ArticleProceedings of the National Academy of Sciences of the United States of America2016
Paradoxical signaling regulates structural plasticity in dendritic spines.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Mechanochemical modeling of exercise-induced skeletal muscle hypertrophy.PLoS computational biology · 2026Article
- Calcium dynamics in small spaces: Lessons learned from modeling in dendritic spines.Biophysical journal · 2025Review
- Systems modeling and uncertainty quantification of AMP-activated protein kinase signaling.NPJ systems biology and applications · 2025Article
- Spatiotemporal orchestration of calcium-cAMP oscillations on AKAP/AC nanodomains is governed by an incoherent feedforward loop.PLoS computational biology · 2024Article
- Hub stability in the calcium calmodulin-dependent protein kinase II.Communications biology · 2024Article
- Real-time single-molecule imaging of CaMKII-calmodulin interactions.Biophysical journal · 2024Article
- Biophysical Modeling of Actin-Mediated Structural Plasticity Reveals Mechanical Adaptation in Dendritic Spines.eNeuro · 2024Article
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Dendritic Spines: Synaptogenesis and Synaptic Pruning for the Developmental Organization of Brain Circuits.Advances in neurobiology · 2023Article
- Methodology for development of single cell dendritic spine (SCDS) synaptic tagging and capture model using Virtual Cell (VCell).MethodsX · 2023Article
- Activation of NMDA receptors in brain endothelial cells increases transcellular permeability.Fluids and barriers of the CNS · 2022Article
- Dynamics and Sensitivity of Signaling Pathways.Current pathobiology reports · 2022Article
- Regulation of Cdc42 signaling by the dopamine D2 receptor in a mouse model of Parkinson's disease.Aging cell · 2022Article
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- Oxidative stress and Rho GTPases in the biogenesis of tunnelling nanotubes: implications in disease and therapy.Cellular and molecular life sciences : CMLS · 2021Article
- Temporal pattern and synergy influence activity of ERK signaling pathways during L-LTP induction.eLife · 2021Article
- Functional repertoire of protein kinases and phosphatases in synaptic plasticity and associated neurological disorders.Neural regeneration research · 2021Review
- Zc3h10 regulates adipogenesis by controlling translation and F-actin/mitochondria interaction.The Journal of cell biology · 2021Article
- Quantifying the roles of space and stochasticity in computer simulations for cell biology and cellular biochemistry.Molecular biology of the cell · 2021Article
- Mechanical Principles Governing the Shapes of Dendritic Spines.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Transient spine enlargement (3- to 5-min timescale) is an important event associated with the structural plasticity of dendritic spines. Many of the molecular mechanisms associated with transient spine enlargement have been identified experimentally. Here, we use a systems biology approach to construct a mathematical model of biochemical signaling and actin-mediated transient spine expansion in response to calcium influx caused by NMDA receptor activation. We have identified that a key feature of this signaling network is the paradoxical signaling loop. Paradoxical components act bifunctionally in signaling networks, and their role is to control both the activation and the inhibition of a desired response function (protein activity or spine volume). Using ordinary differential equation (ODE)-based modeling, we show that the dynamics of different regulators of transient spine expansion, including calmodulin-dependent protein kinase II (CaMKII), RhoA, and Cdc42, and the spine volume can be described using paradoxical signaling loops. Our model is able to capture the experimentally observed dynamics of transient spine volume. Furthermore, we show that actin remodeling events provide a robustness to spine volume dynamics. We also generate experimentally testable predictions about the role of different components and parameters of the network on spine dynamics.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.