ArticleOncogene1999
Control of E2F activity by p21Waf1/Cip1.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
56 citing papers in PubMed, 142 citations in OpenAlex.
- SMAD2/3-SMYD2 and developmental transcription factors cooperate with cell-cycle inhibitors to guide tissue formation.Protein & cell · 2025Article
- The Emerging Role of p21 in Diabetes and Related Metabolic Disorders.International journal of molecular sciences · 2024Review
- p21/Zbtb18 repress the expression of cKit to regulate the self-renewal of hematopoietic stem cells.Protein & cell · 2024Article
- May I Help You with Your Coat? HIV-1 Capsid Uncoating and Reverse Transcription.International journal of molecular sciences · 2024Review
- Lunasin and Its Epigenetic Impact in Cancer Chemoprevention.International journal of molecular sciences · 2023Review
- Fanconi anemia pathway regulation by FANCI in prostate cancer.Frontiers in oncology · 2023Article
- Nucleotide biosynthesis links glutathione metabolism to ferroptosis sensitivity.Life science alliance · 2022Article
- Identification of RUNX1T1 as a potential epigenetic modifier in small-cell lung cancer.Molecular oncology · 2021Article
- Clofarabine‑phytochemical combination exposures in CML cells inhibit DNA methylation machinery, upregulate tumor suppressor genes and promote caspase‑dependent apoptosis.Molecular medicine reports · 2019Article
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
- Thr55 phosphorylation of p21 by MPK38/MELK ameliorates defects in glucose, lipid, and energy metabolism in diet-induced obese mice.Cell death & disease · 2019Article
- Anti-apoptotic role of spermine against lead and/or gamma irradiation-induced hepatotoxicity in male rats.Environmental science and pollution research international · 2017Article
- Negative control of CSL gene transcription by stress/DNA damage response and p53.Cell cycle (Georgetown, Tex.) · 2016Article
- p21 deficiency is susceptible to osteoarthritis through STAT3 phosphorylation.Arthritis research & therapy · 2015Article
- MicroRNA-10b inhibition reduces E2F1-mediated transcription and miR-15/16 activity in glioblastoma.Oncotarget · 2015Article
- The activity and stability of the intrinsically disordered Cip/Kip protein family are regulated by non-receptor tyrosine kinases.Journal of molecular biology · 2015Article
- Article
- A p21-ZEB1 complex inhibits epithelial-mesenchymal transition through the microRNA 183-96-182 cluster.Molecular and cellular biology · 2014Article
- Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance.Nature neuroscience · 2013Article
- p21-mediated RNR2 repression restricts HIV-1 replication in macrophages by inhibiting dNTP biosynthesis pathway.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclin-dependent kinase inhibitors (cdkis), such as p21, are believed to control proliferation through an ability to function as stoichiometric antagonists of cyclin-dependent kinases (cdks). The p21 gene is a direct transcriptional target for the p53 protein, and its activation is likely to be important in effecting the p53 response. It is widely accepted that p21 can influence cell cycle progression by controlling the activity of cdks that act on the retinoblastoma tumour suppressor protein (pRb) which, in a hypophosphorylated state, associates with E2F transcription factors to prevent the activation of genes required for progression into S phase. Phosphorylation of pRb by G1 cdk complexes releases E2F and thereby enables progress through the cell cycle. Here, we describe results which suggest a p21-dependent mechanism that facilitates the regulation of E2F through a pathway that is independent of the cdk control of pRb activity. As p21 can associate with E2F subunits, it is possible that these effects are exerted through a complex with E2F. Furthermore, we find that p21 can regulate transcription in vitro. The results suggest that p21 may control E2F activity through a pathway that acts independently of pRb.
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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.