Disease relevance of tnnt2

• Importantly, altered expression of cardiac sarcomere components, including cardiac troponin T2 and multiple myosin isoforms, was consistent with the hypothesis that TCDD causes dilated cardiomyopathy [1].

High impact information on tnnt2

• This interdependence of thin-filament protein expression led us to postulate that some mutations in tnnt2 may trigger misregulation of thin-filament protein expression, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutations in mice and humans [2].
• Cardiac troponin T is essential in sarcomere assembly and cardiac contractility [2].
• Despite the importance of cardiac troponin T in human disease, its loss-of-function phenotype has not been described [2].
• Troponin T (Tnnt), a troponin component, interacts with tropomyosin and is crucial to the regulation of striated muscle contraction [3].
• Molecular structure and developmental expression of three muscle-type troponin T genes in zebrafish [3].

Biological context of tnnt2

• In addition, we show that mutation of the poly-ADP ribose polymerase-I (PARP-I) binding site adjacent to the distal MCAT element in the chicken cTnT promoter produced a non-cell-specific promoter in vitro and in the zebrafish [4].

Anatomical context of tnnt2

• We examined the regulation of the chicken cTnT gene in vivo in zebrafish embryos, and in vitro in cardiomyocyte, myoblast, and fibroblast cultures [4].

Associations of tnnt2 with chemical compounds

• Exposure to the three-ring PAHs dibenzothiophene and phenanthrene alone was sufficient to induce the characteristic suite of defects, as was genetic ablation of cardiac function using a cardiac troponin T antisense morpholino oligonucleotide [5].

References