ArticleCell adhesion & migration
ERK-ERF-EGR1, a novel switch underlying acquisition of a motile phenotype.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Differential functions of ERK1 and ERK2 in lung metastasis processes in triple-negative breast cancer.Scientific reports · 2020Article
- CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2A.Oncogene · 2018Article
- Tumor suppression by the EGR1, DMP1, ARF, p53, and PTEN Network.Cancer investigation · 2018Article
- A Positive Feed-forward Loop Associating EGR1 and PDGFA Promotes Proliferation and Self-renewal in Glioblastoma Stem Cells.The Journal of biological chemistry · 2016Article
- LL-37 stimulates the functions of adipose-derived stromal/stem cells via early growth response 1 and the MAPK pathway.Stem cell research & therapy · 2016Article
- Transcriptome study and identification of potential marker genes related to the stable expression of recombinant proteins in CHO clones.BMC biotechnology · 2015Article
- CDKN2B Loss Promotes Progression from Benign Melanocytic Nevus to Melanoma.Cancer discovery · 2015Article
- Steering tumor progression through the transcriptional response to growth factors and stroma.FEBS letters · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unlike the well-characterized checkpoints of the cell cycle, which establish commitment to cell division, signaling pathways and gene expression programs that commit cells to migration are incompletely understood. Apparently, several molecular switches are activated in response to an extracellular cue, such as the epidermal growth factor (EGF), and they simultaneously confer distinct features of an integrated motile phenotype. Here we review such early (transcription-independent) and late switches, in light of a novel ERK-ERF-EGR1 switch we recently reported in the FASEB Journal. The study employed human mammary cells and two stimuli: EGF, which induced mammary cell migration, and serum factors, which stimulated cell growth. By contrasting the underlying pathways we unveiled a cascade that allows the active form of the ERK mitogen-activated protein kinase (MAPK) cascade to export the ERF repressor from the nucleus, thereby permitting tightly balanced stimulation of an EGR1-centered gene expression program.
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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.