Troponin C—troponin I interactions and molecular signalling in cardiac myofilaments
RJ Solaro - Molecular and subcellular cardiology: effects of …, 1995 - Springer
Molecular and subcellular cardiology: effects of structure and function, 1995•Springer
This chapter describes a current perception of the molecular interactions regulating
myofilament activity in heart cells. The focus is on the interaction between troponin-C (TnC),
the Ca 2+-receptor and troponin I (TnI), an inhibitory protein. It is this interaction that appears
to form a molecular switch that turns on the thin filament. It will be seen that control of the
actin-myosin reaction is not only through Ca 2+-binding to TnC, but also through steric,
cooperative and allosteric processes involving all of the main myofilament proteins-actin …
myofilament activity in heart cells. The focus is on the interaction between troponin-C (TnC),
the Ca 2+-receptor and troponin I (TnI), an inhibitory protein. It is this interaction that appears
to form a molecular switch that turns on the thin filament. It will be seen that control of the
actin-myosin reaction is not only through Ca 2+-binding to TnC, but also through steric,
cooperative and allosteric processes involving all of the main myofilament proteins-actin …
Abstract
This chapter describes a current perception of the molecular interactions regulating myofilament activity in heart cells. The focus is on the interaction between troponin-C (TnC), the Ca2+-receptor and troponin I (TnI), an inhibitory protein. It is this interaction that appears to form a molecular switch that turns on the thin filament. It will be seen that control of the actin-myosin reaction is not only through Ca2+-binding to TnC, but also through steric, cooperative and allosteric processes involving all of the main myofilament proteins-actin, myosin, tropomyosin (Tm), troponin T (TnT), TnC, and TnI. The process is modulated by covalent and non-covalent mechanisms. The process is altered in diverse myopathies and pathologies of the heart and is a target for pharmacological manipulation by a new class of inotropic agents, the “Ca2+-sensitizers”.
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