ArticleOncogene2008
PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals.eLife · 2025Article
- Role of the SPI1/CDKN2A/p53 signaling pathway in cuproptosis of lung adenocarcinoma cells.Oncology letters · 2025Article
- A system-level model reveals that transcriptional stochasticity is required for hematopoietic stem cell differentiation.NPJ systems biology and applications · 2024Article
- A multi-omics approach for biomarker discovery in neuroblastoma: a network-based framework.NPJ systems biology and applications · 2024Article
- NOL12 as an Oncogenic Biomarker Promotes Hepatocellular Carcinoma Growth and Metastasis.Oxidative medicine and cellular longevity · 2022Article
- Comprehensive Analysis of Immune Implications and Prognostic Value of SPI1 in Gastric Cancer.Frontiers in oncology · 2022Article
- Therapeutic targeting of SPIB/SPI1-facilitated interplay of cancer cells and neutrophils inhibits aerobic glycolysis and cancer progression.Clinical and translational medicine · 2021Article
- Effect of Th9/IL-9 on the growth of gastric cancer in nude mice.OncoTargets and therapy · 2019Article
- High expression of PU.1 is associated with Her-2 and shorter survival in patients with breast cancer.Oncology letters · 2017Article
- Oncopig Soft-Tissue Sarcomas Recapitulate Key Transcriptional Features of Human Sarcomas.Scientific reports · 2017Article
- PU.1 supports TRAIL-induced cell death by inhibiting NF-κB-mediated cell survival and inducing DR5 expression.Cell death and differentiation · 2017Article
- PC-TraFF: identification of potentially collaborating transcription factors using pointwise mutual information.BMC bioinformatics · 2015Article
- Low DICER1 expression is associated with attenuated neutrophil differentiation and autophagy of NB4 APL cells.Journal of leukocyte biology · 2015Article
- The granulocyte orphan receptor CEACAM4 is able to trigger phagocytosis of bacteria.Journal of leukocyte biology · 2015Article
- Pathway analyses identify TGFBR2 as potential breast cancer susceptibility gene: results from a consortium study among Asians.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012Article
- PU.1 is linking the glycolytic enzyme HK3 in neutrophil differentiation and survival of APL cells.Blood · 2012Article
- CLEC5A (MDL-1) is a novel PU.1 transcriptional target during myeloid differentiation.Molecular immunology · 2011Article
- MIRTFnet: analysis of miRNA regulated transcription factors.PloS one · 2011Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression. It has been hypothesized that p53-mediated expression of the p21(Cip1) cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function. In addition to the blockage of erythroblast differentiation provided by increased levels of PU.1, we propose that PU.1 alters p53 function. We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis. Inhibition is mediated through binding of PU.1 to the DNA-binding and/or oligomerization domains of p53/p73 proteins. Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21(Cip1).
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.