ArticlePhysical review. E2017
Stochastic dynamics of genetic broadcasting networks.
Article in Physical review. E, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- OPTIMIS: Optimizing Personalized Therapies through Integrated Multiscale Intelligent Simulation.bioRxiv : the preprint server for biology · 2026Article
- The multifunctional role of intrinsic disorder in NF-κB signaling.Biochemical Society transactions · 2023Review
- The nonequilibrium mechanism of noise-enhanced drug synergy in HIV latency reactivation.iScience · 2022Article
- Force-Dependent Facilitated Dissociation Can Generate Protein-DNA Catch Bonds.Biophysical journal · 2019Article
- Exclusivity and Compensation in NFκB Dimer Distributions and IκB Inhibition.Biochemistry · 2019Article
- Exploring intermediate cell states through the lens of single cells.Current opinion in systems biology · 2018Article
- Resolving the NFκB Heterodimer Binding Paradox: Strain and Frustration Guide the Binding of Dimeric Transcription Factors.Journal of the American Chemical Society · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The complex genetic programs of eukaryotic cells are often regulated by key transcription factors occupying or clearing out of a large number of genomic locations. Orchestrating the residence times of these factors is therefore important for the well organized functioning of a large network. The classic models of genetic switches sidestep this timing issue by assuming the binding of transcription factors to be governed entirely by thermodynamic protein-DNA affinities. Here we show that relying on passive thermodynamics and random release times can lead to a "time-scale crisis" for master genes that broadcast their signals to a large number of binding sites. We demonstrate that this time-scale crisis for clearance in a large broadcasting network can be resolved by actively regulating residence times through molecular stripping. We illustrate these ideas by studying a model of the stochastic dynamics of the genetic network of the central eukaryotic master regulator NFκB which broadcasts its signals to many downstream genes that regulate immune response, apoptosis, etc.
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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.