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Troponin is a central regulatory protein of striated muscle contraction, and together with tropomyosin, is located on the actin filament. Zusätzlich bieten wir Ihnen TNNC1 Proteine (18) und TNNC1 Kits (11) und viele weitere Produktgruppen zu diesem Protein an.
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Our results (i) confirm that genetic backgrounds of hypertrophic cardiomyopathy and restrictive cardiomyopathy overlap and (ii) indicate that TNNC1 is a likely novel gene for autosomal recessive restrictive cardiomyopathy.
Data suggest that modulation of structural dynamics far from the regulatory Ca2 (zeige CA2 Antikörper)+-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 (zeige TNNI2 Antikörper)(SW)] switch peptide binds to TNNC1 and stabilizes the open TNNC1 conformation.
Data suggest that mutations in troponin C (TnC (zeige TNNC2 Antikörper)) found in patients with hypertrophic cardiomyopathy (A8V, C84Y, and D145E) stabilize the active state of regulated actin (the actin-tropomyosin (zeige TPM2 Antikörper)-troponin complex) to various extents; at a saturating Ca2 (zeige CA2 Antikörper)+ concentration, all TnC (zeige TNC Antikörper) 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 (zeige TNC Antikörper) 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 (zeige PTK2 Antikörper)/CREB (zeige CREB1 Antikörper)/TNNC1 has a role in mediating the effect of stromal MFAP5 (zeige MFAP5 Antikörper) on ovarian cancer metastatic potential
Mutations in cTnC have been associated with hypertrophic or dilated cardiomyopathy.[review]
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 (zeige CA2 Antikörper)+) sensitivity in skinned fibers was identified, an the F27W reporter mutation affected Ca(2 (zeige CA2 Antikörper)+) sensitivity, maximal force, and ATPase (zeige DNAH8 Antikörper) activation of some mutants.
Overexpression of sTnC (zeige TNNC2 Antikörper) 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