Mouse dead end 1-β interacts with c-Jun and stimulates activator protein 1 transactivation

Zhang,Yong; Su,Yan-Lin; Li,Le-Sai; Yang,Zhi; Chen,Si; Xiong,Jie; Fu,Xiao-Hua; Peng,Xiao-Ning

doi:10.3892/mmr.2014.2950

Mouse dead end 1-β interacts with c-Jun and stimulates activator protein 1 transactivation

Authors:
- Yong Zhang
- Yan-Lin Su
- Le-Sai Li
- Zhi Yang
- Si Chen
- Jie Xiong
- Xiao-Hua Fu
- Xiao-Ning Peng
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Affiliations: Department of Internal Medicine, College of Medicine, Hunan Normal University, Changsha, Hunan 410013, P.R. China, Department of Gynecologic Oncology, Cancer Hospital of Xiangya School of Medicine of Central South University, Changsha, Hunan 410013, P.R. China
Published online on: November 14, 2014 https://doi.org/10.3892/mmr.2014.2950
Pages: 1701-1707
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Dead end 1 (Dnd1), important for maintaining the viability of primordial germ cells, is the first protein containing an RNA recognition motif that has been directly implicated as a heritable cause of spontaneous tumorigenesis. In the present study, c-Jun was identified through yeast two-hybrid screening of a 10.5-day old mouse embryo cDNA library as one of the proteins which interact with dnd1-β. The interaction between Dnd1-β and c-Jun was demonstrated to occur by glutathione S‑transferase pull‑down and co-immunoprecipitation. Using confocal microscopy, Dnd1-β was found to be specifically expressed in GC-1 spermatogonia cells, mainly in the nuclei. When transfected into GC-1 cells, Dnd1-β and c-Jun were demonstrated to be co-localized principally in the nuclei. Furthermore, in a dual luciferase reporter assay, the transcriptional activity of activator protein 1 was demonstrated to be significantly increased by co-transfection with Dnd1-β and c-Jun plasmids in GC-1 cells. The identification and confirmation of an additional protein interacting with dnd1-β facilitates the investigation of the functions and molecular mechanisms of Dnd1.

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