| ID | Sequence | Length | GC content |
|---|---|---|---|
| AGUGUCCUCGGGGAGUCUCAAGCAGCCCGGAGGAGACUGACGGUCCCUG… | 843 nt | 0.6109 |
Troponin I (TnI), along with troponin T (TnT) and troponin C (TnC), is one of 3 subunits that form the troponin complex of the thin filaments of striated muscle. TnI is the inhibitory subunit; blocking actin-myosin interactions and thereby mediating striated muscle relaxation. The TnI subfamily contains three genes: TnI-skeletal-fast-twitch, TnI-skeletal-slow-twitch, and TnI-cardiac. This gene encodes the TnI-cardiac protein and is exclusively expressed in cardiac muscle tissues. Mutations in this gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM). Troponin I is useful in making a diagnosis of heart failure, and of ischemic heart disease. An elevated level of troponin is also now used as indicator of acute myocardial injury in patients hospitalized with moderate/severe Coronavirus Disease 2019 (COVID-19). Such elevation has also been associated with higher risk of mortality in cardiovascular disease patients hospitalized due to COVID-19. [provided by RefSeq, Aug 2020]
A study in human cadavers demonstrated that the TNNI3 mRNA expression in blood was significantly higher when the cause of death was mechanical asphyxia compared to other causes like sudden cardiac death (SCD), multiple trauma, or other natural deaths, likely due to a sensitive response to acute systemic hypoxia/ischemia [González-Herrera et al. DOI:10.1016/j.forsciint.2019.109876]. An earlier methodological study confirmed that the TNNI3 mRNA remained stable postmortem, with no significant differences in its gene expression between samples collected at postmortem intervals (PMI) of ≤12 hours and >12 hours, supporting its reliability for forensic analysis [Gonzalez-Herrera et al. DOI:10.1016/J.Forsciint.2013.08.001]. A study in rats and H9c2 cells demonstrated that the TNNI3 was upregulated in ischemic models [Tian et al. DOI:10.1038/s41598-021-84056-5].