Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: ATDC/TRIM29 phosphorylation by ATM/MAPKAP kinase 2 mediates radioresistance in pancreatic cancer cells.

Authors: Wang, Lidong; Yang, Huibin; Palmbos, Phillip L; Ney, Gina; Detzler, Taylor Ann; Coleman, Dawn; Leflein, Jacob; Davis, Mary; Zhang, Min; Tang, Wenhua; Hicks, J Kevin; Helchowski, Corey M; Prasad, Jayendra; Lawrence, Theodore S; Xu, Liang; Yu, Xiaochun; Canman, Christine E; Ljungman, Mats; Simeone, Diane M

Published In Cancer Res, (2014 Mar 15)

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by therapeutic resistance for which the basis is poorly understood. Here, we report that the DNA and p53-binding protein ATDC/TRIM29, which is highly expressed in PDAC, plays a critical role in DNA damage signaling and radioresistance in pancreatic cancer cells. Ataxia-telangiectasia group D-associated gene (ATDC) mediated resistance to ionizing radiation in vitro and in vivo in mouse xenograft assays. ATDC was phosphorylated directly by MAPKAP kinase 2 (MK2) at Ser550 in an ATM-dependent manner. Phosphorylation at Ser-550 by MK2 was required for the radioprotective function of ATDC. Our results identify a DNA repair pathway leading from MK2 and ATM to ATDC, suggesting its candidacy as a therapeutic target to radiosensitize PDAC and improve the efficacy of DNA-damaging treatment.

PubMed ID: 24469230 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

Back
to Top