Replication and homologous recombination repair regulate DNA double-strand break formation by the antitumor alkylator ecteinascidin 743-Reference-Cited by-同舟云学术

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Replication and homologous recombination repair regulate DNA double-strand break formation by the antitumor alkylator ecteinascidin 743

Published:2007-07-26 Issue:32 Volume:104 Page:13062-13067
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Soares D. G.,Escargueil A. E.,Poindessous V.,Sarasin A.,de Gramont A.,Bonatto D.,Henriques J. A. P.,Larsen A. K.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference42 articles.

1. Antiproliferative activity of ecteinascidin 743 is dependent upon transcription-coupled nucleotide-excision repair

2. Unique pattern of ET-743 activity in different cellular systems with defined deficiencies in DNA-repair pathways

3. Ecteinascidin-743 (ET-743), a natural marine compound, with a unique mechanism of action

4. The inefficiency of incisions of ecteinascidin 743–DNA adducts by the UvrABC nuclease and the unique structural feature of the DNA adducts can be used to explain the repair-dependent toxicities of this antitumor agent

5. Anti-tumour compounds illudin S and Irofulven induce DNA lesions ignored by global repair and exclusively processed by transcription- and replication-coupled repair pathways

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