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Troponin is a central regulatory protein of striated muscle contraction, and together with tropomyosin, is located on the actin filament. Additionally we are shipping TNNC1 Antibodies (69) and TNNC1 Proteins (15) and many more products for this protein.
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Data suggest that modulation of structural dynamics far from the regulatory Ca2 (show CA2 ELISA Kits)+-binding site is the underlying molecular mechanism for many TNNC1 mutations in patients with hypertrophic cardiomyopathies or familial hypertrophic cardiomyopathies; many mutations affect balance between open and closed conformations; troponin I switch peptide [TnI (show TNNI2 ELISA Kits)(SW)] switch peptide binds to TNNC1 and stabilizes the open TNNC1 conformation.
Data suggest that mutations in troponin C (TnC (show TNNC2 ELISA Kits)) found in patients with hypertrophic cardiomyopathy (A8V, C84Y, and D145E) stabilize the active state of regulated actin (the actin-tropomyosin (show TPM2 ELISA Kits)-troponin complex) to various extents; at a saturating Ca2 (show CA2 ELISA Kits)+ concentration, all TnC (show TNC ELISA Kits) mutants investigated increase the level of active M state compared to the wild type.
There was no difference in the test characteristics of the HEART Pathway whether using cTnI or hs-cTnI, with both achieving 100% sensitivity and NPV. Use of hs-cTnT with the HEART Pathway was associated with one missed major adverse cardiac events.
contractility is constantly above normal in hearts made hypertrophic by TnC (show TNC ELISA Kits) with the A8V mutation
We used nuclear magnetic resonance and circular dichroism to solve the structure and characterize the backbone dynamics and stability of the regulatory domain of cTnC with the L29Q mutation.
conclusive evidence that TNNC1 is an uncommon but definitive HCM-susceptibility gene
Troponin C (TnC) and the N-terminal helix of Troponin I (TnI N-helix), which occurs in vivo during muscle contraction.
FAK (show PTK2 ELISA Kits)/CREB (show CREB1 ELISA Kits)/TNNC1 has a role in mediating the effect of stromal MFAP5 (show MFAP5 ELISA Kits) on ovarian cancer metastatic potential
Mutations in cTnC have been associated with hypertrophic or dilated cardiomyopathy.[review]
Data suggest that mutation A162H in switch region of troponin I induces transitory curved conformation and promotes contraction of troponin I bound to regulatory domain of troponin C; this is countered by residue E164 to ensure proper relaxation.
These results demonstrate that the L29Q mutation enhances the Ca(2+)-binding characteristics of cTnC and that when incorporated into cardiac myocytes, this mutant alters myocyte contractility.
Calcium binding kinetics of troponin C strongly modulate cooperative activation and tension kinetics in cardiac muscle.
A region in cTnC associated with increased Ca(2 (show CA2 ELISA Kits)+) sensitivity in skinned fibers was identified, an the F27W reporter mutation affected Ca(2 (show CA2 ELISA Kits)+) sensitivity, maximal force, and ATPase (show DNAH8 ELISA Kits) activation of some mutants.
Overexpression of sTnC (show TNNC2 ELISA Kits) polypeptide in muscle cells is controlled by its rapid degradation.
Troponin is a central regulatory protein of striated muscle contraction, and together with tropomyosin, is located on the actin filament. Troponin consists of 3 subunits: TnI, which is the inhibitor of actomyosin ATPase\; TnT, which contains the binding site for tropomyosin\; and TnC, the protein encoded by this gene. The binding of calcium to TnC abolishes the inhibitory action of TnI, thus allowing the interaction of actin with myosin, the hydrolysis of ATP, and the generation of tension. Mutations in this gene are associated with cardiomyopathy dilated type 1Z.
cardiac troponin C
, slow twitch skeletal/cardiac muscle troponin C
, troponin C, slow skeletal and cardiac muscles
, troponin C1, slow
, troponin C, cardiac/slow skeletal
, Troponin C, slow skeletal and cardiac muscles