AI Article Synopsis
- The text examines how phosphorylation of cardiac troponin I affects thin filament activity, which is crucial for maintaining heart function and responding to stress.
- It highlights the role of cardiac troponin I in the A-band of the sarcomere and its interactions with other regions like the Z-disk and M-band to facilitate this process.
- The review emphasizes the integration of phosphorylation signaling in cardiac function, influencing various physiological processes, including heartbeat generation, muscle growth, and energy metabolism.
Article Abstract
We focus here on the modulation of thin filament activity by cardiac troponin I phosphorylation as an integral and adaptive mechanism in cardiac homeostasis and as a mechanism vulnerable to maladaptive response to stress. We discuss a current concept of cardiac troponin I function in the A-band region of the sarcomere and potential signaling to cardiac troponin I in a network involving the ends of the thin filaments at the Z-disk and the M-band regions. The cardiac sarcomere represents a remarkable set of interacting proteins that functions not only as a molecular machine generating the heartbeat but also as a hub of signaling. We review how phosphorylation signaling to cardiac troponin I is integrated, with parallel signals controlling excitation-contraction coupling, hypertrophy, and metabolism.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567448 | PMC |
| http://dx.doi.org/10.1161/CIRCRESAHA.112.268672 | DOI Listing |
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