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Cited by 234

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation

Open access
Sun, Yingli, Jiang, Xiaofeng, Chen, Shujuan, Price, Brendan D.·2006·FEBS Letters

Abstract

Histone acetyltransferases (HATs) regulate transcription, chromatin structure and DNA repair. Here, we utilized a novel HAT inhibitor, anacardic acid, to examine the role of HATs in the DNA damage response. Anacardic acid inhibits the Tip60 HAT in vitro, and blocks the Tip60‐dependent activation of the ATM and DNA–PKcs protein kinases by DNA damage in vivo. Further, anacardic acid sensitizes human tumor cells to the cytotoxic effects of ionizing radiation. These results demonstrate a central role for HATs such as Tip60 in regulating the DNA damage response. HAT inhibitors provide a novel therapeutic approach for increasing the sensitivity of tumors to radiation therapy.

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Metadata

Authors
Sun, Y., Jiang, X., Chen, S., & Price, B. D.
Venue
FEBS Letters
Publisher
Wiley
Published
2006-07-10
Volume
580
Issue
18
Pages
4353-4356
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2143716699
Cited by
234
References
2
FWCI
3.07
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation. https://app.cochat.ai/papers/10.1016/j.febslet.2006.06.092
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Sun, Y., Jiang, X., Chen, S., & Price, B. D. (2006). Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation. FEBS Letters. https://doi.org/10.1016/j.febslet.2006.06.092

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.