Suppression of cell cycle progression by Jun dimerization protein (JDP2) involves down-regulation of cyclin A2
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- Institute of Animal Husbandry and Veterinary, Zhejiang Academy of Agricultural Sciences, Animal Molecular Biotechnology Laboratory
- RIKEN BRC, Gene Engineering Division
- Graduate School of Pharmaceutical Sciences, Chiba University, Department of Molecular Cell Biology
- KMU, Gradiate Institute of Medicine
- RIKEN BRC, Experimental Animal Division
- Chiba University
- RIKEN BRC, President
- Kaohsiung Medical University, Graduate Institute of Medicine
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- Document Type:
- Manuscript
- Date:
- Received 08 October 2009 07:50 UTC; Posted 08 October 2009
- Subjects:
- Cancer
- Abstract:
We report here a novel role for Jun dimerization protein-2 (JDP2) as a regulator of the progression of normal cells through the cell cycle. To determine the role of JDP2 in vivo, we generated Jdp2 knock-out (Jdp2KO) mice by targeting exon 1 to disrupt the site of initiation of transcription. The healing of wounded skin of Jdp2KO mice proceeded more rapidly than that of control mice and more proliferating cells were found at wound margins. Fibroblasts derived from embryos of Jdp2KO mice proliferated more rapidly and formed more colonies than wild-type fibroblasts. JDP2 was recruited to the promoter of the gene for cyclin A2 (ccna2) at a previously unidentified AP-1 site. Cells lacking Jdp2 had elevated levels of cyclin A2 mRNA. Moreover, reintroduction of JDP2 resulted in repression of transcription of ccna2 and of cell cycle progression. Thus, transcription of the gene for cyclin A2 appears to be a direct target of JDP2 in the suppression of cell proliferation.
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- This document is licensed to the public under the Creative Commons Attribution 3.0 License
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Pan, Jianzhi, Nakade, Koji, Masuzaki, Satoko, Hasegawa, Hitomi, Huang, Yu-Chang, Murata, Takehide, Yoshiki, Atsushi, Yamaguchi, Naoto, Obata, Yuichi, and Yokoyama, Kazunari. Suppression of cell cycle progression by Jun dimerization protein (JDP2) involves down-regulation of cyclin A2. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2009.3840.1> (2009)
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