ArticleMolecular and cellular biology2004
An extracellular signal-regulated kinase 1- and 2-dependent program of chromatin trafficking of c-Fos and Fra-1 is required for cyclin D1 expression during cell cycle reentry.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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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Who cites it
37 citing papers in PubMed, 89 citations in OpenAlex.
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- Role of the renin-angiotensin system in NETosis in the coronavirus disease 2019 (COVID-19).Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Role of the Transcription Factor FOSL1 in Organ Development and Tumorigenesis.International journal of molecular sciences · 2022Review
- LPS-induced inflammatory response and apoptosis are mediated by Fra-1 upregulation and binding to YKL-40 in A549 cells.Experimental and therapeutic medicine · 2021Article
- Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers.Nucleic acids research · 2021Article
- From Melanoma Development to RNA-Modified Dendritic Cell Vaccines: Highlighting the Lessons From the Past.Frontiers in immunology · 2021Review
- Temporal integration of mitogen history in mother cells controls proliferation of daughter cells.Science (New York, N.Y.) · 2020Article
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- The role of AP-1 in self-sufficient proliferation and migration of cancer cells and its potential impact on an autocrine/paracrine loop.Oncotarget · 2018Article
- Activation of adrenergic receptor in H9c2 cardiac myoblasts co-stimulates Nox2 and the derived ROS mediate the downstream responses.Molecular and cellular biochemistry · 2017Article
- MLK3 regulates FRA-1 and MMPs to drive invasion and transendothelial migration in triple-negative breast cancer cells.Oncogenesis · 2017Article
- Involvement of Fra-1 in Retinal Ganglion Cell Apoptosis in Rat Light-Induced Retina Damage Model.Cellular and molecular neurobiology · 2017Article
- Small molecule inhibition of cAMP response element binding protein in human acute myeloid leukemia cells.Leukemia · 2016Article
- Small molecule screen for inhibitors of expression from canonical CREB response element-containing promoters.Oncotarget · 2016Article
- p53 protein-mediated up-regulation of MAP kinase phosphatase 3 (MKP-3) contributes to the establishment of the cellular senescent phenotype through dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2).The Journal of biological chemistry · 2015Article
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- Ischemic preconditioning affects long-term cell fate through DNA damage-related molecular signaling and altered proliferation.The American journal of pathology · 2014Article
- Retinoblastoma protein and MyoD function together to effect the repression of Fra-1 and in turn cyclin D1 during terminal cell cycle arrest associated with myogenesis.The Journal of biological chemistry · 2014Article
- Mitochondrial-targeted nitroxides disrupt mitochondrial architecture and inhibit expression of peroxiredoxin 3 and FOXM1 in malignant mesothelioma cells.Journal of cellular physiology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitogens activate cell signaling and gene expression cascades that culminate in expression of cyclin D1 during the G(0)-to-G(1) transition of the cell cycle. Using cell cycle arrest in response to oxidative stress, we have delineated a dynamic program of chromatin trafficking of c-Fos and Fra-1 required for cyclin D1 expression during cell cycle reentry. In serum-stimulated lung epithelial cells, c-Fos was expressed, recruited to chromatin, phosphorylated at extracellular signal-regulated kinase 1- and 2 (ERK1,2)-dependent sites, and degraded prior to prolonged recruitment of Fra-1 to chromatin. Immunostaining showed that expression of nuclear c-Fos and that of cyclin D1 are mutually exclusive, whereas nuclear Fra-1 and cyclin D1 are coexpressed as cells traverse G(1). Oxidative stress prolonged the accumulation of phospho-ERK1,2 and phospho-c-Fos on chromatin, inhibited entry of Fra-1 into the nucleus, and blocked cyclin D1 expression. After induction of the immediate-early gene response in the presence of oxidative stress, inhibition of ERK1,2 signaling promoted degradation of c-Fos, recruitment of Fra-1 to chromatin, and expression of cyclin D1. Our data indicate that termination of nuclear ERK1,2 signaling is required for an exchange of Fra-1 for c-Fos on chromatin and initiation of cyclin D1 expression at the G(0)-to-G(1) transition of the cell cycle.
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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.