ArticleThe Journal of biological chemistry2009
The fanconi anemia core complex acts as a transcriptional co-regulator in hairy enhancer of split 1 signaling.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Fanconi anemia pathway regulation by FANCI in prostate cancer.Frontiers in oncology · 2023Article
- FANCD2 and HES1 suppress inflammation-induced PPARɣ to prevent haematopoietic stem cell exhaustion.British journal of haematology · 2021Article
- Fanconi anemia pathway as a prospective target for cancer intervention.Cell & bioscience · 2020Review
- Fanconi anemia core complex-dependent HES1 mono-ubiquitination regulates its transcriptional activity.BMC research notes · 2018Article
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- Inflammation-mediated notch signaling skews fanconi anemia hematopoietic stem cell differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Fanconi anemia complementation group A (FANCA) protein has intrinsic affinity for nucleic acids with preference for single-stranded forms.The Journal of biological chemistry · 2012Article
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- Ubiquitin signalling in DNA replication and repair.Nature reviews. Molecular cell biology · 2010Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in one of the 13 Fanconi anemia (FA) genes cause a progressive bone marrow failure disorder associated with developmental abnormalities and a predisposition to cancer. Although FA has been defined as a DNA repair disease based on the hypersensitivity of patient cells to DNA cross-linking agents, FA patients develop various developmental defects such as skeletal abnormalities, microphthalmia, and endocrine abnormalities that may be linked to transcriptional defects. Recently, we reported that the FA core complex interacts with the transcriptional repressor Hairy Enhancer of Split 1 (HES1) suggesting that the core complex plays a role in transcription. Here we show that the FA core complex contributes to transcriptional regulation of HES1-responsive genes, including HES1 and the cyclin-dependent kinase inhibitor p21(cip1/waf1). Chromatin immunoprecipitation studies show that the FA core complex interacts with the HES1 promoter but not the p21(cip1/waf1) promoter. Furthermore, we show that the FA core complex interferes with HES1 binding to the co-repressor transducin-like-Enhancer of Split, suggesting that the core complex affects transcription both directly and indirectly. Taken together these data suggest a novel function of the FA core complex in transcriptional regulation.
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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.