ArticleNucleic acids research2008
Transcriptional activation of the tumor suppressor and differentiation gene S100A2 by a novel p63-binding site.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 37 citations in OpenAlex.
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- Role of S100 family proteins in colorectal cancer (CRC): an overview of their potential function as new biomarkers and therapeutic agents.Expert reviews in molecular medicine · 2025Review
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.Nature communications · 2024Article
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.bioRxiv : the preprint server for biology · 2023Article
- Type 2 inflammation drives an airway basal stem cell program through insulin receptor substrate signaling.The Journal of allergy and clinical immunology · 2023Article
- Pathogenic role of S100 proteins in psoriasis.Frontiers in immunology · 2023Review
- Influence of S100A2 in Human Diseases.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- Article
- The Role of lncRNAs TAPIR-1 and -2 as Diagnostic Markers and Potential Therapeutic Targets in Prostate Cancer.Cancers · 2020Article
- DREAM and RB cooperate to induce gene repression and cell-cycle arrest in response to p53 activation.Nucleic acids research · 2019Article
- The p53-S100A2 Positive Feedback Loop Negatively Regulates Epithelialization in Cutaneous Wound Healing.Scientific reports · 2018Article
- Prognostic Roles of mRNA Expression of S100 in Non-Small-Cell Lung Cancer.BioMed research international · 2018Article
- Article
- Article
- Human papilloma virus E7 oncoprotein abrogates the p53-p21-DREAM pathway.Scientific reports · 2017Article
- S100A2 is a BRCA1/p63 coregulated tumour suppressor gene with roles in the regulation of mutant p53 stability.Cell death & disease · 2014Article
- Polo-like kinase 4 transcription is activated via CRE and NRF1 elements, repressed by DREAM through CDE/CHR sites and deregulated by HPV E7 protein.Nucleic acids research · 2014Article
- The CHR site: definition and genome-wide identification of a cell cycle transcriptional element.Nucleic acids research · 2014Article
- p53 can repress transcription of cell cycle genes through a p21(WAF1/CIP1)-dependent switch from MMB to DREAM protein complex binding at CHR promoter elements.Cell cycle (Georgetown, Tex.) · 2012Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A2 is generally found expressed in the epidermis and was recently shown to play a crucial role in the differentiation of keratinocytes. Also known as CaN19, S100A2 was identified as a potential tumor suppressor. Expression of S100A2 is upregulated by p53. The proteins p63 and p73 are related to p53 and are expressed as several splice variants with partially overlapping tasks but also functions different from p53. It had been shown that p63 proteins with mutations in their DNA-binding domain cause severe phenotypes in man as autosomal dominantly inherited disease including EEC, AEC, SHFM, LMS and ADULT syndromes. Here we show that S100A2 is a transcriptional target of p63/p73 family members, particularly the p63 splice variant TAp63gamma. The regulation is mediated by a novel transcriptional element in the S100A2 promoter which is bound by TAp63gamma but not by p53. Mutant p63 proteins derived from EEC and ADULT syndrome patients cannot activate S100A2 transcription whereas SHFM-related mutants still can stimulate the S100A2 promoter. Consistent with a function in tumor suppression S100A2 expression is stimulated upon DNA damage. After doxorubicin treatment p63gamma proteins are recruited to the S100A2 promoter in vivo. This may indicate a function of the p63-dependent S100A2 regulation in tumor suppression.
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.