Skip Navigation


Carcinogenesis Advance Access originally published online on February 4, 2004
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
25/6/889    most recent
bgh099v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Habu, T.
Right arrow Articles by Morita, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Habu, T.
Right arrow Articles by Morita, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 25, No. 6, 889-893, June 2004
Carcinogenesis vol.25 no.6 © Oxford University Press 2004; all rights reserved.

ARTICLE

p53 protein interacts specifically with the meiosis-specific mammalian RecA-like protein DMC1 in meiosis

Toshiyuki Habu1,4, Nobunao Wakabayashi1,5, Kayo Yoshida3, Kenntaro Yomogida2, Yoshitake Nishimune2 and Takashi Morita3,6

1 Department of Molecular Embryology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565, Japan, 2 Department of Science for Laboratory Animal Experimentation, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565, Japan and 3 Department of Molecular Genetics, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi, Abeno, Osaka 545-8585, Japan
Present addresses: 4 Radiation Biology Center, Kyoto University, Yoshidakonoe-cho, Sakyou-ku, Kyoto 606-8501, Japan and 5 Johns Hopkins University, Bloomberg School of Public Health, Division of Toxicological Sciences, 615 North Wolfe Street, Room 7032, Baltimore, MD 21205, USA

6 To whom correspondence should be addressed. Email: tmorita{at}med.osaka-cu.ac.jp

The tumor suppressor protein p53 is specifically expressed during meiosis in spermatocytes. Subsets of p53 knockout mice exhibit testicular giant cell degenerative syndrome, which suggests p53 may be associated with meiotic cell cycle and/or DNA metabolism. Here, we show that p53 binds to the mouse meiosis-specific RecA-like protein Mus musculus DMC1 (MmDMC1). The C-terminal domain (amino acid 234–340) of MmDMC1 binds to DNA-binding domain of p53 protein. p53 might be involved in homologous recombination and/or checkpoint function by directly binding to DMC1 protein to repress genomic instability in meiotic germ cells.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Hum ReprodHome page
F. Ghafari, S. Pelengaris, E. Walters, and G.M. Hartshorne
Influence of p53 and genetic background on prenatal oogenesis and oocyte attrition in mice
Hum. Reprod., June 1, 2009; 24(6): 1460 - 1472.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. Sauvageau, A. Z. Stasiak, I. Banville, M. Ploquin, A. Stasiak, and J.-Y. Masson
Fission Yeast Rad51 and Dmc1, Two Efficient DNA Recombinases Forming Helical Nucleoprotein Filaments
Mol. Cell. Biol., June 1, 2005; 25(11): 4377 - 4387.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.