland et al., 1989). In addition, studies using reconstituted fibers and mutational analysis have shown that PKC phosphorylation of TnI (largely at Ser43) inhibits the actin-cross bridge reaction and reduces the Ca++ dependent actomyosin ATPase rate as well as the calcium sensitivity of force generation (Noland, Jr. and Kuo, 1991). Phosphorylation at Thr144 (mediated by several PKC isoforms) reduces maximal tension development and cross-bridge cycling rates (Sumandea et al., 2008). Importantly, changes in the phosphorylation at each of these sites have been shown to be stage-specific with regard to cardiac disease progression (Walker et al., 2010).