ArticlePloS one2011
Fanconi anemia core complex gene promoters harbor conserved transcription regulatory elements.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Oncogenic properties of wild-type DNA repair gene FANCA in breast cancer.Cell reports · 2025Article
- Epigenetic Regulation of Fanconi Anemia Genes Implicates PRMT5 Blockage as a Strategy for Tumor Chemosensitization.Molecular cancer research : MCR · 2021Article
- Article
- ConstitutiveCancers · 2019Article
- Analysis of Genomes and Transcriptomes of Hepatocellular Carcinomas Identifies Mutations and Gene Expression Changes in the Transforming Growth Factor-β Pathway.Gastroenterology · 2018Article
- Alcohol, stem cells and cancer.Genes & cancer · 2017Review
- – (-) Menthol Induces Reversal of Promoter Hypermethylation and Associated Up-Regulation of the FANCF Gene in the SiHa Cell LineAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Reduced PAK1 activity sensitizes FA/BRCA-proficient breast cancer cells to PARP inhibition.Oncotarget · 2016Article
- Substantial interindividual and limited intraindividual genomic diversity among tumors from men with metastatic prostate cancer.Nature medicine · 2016Article
- Enamel matrix derivative promote primary human pulp cell differentiation and mineralization.International journal of molecular sciences · 2014Article
- Coregulation of FANCA and BRCA1 in human cells.SpringerPlus · 2014Article
- DNA methyltransferases, DNA damage repair, and cancer.Advances in experimental medicine and biology · 2013Review
- Hepatic stem cells and transforming growth factor β in hepatocellular carcinoma.Nature reviews. Gastroenterology & hepatology · 2012Review
- Inferring the regulatory network behind a gene expression experiment.Nucleic acids research · 2012Article
- Molecular scores to predict ovarian cancer outcomes: a worthy goal, but not ready for prime time.Journal of the National Cancer Institute · 2012Article
- TSN Disrupts Fanconi Anemia Pathway Activation Through JAK/STAT1-Mediated Transcriptional Repression of FA Core Subunits in Bladder Cancer.Dose-response : a publication of International Hormesis SocietyArticle
- Ginsenoside Rh2 Suppresses the Fanconi Anemia Pathway by Inhibiting NF-κB-Mediated FANCL Transcription in Bladder Cancer.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Fanconi anemia (FA) gene family is a recent addition to the complex network of proteins that respond to and repair certain types of DNA damage in the human genome. Since little is known about the regulation of this novel group of genes at the DNA level, we characterized the promoters of the eight genes (FANCA, B, C, E, F, G, L and M) that compose the FA core complex. The promoters of these genes show the characteristic attributes of housekeeping genes, such as a high GC content and CpG islands, a lack of TATA boxes and a low conservation. The promoters functioned in a monodirectional way and were, in their most active regions, comparable in strength to the SV40 promoter in our reporter plasmids. They were also marked by a distinctive transcriptional start site (TSS). In the 5' region of each promoter, we identified a region that was able to negatively regulate the promoter activity in HeLa and HEK 293 cells in isolation. The central and 3' regions of the promoter sequences harbor binding sites for several common and rare transcription factors, including STAT, SMAD, E2F, AP1 and YY1, which indicates that there may be cross-connections to several established regulatory pathways. Electrophoretic mobility shift assays and siRNA experiments confirmed the shared regulatory responses between the prominent members of the TGF-β and JAK/STAT pathways and members of the FA core complex. Although the promoters are not well conserved, they share region and sequence specific regulatory motifs and transcription factor binding sites (TBFs), and we identified a bi-partite nature to these promoters. These results support a hypothesis based on the co-evolution of the FA core complex genes that was expanded to include their promoters.
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.