ArticlePloS one2015
Protein copy number distributions for a self-regulating gene in the presence of decoy binding sites.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 42 citations in OpenAlex.
- Optimisation of gene expression noise for cellular persistence against lethal events.Journal of theoretical biology · 2025Article
- Holimap: an accurate and efficient method for solving stochastic gene network dynamics.Nature communications · 2024Article
- Controlling gene expression timing through gene regulatory architecture.PLoS computational biology · 2022Article
- Enhancement of gene expression noise from transcription factor binding to genomic decoy sites.Scientific reports · 2020Article
- Stochastic Modeling of Autoregulatory Genetic Feedback Loops: A Review and Comparative Study.Biophysical journal · 2020Review
- What is Normalization? The Strategies Employed in Top-Down and Bottom-Up Proteome Analysis Workflows.Proteomes · 2019Review
- Exponential equilibration of genetic circuits using entropy methods.Journal of mathematical biology · 2019Article
- Gene expression noise is affected differentially by feedback in burst frequency and burst size.Journal of mathematical biology · 2017Article
- Effect of transcription factor resource sharing on gene expression noise.PLoS computational biology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A single transcription factor may interact with a multitude of targets on the genome, some of which are at gene promoters, others being part of DNA repeat elements. Being sequestered at binding sites, protein molecules can be prevented from partaking in other pathways, specifically, from regulating the expression of the very gene that encodes them. Acting as decoys at the expense of the autoregulatory loop, the binding sites can have a profound impact on protein abundance--on its mean as well as on its cell-to-cell variability. In order to quantify this impact, we study in this paper a mathematical model for pulsatile expression of a transcription factor that autoregulates its expression and interacts with decoys. We determine the exact stationary distribution for protein abundance at the single-cell level, showing that in the case of non-cooperative positive autoregulation, the distribution can be bimodal, possessing a basal expression mode and a distinct, up-regulated, mode. Bimodal protein distributions are more feasible if the rate of degradation is the same irrespective of whether protein is bound or not. Contrastingly, the presence of decoy binding sites which protect the protein from degradation reduces the availability of the bimodal scenario.
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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 OpenQuestion graph.