Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Jul;136(1):13-9.
doi: 10.1085/jgp.201010462.

The curious role of sarcomeric proteins in control of diverse processes in cardiac myocytes

R John Solaro  1 , Katherine A Sheehan, Ming Lei, Yunbo Ke
Affiliations

The curious role of sarcomeric proteins in control of diverse processes in cardiac myocytes

R John Solaro et al. J Gen Physiol. 2010 Jul.
No abstract available

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
A section of cardiac thin filaments illustrating the position of troponin components with Tm in the OFF state (left) and ON state (right). Thin filaments are shown containing TnI, TnT, and TnC. cTnC, a dumbbell-shaped protein with an N lobe containing a single regulatory Ca-binding site (yellow spheres) and a C lobe containing slowly exchanged Ca2+/Mg2+ sites. In the OFF state, Tm is immobile and held in place by TnI, which is shown tethered to actin on an actin strand by an Ip and a second actin-binding region flanking a switch peptide (Sw), which interacts with cTnC upon Ca activation. Note that the Ip of cTnI binds to one actin strand, whereas the N-terminal tail of TnT interacts with Tm on the adjacent actin strand. The distal C-terminal end of cTnI drapes across azimuthal actins and may interact with Tm. TnI has a unique stretch of N-terminal amino acids, which contain phosphorylation sites at S23 and S24. The N peptide interacts with the N lobe of cTnC, but it is released upon phosphorylation. With release of Ca2+, there is a release of cTnI from actin and binding of the switch peptide to cTnC. Activation is associated with release of Tm from an immobilized state by protein signaling to cTnT and possible release of Tm from an interaction with the C-terminal end of cTnI. See Are kinetic processes intrinsic to… for further description.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Backx P.H., Gao W.D., Azan-Backx M.D., Marban E. 1995. The relationship between contractile force and intracellular [Ca2+] in intact rat cardiac trabeculae. J. Gen. Physiol. 105:1–19 10.1085/jgp.105.1.1 - DOI - PMC - PubMed
    1. Baran D., Ogino K., Stennett R., Schnellbacher M., Zwas D., Morgan J.P., Burkhoff D. 1997. Interrelating of ventricular pressure and intracellular calcium in intact hearts. Am. J. Physiol. 273:H1509–H1522 - PubMed
    1. Bers D.M. 2000. Calcium fluxes involved in control of cardiac myocyte contraction. Circ. Res. 87:275–281 - PubMed
    1. Biesiadecki B.J., Kobayashi T., Walker J.S., John Solaro R., de Tombe P.P. 2007. The troponin C G159D mutation blunts myofilament desensitization induced by troponin I Ser23/24 phosphorylation. Circ. Res. 100:1486–1493 10.1161/01.RES.0000267744.92677.7f - DOI - PubMed
    1. Burkhoff D. 1994. Explaining load dependence of ventricular contractile properties with a model of excitation-contraction coupling. J. Mol. Cell. Cardiol. 26:959–978 10.1006/jmcc.1994.1117 - DOI - PubMed

Publication types

MeSH terms