ArticleMolecular cell2011
Two phases of mitogenic signaling unveil roles for p53 and EGR1 in elimination of inconsistent growth signals.
Article in Molecular cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Reusable rule-based cell cycle model explains compartment-resolved dynamics of 16 observables in RPE-1 cells.PLoS computational biology · 2024Article
- A guide to ERK dynamics, part 2: downstream decoding.The Biochemical journal · 2023Article
- Relating individual cell division events to single-cell ERK and Akt activity time courses.Scientific reports · 2022Article
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- The ERK mitogen-activated protein kinase signaling network: the final frontier in RAS signal transduction.Biochemical Society transactions · 2021Review
- The Basally Expressed p53-Mediated Homeostatic Function.Frontiers in cell and developmental biology · 2021Review
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- Receptor-Driven ERK Pulses Reconfigure MAPK Signaling and Enable Persistence of Drug-Adapted BRAF-Mutant Melanoma Cells.Cell systems · 2020Article
- ERK signalling: a master regulator of cell behaviour, life and fate.Nature reviews. Molecular cell biology · 2020Review
- MDMX phosphorylation-dependent p53 downregulation contributes to an immunosuppressive tumor microenvironment.Journal of molecular cell biology · 2020Article
- Expression and prognostic value of the transcription factors EGR1 and EGR3 in gliomas.Scientific reports · 2020Article
- A Live-Cell Screen for Altered Erk Dynamics Reveals Principles of Proliferative Control.Cell systems · 2020Article
- De-ubiquitination of ELK-1 by USP17 potentiates mitogenic gene expression and cell proliferation.Nucleic acids research · 2019Article
1 more citing papers are in PubMed but not listed here.
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16 authors.
Funding
Abstract
Normal cells require continuous exposure to growth factors in order to cross a restriction point and commit to cell-cycle progression. This can be replaced by two short, appropriately spaced pulses of growth factors, where the first pulse primes a process, which is completed by the second pulse, and enables restriction point crossing. Through integration of comprehensive proteomic and transcriptomic analyses of each pulse, we identified three processes that regulate restriction point crossing: (1) The first pulse induces essential metabolic enzymes and activates p53-dependent restraining processes. (2) The second pulse eliminates, via the PI3K/AKT pathway, the suppressive action of p53, as well as (3) sets an ERK-EGR1 threshold mechanism, which digitizes graded external signals into an all-or-none decision obligatory for S phase entry. Together, our findings uncover two gating mechanisms, which ensure that cells ignore fortuitous growth factors and undergo proliferation only in response to consistent mitogenic signals.
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