The troponin complex of cardiac thin filaments, specifically cTnI and cTnT, plays a major role in phosphoryl group transfer reactions essential for cardiac function homeostasis.
Homeostasis of cardiac function requires significant adjustments in sarcomeric protein phosphorylation. The existence of unique peptides in cardiac sarcomeres, which are substrates for a multitude of kinases, strongly supports this concept (1). We focus here on the troponin complex of the thin filaments, which contain two major proteins that participate in these phosphoryl group transfer reactions: the inhibitory protein (cardiac troponin (cTn)2 I) and the tropomyosin (Tm)-binding protein (cTnT).
Solaro et al. (Sat,) conducted a review in Cardiac function and sarcomeric protein phosphorylation. The troponin complex of cardiac thin filaments, specifically cTnI and cTnT, plays a major role in phosphoryl group transfer reactions essential for cardiac function homeostasis.