ArticleOncogene2002
Transcriptional activation by the oestrogen receptor alpha is modulated through inhibition of cyclin-dependent kinases.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- Crosstalk of methylation and tamoxifen in breast cancer (Review).Molecular medicine reports · 2024Review
- Network-informed discovery of multidrug combinations for ERα+/HER2-/PI3Kα-mutant breast cancer.Cellular and molecular life sciences : CMLS · 2023Article
- The Role of the Cyclin Dependent Kinase Inhibitor p21Cancers · 2019Review
- Role of WISP-2/CCN5 in the maintenance of a differentiated and noninvasive phenotype in human breast cancer cells.Molecular and cellular biology · 2008Article
- Proliferation-associated Brn-3b transcription factor can activate cyclin D1 expression in neuroblastoma and breast cancer cells.Oncogene · 2008Article
- Cyclin dependent kinase 2 and the regulation of human progesterone receptor activity.Steroids · 2007Review
- p21WAF1/CIP1 selectively controls the transcriptional activity of estrogen receptor alpha.Molecular and cellular biology · 2005Article
- Advances in estrogen receptor biology: prospects for improvements in targeted breast cancer therapy.Breast cancer research : BCR · 2004Review
- Intratumoural mRNA expression of genes from the oestradiol metabolic pathway and clinical and histopathological parameters of breast cancer.Breast cancer research : BCR · 2004Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the interaction between the expression of p21(WAF1/CIP1/SDI1), a stoichiometric inhibitor of Cdk, and the transcriptional activity of the oestrogen receptor alpha (ER(alpha). Transient transfection experiments demonstrated that the expression of p21(WAF1/CIP1/SDI1) amplified the transcriptional activation by ER(alpha). A dominant negative mutant of Cdk2 also enhanced the ER(alpha) transcriptional activity, indicating that the underlying mechanism relies on the inhibition of Cdk2 activity and cell cycle arrest. In agreement with this conclusion, experiments with p21(WAF1/CIP1/SDI1) mutants demonstrated that the domain involved in the binding of p21(WAF1/CIP1/SDI1) to Cdks was indispensable for the modulation of ER(alpha) activity. In addition, we show that expression of p21(WAF1/CIP1/SDI1) alleviates the block on CBP function mediated by Cdk2 and in turn stimulates transcriptional activation by ER(alpha) in a CBP-histone acetyltransferase (HAT)-dependent manner. These results suggest a novel mechanism by which p21(WAF1/CIP1/SDI1) functions as an enhancer of ER(alpha) activity through the modulation of CBP function.
Indexed as
Identifiers
What OpenQuestion holds
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.