ArticleThe Journal of clinical investigation1998
Role of c-fos and E2F in the induction of cyclin A transcription and vascular smooth muscle cell proliferation.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 76 citations in OpenAlex.
- NQO1 regulates cell cycle progression at the G2/M phase.Theranostics · 2023Article
- Punicalagin Attenuates Disturbed Flow-Induced Vascular Dysfunction by Inhibiting Force-Specific Activation of Smad1/5.Frontiers in cell and developmental biology · 2021Article
- RING finger protein 10 is a potential drug target for diabetic vascular complications.Molecular medicine reports · 2019Article
- Cocaine promotes primary human astrocyte proliferation via JNK-dependent up-regulation of cyclin A2.Restorative neurology and neuroscience · 2016Article
- COUGER--co-factors associated with uniquely-bound genomic regions.Nucleic acids research · 2014Article
- The intermediate conductance calcium-activated potassium channel KCa3.1 regulates vascular smooth muscle cell proliferation via controlling calcium-dependent signaling.The Journal of biological chemistry · 2013Article
- Redox control of the cell cycle in health and disease.Antioxidants & redox signaling · 2009Review
- PGC-1alpha inhibits oleic acid induced proliferation and migration of rat vascular smooth muscle cells.PloS one · 2007Article
- Phosphorylation of the cyclic AMP response element binding protein mediates transforming growth factor beta-induced downregulation of cyclin A in vascular smooth muscle cells.Molecular and cellular biology · 2007Article
- Fra-1 promotes growth and survival in RAS-transformed thyroid cells by controlling cyclin A transcription.The EMBO journal · 2007Article
- Brd2 is a TBP-associated protein and recruits TBP into E2F-1 transcriptional complex in response to serum stimulation.Molecular and cellular biochemistry · 2007Article
- Regulation of vascular smooth muscle proliferation by heparin: inhibition of cyclin-dependent kinase 2 activity by p27(kip1).The Journal of biological chemistry · 2005Article
- Bromodomain analysis of Brd2-dependent transcriptional activation of cyclin A.The Biochemical journal · 2005Article
- Article
- Transcriptional activation of the cyclin A gene by the architectural transcription factor HMGA2.Molecular and cellular biology · 2003Article
- Activation of transcription factors AP-1 and NF-kappa B in murine Chagasic myocarditis.Infection and immunity · 2003Article
- Distinct effects of mitogens and the actin cytoskeleton on CREB and pocket protein phosphorylation control the extent and timing of cyclin A promoter activity.Molecular and cellular biology · 2001Article
- Inhibition of the cyclin D1/E2F pathway by PCA-4230, a potent repressor of cellular proliferation.British journal of pharmacology · 2001Article
- Reactive oxygen intermediates involved in cellular regulation.Protoplasma · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Excessive proliferation of vascular smooth muscle cells (VSMCs) contributes to vessel renarrowing after angioplasty. Here we investigated the transcriptional regulation of the cyclin A gene, a key positive regulator of S phase that is induced after angioplasty. We show that Ras-dependent mitogenic signaling is essential for the normal stimulation of cyclin A promoter activity and DNA synthesis in VSMCs. Overexpression of the AP-1 transcription factor c-fos can circumvent this requirement via interaction with the cAMP-responsive element (CRE) in the cyclin A promoter. Moreover, c-fos overexpression in serum-starved VSMCs results in the induction of cyclin A promoter activity in a CRE-dependent manner, and increased binding of endogenous c-fos protein to the cyclin A CRE precedes the onset of DNA replication in VSMCs induced by serum in vitro and by angioplasty in vivo. We also show that E2F function is essential for both serum- and c-fos-dependent induction of cyclin A expression. Taken together, these findings suggest that c-fos and E2F are important components of the signaling cascade that link Ras activity to cyclin A transcription in VSMCs. These studies illustrate a novel link between the transcriptional and cell cycle machinery that may be relevant to the pathogenesis of vascular proliferative disorders.
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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.