The Fanconi Anemia Pathway in Replication Stress and DNA Crosslink Repair

Overview

Journal Cell Mol Life Sci

Publisher Springer

Specialty Biology

Date 2012 Jun 30

PMID 22744751

Citations 12

Authors

Mathew J K Jones

Tony T Huang

Affiliations

Soon will be listed here.

Abstract

Interstand crosslinks (ICLs) are DNA lesions where the bases of opposing DNA strands are covalently linked, inhibiting critical cellular processes such as transcription and replication. Chemical agents that generate ICLs cause chromosomal abnormalities including breaks, deletions and rearrangements, making them highly genotoxic compounds. This toxicity has proven useful for chemotherapeutic treatment against a wide variety of cancer types. The majority of our understanding of ICL repair in humans has been uncovered through analysis of the rare genetic disorder Fanconi anemia, in which patients are extremely sensitive to crosslinking agents. Here, we discuss recent insights into ICL repair gained using new repair assays and highlight the role of the Fanconi anemia repair pathway during replication stress.

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