ArticleMolecular biology of the cell2016
Defined spatiotemporal features of RAS-ERK signals dictate cell fate in MCF-7 mammary epithelial cells.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Changes in Ras and Ras-Associated GTPases During Maturation of Porcine Cumulus Cells and Oocytes.Animals : an open access journal from MDPI · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- Review
- PDGFR dimer-specific activation, trafficking and downstream signaling dynamics.Journal of cell science · 2022Article
- Review
- Palmitoylation as a Key Regulator of Ras Localization and Function.Frontiers in molecular biosciences · 2021Review
- Spatial regulation and generation of diversity in signaling pathways.Journal of biosciences · 2021Review
- RAS Subcellular Localization Inversely Regulates Thyroid Tumor Growth and Dissemination.Cancers · 2020Article
- Signaling diversity enabled by Rap1-regulated plasma membrane ERK with distinct temporal dynamics.eLife · 2020Article
- Epigenetic Alterations in Renal Cell Cancer With TKIs Resistance: From Mechanisms to Clinical Applications.Frontiers in genetics · 2020Review
- DNA methylation-regulated QPCT promotes sunitinib resistance by increasing HRAS stability in renal cell carcinoma.Theranostics · 2019Article
- Diepoxybutane-induced apoptosis is mediated through the ERK1/2 pathway.Human & experimental toxicology · 2018Article
- RAS at the Golgi antagonizes malignant transformation through PTPRκ-mediated inhibition of ERK activation.Nature communications · 2018Article
- Article
- Emerging themes of regulation at the Golgi.Current opinion in cell biology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signals conveyed through the RAS-ERK pathway are essential for the determination of cell fate. It is well established that signal variability is achieved in the different microenvironments in which signals unfold. It is also known that signal duration is critical for decisions concerning cell commitment. However, it is unclear how RAS-ERK signals integrate time and space in order to elicit a given biological response. To investigate this, we used MCF-7 cells, in which EGF-induced transient ERK activation triggers proliferation, whereas sustained ERK activation in response to heregulin leads to adipocytic differentiation. We found that both proliferative and differentiating signals emanate exclusively from plasma membrane-disordered microdomains. Of interest, the EGF signal can be transformed into a differentiating stimulus by HRAS overexpression, which prolongs ERK activation, but only if HRAS localizes at disordered membrane. On the other hand, HRAS signals emanating from the Golgi complex induce apoptosis and can prevent heregulin-induced differentiation. Our results indicate that within the same cellular context, RAS can exert different, even antagonistic, effects, depending on its sublocalization. Thus cell destiny is defined by the ability of a stimulus to activate RAS at the appropriate sublocalization for an adequate period while avoiding switching on opposing RAS signals.
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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.