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(Circulation Research. 2002;91:449.)
© 2002 American Heart Association, Inc.

Editorials

Troponin I

In Sickness and In Health—and Normal Development

Anne M. Murphy

From the Division of Cardiology, Department of Pediatrics and Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Baltimore, Md.

Correspondence to Anne M. Murphy, Division of Cardiology, Department of Pediatrics and Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Ross 1144, 720 Rutland Ave, Baltimore, MD 21205. E-mail murphy@jhmi.edu

Key Words: troponin • hypertrophic cardiomyopathy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Troponin is the key component of the calcium-dependent switch of the contractile apparatus in striated muscle. There are three subunits of troponin: troponin C, a Ca²⁺-binding calmodulin-like protein; troponin T, which attaches the complex to tropomyosin, anchoring it to the thin filament as well as having a regulatory role; and troponin I (TnI), named for its ability to inhibit actin-myosin interactions at diastolic levels of Ca²⁺. As cytosolic Ca²⁺ increases in systole, it binds to a regulatory Ca²⁺-binding site on TnC, leading to increasing affinity of TnC for TnI and weakening the interactions of TnI and actin. This permits movement of tropomyosin-troponin on the thin filament such that the inhibition of actin-myosin interaction is diminished, increasing the probability of crossbridge cycling and muscle shortening. The ability to inhibit the actin-myosin interaction resides within a 12-amino acid region of the TnI molecule, although its inhibitory function is modulated by other regions of TnI.¹

In mature mammals, a different TnI gene is expressed specifically in each of the three types of striated muscle: fast twitch (fsTnI), slow twitch (ssTnI), and cardiac (cTnI). The fetal and neonatal cardiac atria and ventricle also express ssTnI, and there is a gradual downregulation of the mRNA for ssTnI and increased expression of cTnI with maturation.² This gene switch occurs in all mammalian species studied to date, including human. The tight regulation of this process was made apparent when the cTnI gene was subjected to targeted deletion in mice by Huang et al.³ Rather . . . [Full Text of this Article]

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