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dc.contributor.authorMaltsev, AVen_US
dc.contributor.authorMaltsev, VAen_US
dc.contributor.authorStern, MDen_US
dc.date.accessioned2017-08-23T09:15:57Z
dc.date.available2017-05-31en_US
dc.date.issued2017-07-18en_US
dc.date.submitted2017-08-16T09:18:18.024Z
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/25404
dc.description.abstractIntracellular Ca signals represent a universal mechanism of cell function. Messages carried by Ca are local, rapid, and powerful enough to be delivered over the thermal noise. A higher signal-to-noise ratio is achieved by a cooperative action of Ca release channels such as IP3 receptors or ryanodine receptors arranged in clusters (release units) containing a few to several hundred release channels. The channels synchronize their openings via Ca-induced Ca release, generating high-amplitude local Ca signals known as puffs in neurons and sparks in muscle cells. Despite the positive feedback nature of the activation, Ca signals are strictly confined in time and space by an unexplained termination mechanism. Here we show that the collective transition of release channels from an open to a closed state is identical to the phase transition associated with the reversal of magnetic field in an Ising ferromagnet. Our simple quantitative criterion closely predicts the Ca store depletion level required for spark termination for each cluster size. We further formulate exact requirements that a cluster of release channels should satisfy in any cell type for our mapping to the Ising model and the associated formula to remain valid. Thus, we describe deterministically the behavior of a system on a coarser scale (release unit) that is random on a finer scale (release channels), bridging the gap between scales. Our results provide exact mapping of a nanoscale biological signaling model to an interacting particle system in statistical physics, making the extensive mathematical apparatus available to quantitative biology.en_US
dc.format.extent7525 - 7530en_US
dc.languageengen_US
dc.relation.ispartofProc Natl Acad Sci U S Aen_US
dc.rightsThis is a pre-copyedited, author-produced version of an article accepted for publication in Proceedings of the National Academy of Sciences following peer review. The version of record is available http://www.pnas.org/content/114/29/7525
dc.subjectcalciumen_US
dc.subjectcalcium sparken_US
dc.subjectexcitation–contraction couplingen_US
dc.subjecthearten_US
dc.subjectryanodine receptoren_US
dc.subjectAnimalsen_US
dc.subjectCalciumen_US
dc.subjectCalcium Channelsen_US
dc.subjectCalcium Signalingen_US
dc.subjectCytoplasmen_US
dc.subjectHearten_US
dc.subjectHot Temperatureen_US
dc.subjectLipid Bilayersen_US
dc.subjectMagnetic Fieldsen_US
dc.subjectModels, Biologicalen_US
dc.subjectModels, Statisticalen_US
dc.subjectRyanodine Receptor Calcium Release Channelen_US
dc.subjectSarcoplasmic Reticulumen_US
dc.subjectSignal-To-Noise Ratioen_US
dc.titleClusters of calcium release channels harness the Ising phase transition to confine their elementary intracellular signals.en_US
dc.typeArticle
dc.rights.holder© 2017 National Academy of Sciences
dc.identifier.doi10.1073/pnas.1701409114en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/28674006en_US
pubs.issue29en_US
pubs.notesNot knownen_US
pubs.organisational-group/Queen Mary University of London
pubs.organisational-group/Queen Mary University of London/Faculty of Science & Engineering
pubs.organisational-group/Queen Mary University of London/Faculty of Science & Engineering/Mathematical Sciences - Staff and Research Students
pubs.organisational-group/Queen Mary University of London/REF
pubs.organisational-group/Queen Mary University of London/REF/REF - UoA 10
pubs.publication-statusPublisheden_US
pubs.volume114en_US


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