ArticleScientific reports2020
Activity-dependent compensation of cell size is vulnerable to targeted deletion of ion channels.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Aging Alters Hair Cell Physiological Properties in Mice With Late-Onset Age-Related Hearing Loss.Aging cell · 2026Article
- Persistent adaptation through dual-timescale regulation of ion channel properties.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Persistent Adaptation through Dual-Timescale Regulation of Ion Channel Properties.bioRxiv : the preprint server for biology · 2025Article
- The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.Frontiers in physiology · 2025Article
- A possible path to persistent re-entry waves at the outlet of the left pulmonary vein.NPJ systems biology and applications · 2024Article
- Do calcium channel blockers applied to cardiomyocytes cause increased channel expression resulting in reduced efficacy?NPJ systems biology and applications · 2024Article
- Gating of homeostatic regulation of intrinsic excitability produces cryptic long-term storage of prior perturbations.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neuronal morphology enhances robustness to perturbations of channel densities.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Heterogeneous off-target impact of ion-channel deletion on intrinsic properties of hippocampal model neurons that self-regulate calcium.Frontiers in cellular neuroscience · 2023Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
In many species, excitable cells preserve their physiological properties despite significant variation in physical size across time and in a population. For example, neurons in crustacean central pattern generators generate similar firing patterns despite several-fold increases in size between juveniles and adults. This presents a biophysical problem because the electrical properties of cells are highly sensitive to membrane area and channel density. It is not known whether specific mechanisms exist to sense membrane area and adjust channel expression to keep a consistent channel density, or whether regulation mechanisms that sense activity alone are capable of compensating cell size. We show that destabilising effects of growth can be specifically compensated by feedback mechanism that senses average calcium influx and jointly regulate multiple conductances. However, we further show that this class of growth-compensating regulation schemes is necessarily sensitive to perturbations that alter the expression of subsets of ion channel types. Targeted perturbations of specific ion channels can trigger a pathological response of the regulation mechanism and a failure of homeostasis. Our findings suggest that physiological regulation mechanisms that confer robustness to growth may be specifically vulnerable to deletions or mutations that affect subsets of ion channels.
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Registered trials
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 Socratic graph.