ArticleMolecular biology of the cell2018
A data-entrained computational model for testing the regulatory logic of the vertebrate unfolded protein response.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- A beneficial adaptive role for CHOP in driving cell fate selection during ER stress.EMBO reports · 2024Article
- A systems biological analysis of the ATF4-GADD34-CHOP regulatory triangle upon endoplasmic reticulum stress.FEBS open bio · 2022Article
- Temporal control of the integrated stress response by a stochastic molecular switch.Science advances · 2022Article
- Unfolded protein response in colorectal cancer.Cell & bioscience · 2021Review
- Arsenic induced redox imbalance triggers the unfolded protein response in the liver of zebrafish.Toxicology and applied pharmacology · 2020Article
- Development of a hybrid model for a partially known intracellular signaling pathway through correction term estimation and neural network modeling.PLoS computational biology · 2020Article
- ATF6 Is a Critical Determinant of CHOP Dynamics during the Unfolded Protein Response.iScience · 2020Article
- Targeting the unfolded protein response in head and neck and oral cavity cancers.Experimental cell research · 2019Review
- Identification of a time-varying intracellular signalling model through data clustering and parameter selection: application to NF-[inline-formula removed]B signalling pathway induced by LPS in the presence of BFA.IET systems biology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The vertebrate unfolded protein response (UPR) is characterized by multiple interacting nodes among its three pathways, yet the logic underlying this regulatory complexity is unclear. To begin to address this issue, we created a computational model of the vertebrate UPR that was entrained upon and then validated against experimental data. As part of this validation, the model successfully predicted the phenotypes of cells with lesions in UPR signaling, including a surprising and previously unreported differential role for the eIF2α phosphatase GADD34 in exacerbating severe stress but ameliorating mild stress. We then used the model to test the functional importance of a feedforward circuit within the PERK/CHOP axis and of cross-regulatory control of BiP and CHOP expression. We found that the wiring structure of the UPR appears to balance the ability of the response to remain sensitive to endoplasmic reticulum stress and to be deactivated rapidly by improved protein-folding conditions. This model should serve as a valuable resource for further exploring the regulatory logic of the UPR.
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