Abstract
Store-operated calcium (SOC) entry is the most prominent mode of calcium entry in nonexcitable cells, although important questions remain regarding its mechanism(s) of activation and the molecular identity of SOC entry channels. Recent work using Drosophila melanogaster and mammalian cells suggest that myosin may play a central role in regulation of the open state of SOC entry channels. The most direct evidence for such a role for myosin motor function is in the Drosophila rhabdomere, where a myosin homolog appears to terminate channel signaling. Studies directly examining the contribution of myosin to mammalian SOC entry are lacking. However, several indirect lines of evidence support a role for myosin motor function in the control of calcium entry. Both inhibition of myosin light-chain kinase (the kinase responsible for myosin activation) and disruption of filamentous actin (the track for actomyosin motor function) reduces SOC entry and appear to prevent activation of a calcium-selective SOC entry current. Thus, this review summarizes data-emphasizing recent evidence in mammalian systems-implicating myosin motor function in the control of SOC entry.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.