ArticleProceedings of the National Academy of Sciences of the United States of America2004
Siah-1b is a direct transcriptional target of p53: identification of the functional p53 responsive element in the siah-1b promoter.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- A noninvasive iRFP713 p53 reporter reveals dynamic p53 activity in response to irradiation and liver regeneration in vivo.Science signaling · 2022Article
- E3 ubiquitin ligase-mediated regulation of vertebrate ocular development; new insights into the function of SIAH enzymes.Biochemical Society transactions · 2021Review
- Host cell factors stimulate HIV-1 transcription by antagonizing substrate-binding function of Siah1 ubiquitin ligase to stabilize transcription elongation factor ELL2.Nucleic acids research · 2020Article
- Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer.International journal of molecular sciences · 2020Review
- Mutant p53 Gain-of-Function: Role in Cancer Development, Progression, and Therapeutic Approaches.Frontiers in cell and developmental biology · 2020Review
- An investigation of the correlation between the S-glutathionylated GAPDH levels in blood and Alzheimer's disease progression.PloS one · 2020Article
- S-Nitrosylation: An Emerging Paradigm of Redox Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- Plakoglobin restores tumor suppressor activity of p53Cancer science · 2018Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
- Seven in Absentia E3 Ubiquitin Ligases: Central Regulators of Neural Cell Fate and Neuronal Polarity.Frontiers in cellular neuroscience · 2017Review
- Protein Recognition in Drug-Induced DNA Alkylation: When the Moonlight Protein GAPDH Meets S23906-1/DNA Minor Groove Adducts.International journal of molecular sciences · 2015Review
- Cellular reprogramming in skin cancer.Seminars in cancer biology · 2015Review
- Critical protein GAPDH and its regulatory mechanisms in cancer cells.Cancer biology & medicine · 2015Review
- Article
- Genomic DNA hypomethylation is associated with neural tube defects induced by methotrexate inhibition of folate metabolism.PloS one · 2015Article
- SIAH2 antagonizes TYK2-STAT3 signaling in lung carcinoma cells.Oncotarget · 2014Article
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Regulators and effectors of Siah ubiquitin ligases.Cell biochemistry and biophysics · 2013Review
- Roles of p53 in herpes simplex virus 1 replication.Journal of virology · 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
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Siah proteins are E3 ubiquitin ligases. They are homologues of the Drosophila seven in absentia (Sina), a protein required for the R7 photoreceptor development. We have previously found that the expression of human siah-1 and its mouse homologue siah-1b are induced by p53 during apoptosis and tumor reversion. So far, no evidence that the siah-1b gene is a direct transcriptional target of p53 has been provided. In the present study we investigate this issue. Northern blot analysis with a specific probe demonstrates an increase in siah-1b transcription on activation of endogenous and inducible exogenous p53. To explore whether this effect is directly mediated by p53 we analyzed 20 kb of chromosome X DNA, containing the siah-1b locus. A p53-binding site was identified in the siah-1b promoter, located at nucleotides -2155/-2103 relative to the translational start site. This site is composed of two half-sites, conforming to the p53-binding consensus sequence but separated by a nonclassical 33-bp spacer. In luciferase assays, p53 induces a substantial increase in siah-1b promoter activity. Gel shift and DNase-I-footprinting studies, combined with mutational analysis and chromatin immunoprecipitation, indicate that p53 effectively binds the siah-1b promoter in vitro and in vivo. Thus, the siah-1b gene is a direct transcriptional target of p53.
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.