ArticleScientific reports2016
Modelling intracellular competition for calcium: kinetic and thermodynamic control of different molecular modes of signal decoding.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- A Modeling and Analysis Study Reveals That CaMKII in Synaptic Plasticity Is a Dominant Affecter in CaM Systems in a T286 Phosphorylation-Dependent Manner.Molecules (Basel, Switzerland) · 2022Article
- A model for time interval learning in the Purkinje cell.PLoS computational biology · 2020Article
- Comprehensive Analysis of Differently Expressed and Methylated Genes in Preeclampsia.Computational and mathematical methods in medicine · 2020Article
- Computational Modeling Reveals Frequency Modulation of Calcium-cAMP/PKA Pathway in Dendritic Spines.Biophysical journal · 2019Article
- Competitive Tuning Among CaCellular and molecular bioengineering · 2018Article
- AMPA receptor trafficking and its role in heterosynaptic plasticity.Scientific reports · 2018Article
- Molecular mechanisms of detection and discrimination of dynamic signals.Scientific reports · 2018Article
- Competitive tuning: Competition's role in setting the frequency-dependence of Ca2+-dependent proteins.PLoS computational biology · 2017Article
- Stochastic Induction of Long-Term Potentiation and Long-Term Depression.Scientific reports · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frequently, a common chemical entity triggers opposite cellular processes, which implies that the components of signalling networks must detect signals not only through their chemical natures, but also through their dynamic properties. To gain insights on the mechanisms of discrimination of the dynamic properties of cellular signals, we developed a computational stochastic model and investigated how three calcium ion (Ca(2+))-dependent enzymes (adenylyl cyclase (AC), phosphodiesterase 1 (PDE1), and calcineurin (CaN)) differentially detect Ca(2+) transients in a hippocampal dendritic spine. The balance among AC, PDE1 and CaN might determine the occurrence of opposite Ca(2+)-induced forms of synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD). CaN is essential for LTD. AC and PDE1 regulate, indirectly, protein kinase A, which counteracts CaN during LTP. Stimulations of AC, PDE1 and CaN with artificial and physiological Ca(2+) signals demonstrated that AC and CaN have Ca(2+) requirements modulated dynamically by different properties of the signals used to stimulate them, because their interactions with Ca(2+) often occur under kinetic control. Contrarily, PDE1 responds to the immediate amplitude of different Ca(2+) transients and usually with the same Ca(2+) requirements observed under steady state. Therefore, AC, PDE1 and CaN decode different dynamic properties of Ca(2+) signals.
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