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dc.contributor.authorHernández-Ochoa, E.O.
dc.contributor.authorSchneider, M.F.
dc.date.accessioned2019-04-05T13:55:10Z
dc.date.available2019-04-05T13:55:10Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85050255472&doi=10.1186%2fs13395-018-0167-9&partnerID=40&md5=d49da14cb3600f5f8e763556c84abda9
dc.identifier.urihttp://hdl.handle.net/10713/8782
dc.description.abstractThe process by which muscle fiber electrical depolarization is linked to activation of muscle contraction is known as excitation-contraction coupling (ECC). Our understanding of ECC has increased enormously since the early scientific descriptions of the phenomenon of electrical activation of muscle contraction by Galvani that date back to the end of the eighteenth century. Major advances in electrical and optical measurements, including muscle fiber voltage clamp to reveal membrane electrical properties, in conjunction with the development of electron microscopy to unveil structural details provided an elegant view of ECC in skeletal muscle during the last century. This surge of knowledge on structural and biophysical aspects of the skeletal muscle was followed by breakthroughs in biochemistry and molecular biology, which allowed for the isolation, purification, and DNA sequencing of the muscle fiber membrane calcium channel/transverse tubule (TT) membrane voltage sensor (Cav1.1) for ECC and of the muscle ryanodine receptor/sarcoplasmic reticulum Ca2+ release channel (RyR1), two essential players of ECC in skeletal muscle. In regard to the process of voltage sensing for controlling calcium release, numerous studies support the concept that the TT Cav1.1 channel is the voltage sensor for ECC, as well as also being a Ca2+ channel in the TT membrane. In this review, we present early and recent findings that support and define the role of Cav1.1 as a voltage sensor for ECC. © 2018 The Author(s).en_US
dc.description.sponsorshipThis publication was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number R37-AR055099 (to M. F. S.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.en_US
dc.description.urihttps://dx.doi.org/10.1186/s13395-018-0167-9en_US
dc.language.isoEnglishen_US
dc.publisherBioMed Central Ltd.en_US
dc.relation.ispartofSkeletal Muscle
dc.subjectCa2+ releaseen_US
dc.subjectcharge movementen_US
dc.subjectDHPR/Cav1.1en_US
dc.subjectL-type voltage-gated calcium channelen_US
dc.subjectRyR1en_US
dc.subjectvoltage sensorsen_US
dc.subject.meshExcitation Contraction Couplingen_US
dc.subject.meshMuscle, Skeletalen_US
dc.titleVoltage sensing mechanism in skeletal muscle excitation-contraction coupling: Coming of age or midlife crisis?en_US
dc.typeReviewen_US
dc.identifier.doi10.1186/s13395-018-0167-9
dc.identifier.pmid30025545


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