ArticleMolecular and cellular biology2006
Functional analysis of p53 binding under differential stresses.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 65 citations in OpenAlex.
- UPR-induced intracellular C5aR1 promotes adaptation to the hypoxic tumour microenvironment.Cell death & disease · 2025Article
- TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression.Molecular and cellular biochemistry · 2025Article
- Identification of two novel autism genes,Frontiers in psychiatry · 2023Article
- t(4;12)(q12;p13) ETV6-rearranged AML without eosinophilia does not involve PDGFRA: relevance for imatinib insensitivity.Blood advances · 2022Article
- Characterization ofFrontiers in physiology · 2021Article
- Spermidine/spermine N1-acetyltransferase 1 is a gene-specific transcriptional regulator that drives brain tumor aggressiveness.Oncogene · 2019Article
- High glucose-induced p53 phosphorylation contributes to impairment of endothelial antioxidant system.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- The polyamine catabolic enzyme SAT1 modulates tumorigenesis and radiation response in GBM.Cancer research · 2014Article
- JMJD6 promotes colon carcinogenesis through negative regulation of p53 by hydroxylation.PLoS biology · 2014Article
- Article
- p53 regulates the transcription of the anti-inflammatory molecule developmental endothelial locus-1 (Del-1).Oncotarget · 2013Article
- Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells.Nucleic acids research · 2013Article
- REV3L 3'UTR 460 T>C polymorphism in microRNA target sites contributes to lung cancer susceptibility.Oncogene · 2013Article
- Temozolomide suppresses MYC via activation of TAp63 to inhibit progression of human glioblastoma.Scientific reports · 2013Article
- DNA-protein interactions: methods for detection and analysis.Molecular and cellular biochemistry · 2012Review
- Article
- Distinct p53 genomic binding patterns in normal and cancer-derived human cells.Cell cycle (Georgetown, Tex.) · 2011Article
- Translesion DNA synthesis in the context of cancer research.Cancer cell international · 2011Article
- Reciprocal influence of the p53 and the hypoxic pathways.Cell death & disease · 2011Review
- Human single-nucleotide polymorphisms alter p53 sequence-specific binding at gene regulatory elements.Nucleic acids research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxia and DNA damage stabilize the p53 protein, but the subsequent effect that each stress has on transcriptional regulation of known p53 target genes is variable. We have used chromatin immunoprecipitation followed by CpG island (CGI) microarray hybridization to identify promoters bound by p53 under both DNA-damaging and non-DNA-damaging conditions in HCT116 cells. Using gene-specific PCR analysis, we have verified an association with CGIs of the highest enrichment (> 2.5-fold) (REV3L, XPMC2H, HNRPUL1, TOR1AIP1, glutathione peroxidase 1, and SCFD2), with CGIs of intermediate enrichment (> 2.2-fold) (COX7A2L, SYVN1, and JAG2), and with CGIs of low enrichment (> 2.0-fold) (MYC and PCNA). We found little difference in promoter binding when p53 is stabilized by these two distinctly different stresses. However, expression of these genes varies a great deal: while a few genes exhibit classical induction with adriamycin, the majority of the genes are unchanged or are mildly repressed by either hypoxia or adriamycin. Further analysis using p53 mutated in the core DNA binding domain revealed that the interaction of p53 with CGIs may be occurring through both sequence-dependent and -independent mechanisms. Taken together, these experiments describe the identification of novel p53 target genes and the subsequent discovery of distinctly different expression phenomena for p53 target genes under different stress scenarios.
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.