PIAS3 promotes homology‑directed repair and distal non‑homologous end joining

  • Authors:
    • Shicui Liu
    • Zhongyi Fan
    • Zhengying Geng
    • Hao Zhang
    • Qinong Ye
    • Shunchang Jiao
    • Xiaojie Xu
  • View Affiliations

  • Published online on: July 17, 2013     https://doi.org/10.3892/ol.2013.1472
  • Pages: 1045-1048
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Abstract

A DNA double‑strand break (DSB) is the most severe form of DNA damage and is mainly repaired through homologous recombination (HR), which has a high fidelity, or non‑homologous end joining (NHEJ), which is prone to errors. Defects in the DNA damage response lead to genomic instability and ultimately the predisposition of organs to cancer. Protein inhibitor of activated STAT‑1 (PIAS1), which is a potential small ubiquitin‑related modifier (SUMO) ligase, has been reported to be involved in DSB repair. The present study identified that another member of the PIAS family, PIAS3, is also an enhancer for HR‑ and NHEJ‑mediated DSB repair. Furthermore, the overexpression of PIAS3 was demonstrated to increase the resistance of HeLa cells to ionizing radiation (IR), indicating a significant role for PIAS3 in the DNA damage response (DDR) pathway.
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October 2013
Volume 6 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Copy and paste a formatted citation
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Spandidos Publications style
Liu S, Fan Z, Geng Z, Zhang H, Ye Q, Jiao S and Xu X: PIAS3 promotes homology‑directed repair and distal non‑homologous end joining. Oncol Lett 6: 1045-1048, 2013
APA
Liu, S., Fan, Z., Geng, Z., Zhang, H., Ye, Q., Jiao, S., & Xu, X. (2013). PIAS3 promotes homology‑directed repair and distal non‑homologous end joining. Oncology Letters, 6, 1045-1048. https://doi.org/10.3892/ol.2013.1472
MLA
Liu, S., Fan, Z., Geng, Z., Zhang, H., Ye, Q., Jiao, S., Xu, X."PIAS3 promotes homology‑directed repair and distal non‑homologous end joining". Oncology Letters 6.4 (2013): 1045-1048.
Chicago
Liu, S., Fan, Z., Geng, Z., Zhang, H., Ye, Q., Jiao, S., Xu, X."PIAS3 promotes homology‑directed repair and distal non‑homologous end joining". Oncology Letters 6, no. 4 (2013): 1045-1048. https://doi.org/10.3892/ol.2013.1472