Tnnt2 Antibody

1. Replacement of the functionally corresponding N-terminal end portion of rat fast skeletal cardiac muscle (RfsTnT) into cardiac muscle troponin T (RcTnT), the observed functional differences associate with a sequence variation. PMID: 23357173
2. L48Q cTnC reduced crossbridge dependence of thin filament activation in cardiac muscle and changes in Ca(2+) sensitivity of force in response to changes in sarcomere length are at least partially dependent on properties of thin filament troponin. PMID: 22865385
3. cTnC, cTnI, cTnT and cTm are not only present in myofilaments of ventricular cardiomyocytes in culture but are also within their nuclei; significantly, these four proteins appear between days 3 and 5 in both myofilaments and nuclei PMID: 22364878
4. Early single cTnT measurement correlates with infarct size in rats, and a cutoff value of 5.1 mug/l provides good sensitivity and specificity to predict congestive heart failure with secondary pulmonary hypertension. PMID: 20537565
5. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart. PMID: 20711602
6. a novel role for cTnT as a dual-specificity sarcomeric A-kinase anchoring protein PMID: 21056973
7. Studies show that the rat Tnnt2-rtTA;TetO-Cre mice transgenic line a valuable genetic tool for analysis of spatiotemporal gene function and cardiomyocyte lineage tracing during developmental and postnatal period. PMID: 20014345
8. The mu-calpain-mediated proteolytic modification of TnT may act as an acute mechanism to adjust muscle contractility under stress conditions. PMID: 16981728
9. Overexpression of heat shock protein 27 protects against ischaemia/reperfusion-induced cardiac dysfunction via stabilization of troponin I and T. PMID: 18397962
10. Mdetabolic inhibition of cardiomyocytes induces a parallel release of intact Tnnt3 and its degradation products, starting only after onset of irreversible cardiomyocyte damage. PMID: 18721805
11. Study demonstrate profound energetic alterations in DEL-TNT hearts, supporting the notion that inefficient cellular ATP utilization contributes to the pathogenesis of HCM. PMID: 19189074

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KEGG: rno:24837

STRING: 10116.ENSRNOP00000049297

UniGene: Rn.9965