ArticleMolecular genetics and metabolism
ERCC1 is required for FANCD2 focus formation.
Article in Molecular genetics and metabolism. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Fanconi anemia-associated chromosomal radial formation is dependent on POLθ-mediated alternative end joining.Cell reports · 2023Article
- Transcription-Replication Collisions-A Series of Unfortunate Events.Biomolecules · 2021Review
- A novel role for non-ubiquitinated FANCD2 in response to hydroxyurea-induced DNA damage.Oncogene · 2016Article
- Advances in understanding the complex mechanisms of DNA interstrand cross-link repair.Cold Spring Harbor perspectives in biology · 2013Review
- Loss of ercc1 results in a time- and dose-dependent reduction of proliferating early hematopoietic progenitors.Anemia · 2012Article
- Using synthetic DNA interstrand crosslinks to elucidate repair pathways and identify new therapeutic targets for cancer chemotherapy.Cellular and molecular life sciences : CMLS · 2010Review
- Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle.Environmental and molecular mutagenesis · 2010Review
- DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010Review
- XPF-ERCC1 participates in the Fanconi anemia pathway of cross-link repair.Molecular and cellular biology · 2009Article
- DNA interstrand crosslink repair in mammalian cells.Journal of cellular physiology · 2009Review
- Cellular and molecular consequences of defective Fanconi anemia proteins in replication-coupled DNA repair: mechanistic insights.Mutation research · 2009Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The rare genetic disorder Fanconi anemia, caused by a deficiency in any of at least thirteen identified genes, is characterized by cellular sensitivity to DNA interstrand crosslinks and genome instability. The excision repair cross complementing protein, ERCC1, first identified as a participant in nucleotide excision repair, appears to also act in crosslink repair, possibly in incision and at a later stage. We have investigated the relationship of ERCC1 to the Fanconi anemia pathway, using depletion of ERCC1 by siRNA in transformed normal human fibroblasts and fibroblasts from Fanconi anemia patients. We find that depletion of ERCC1 does not hinder formation of double strand breaks in crosslink repair as indexed by gammaH2AX. However, the monoubiquitination of FANCD2 protein in response to MMC treatment is decreased and the localization of FANCD2 to nuclear foci is eliminated. Arrest of DNA replication by hydroxyurea, producing double strand breaks without crosslinks, also requires ERRC1 for FANCD2 localization to nuclear foci. Our results support a role for ERCC1 after creation of a double strand break for full activation of the Fanconi anemia pathway.
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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.