ArticleProceedings of the National Academy of Sciences of the United States of America2014
The Fanconi anemia pathway has a dual function in Dickkopf-1 transcriptional repression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Fanconi anemia pathway as a prospective target for cancer intervention.Cell & bioscience · 2020Review
- Comparative genomics provides new insights into the remarkable adaptations of the African wild dog (Lycaon pictus).Scientific reports · 2019Article
- Lipidomic Profiling Links the Fanconi Anemia Pathway to Glycosphingolipid Metabolism in Head and Neck Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Genomic analysis of synchronous intracranial meningiomas with different histological grades.Journal of neuro-oncology · 2018Article
- Recent advances in understanding hematopoiesis in Fanconi Anemia.F1000Research · 2018Review
- Wnt signaling in triple-negative breast cancer.Oncogenesis · 2017Review
- The mTOR Complex Controls HIV Latency.Cell host & microbe · 2016Article
- Article
- Review
- Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt Signaling Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair.Nucleic acids research · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is an inherited bone marrow failure syndrome associated with a progressive decline in hematopoietic stem cells, developmental defects, and predisposition to cancer. These various phenotypic features imply a role of FA proteins in molecular events regulating cellular homeostasis. Interestingly, we previously found that the Fanconi C protein (FANCC) interacts with the C-terminal-binding protein-1 (CtBP1) involved in transcriptional regulation. Here we report that FANCC with CtBP1 forms a complex with β-catenin, and that β-catenin activation through glycogen synthase kinase 3β inhibition leads to FANCC nuclear accumulation and FA pathway activation, as measured by the Fanconi D2 protein (FANCD2) monoubiquitination. β-catenin and FANCC nuclear entry is defective in FA mutant cells and in cells depleted of the Fanconi A protein or FANCD2, suggesting that integrity of the FA pathway is required for FANCC nuclear activity. We also report that FANCC with CtBP1 acts as a negative regulator of Dickkopf-1 (DKK1) expression, and that a FA disease-causing mutation in FANCC abrogates this function. Our findings reveal that a defective FA pathway leads to up-regulation of DKK1, a molecule involved in hematopoietic malignancies.
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