Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway
| Autor: | Chih-Chao Liang, Martin A. Cohn, David Lopez-Martinez |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Genome instability Genomic instability DNA Replication Models Molecular DNA Repair DNA repair DNA damage Review Biology 03 medical and health sciences Cellular and Molecular Neuroscience DNA Adducts Fanconi anemia FANCD2 medicine FANCI Animals Humans Phosphorylation UHRF1 Mitotic catastrophe Molecular Biology Pharmacology DNA replication Ubiquitination Cell Biology DNA medicine.disease Fanconi Anemia Complementation Group Proteins Intercalating Agents Cell biology 030104 developmental biology Cross-Linking Reagents Biochemistry SUMO Molecular Medicine Chromosome breakage Protein Processing Post-Translational DNA Damage Signal Transduction |
| Zdroj: | Cellular and Molecular Life Sciences |
| ISSN: | 1420-9071 1420-682X |
| Popis: | Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss the origin of ICLs, comparing various endogenous and exogenous sources. Second, we will describe FA proteins as well as FA-related proteins involved in ICL repair, and the post-translational modifications that regulate these proteins. Finally, we will review the process of how ICLs are repaired by both replication-dependent and replication-independent mechanisms. |
| Databáze: | OpenAIRE |
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