期刊
JOURNAL OF MOLECULAR BIOLOGY
卷 340, 期 2, 页码 295-305出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2004.04.046
关键词
muscle regulation; Ca2+-regulatory switch; troponin; signal transduction; length-dependent activation
资金
- NHLBI NIH HHS [R01 HL080186, HL52508] Funding Source: Medline
The principal task of the Ca2+ activation of striated muscle-is the release of the troponin I (TnI) inhibitory region (TnI-I) from actin. TnI-I release facilitates the repositioning of tropomyosin across the actin surface and the formation of strong, force generating, actin-myosin cross-bridges. Full activation of the Ca2+ regulatory switch (CRS) requires two switching steps in cTnI: binding of the TnI regulatory region to hydrophobic sites in the N-domain of Ca2+-bound troponin C and release of the adjacent TnI-I from actin. Using Forster resonance energy transfer, we have examined the requirements for full activation of the cardiac CRS. In the presence of actin, both Ca2+ and strong cross-bridges are required for full activation. Actin desensitizes the CRS to Ca2+ and produces cooperativity in the Ca2+ activation of the CRS. Strong cross-bridges eliminate cooperativity and re-sensitize the CRS to Ca2+. We propose a kinetic scheme and a structural model to account for these findings. (C) 2004 Elsevier Ltd. All rights reserved.
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