spacer gif spacer gif spacer gif spacer gif Propose a workshop for 2011 spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search    

The fully linked HTML version of this article has now been published.
JCS ePress online publication date 12 Aug 2003
doi: 10.1242/jcs.00714

This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jcs.00714v1
116/19/3917    most recent
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kurki, S.
Right arrow Articles by Laiho, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kurki, S.
Right arrow Articles by Laiho, M.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Research Article

Cellular stress and DNA damage invoke temporally distinct Mdm2, p53 and PML complexes and damage-specific nuclear relocalization


Sari Kurki, Leena Latonen, and Marikki Laiho*
* Author for correspondence (e-mail: marikki.laiho{at}helsinki.fi)

Mdm2 is a nucleoplasmic and nucleolar protein interacting with p53 and alternative reading frame (ARF) tumor suppressor proteins. Here we demonstrate relocalization and novel interactions of Mdm2 with the promyelocytic leukemia (PML) protein following cellular stress and DNA damage. We show that Mdm2 and PML interact directly in vivo and in vitro depending on the Mdm2 RING finger domain and the PML C-terminus, and that Mdm2 is recruited to the PML nuclear bodies by overexpression of PML. Cellular stress and DNA damage caused by UV-radiation, downregulation of the proteasome and arsenic trioxide promoted Mdm2 and PML damage-specific nuclear relocalization and interaction in a p53-independent manner. However, in vitro analyses showed that PML, Mdm2 and p53 form trimeric complexes. UV-radiation caused rapid rearrangements of PML nuclear bodies and promoted PML-p53 and PML-Mdm2 complex formation, coinciding with p53 stabilization and preceding p53-Mdm2 interaction suggesting temporally distinct complexes. The results demonstrate novel associations between Mdm2 and PML and show the capacity of PML to participate in the activation and stabilization of p53 in response to cellular stress through PML interaction with Mdm2.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 JCBHome page
M. Cioce, S. Boulon, A. G. Matera, and A. I. Lamond
UV-induced fragmentation of Cajal bodies
J. Cell Biol., November 6, 2006; 175(3): 401 - 413.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
W. Oh, E.-W. Lee, Y. H. Sung, M.-R. Yang, J. Ghim, H.-W. Lee, and J. Song
Jab1 Induces the Cytoplasmic Localization and Degradation of p53 in Coordination with Hdm2
J. Biol. Chem., June 23, 2006; 281(25): 17457 - 17465.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
R. D. Everett and J. Murray
ND10 Components Relocate to Sites Associated with Herpes Simplex Virus Type 1 Nucleoprotein Complexes during Virus Infection
J. Virol., April 15, 2005; 79(8): 5078 - 5089.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
R. W. Ching, G. Dellaire, C. H. Eskiw, and D. P. Bazett-Jones
PML bodies: a meeting place for genomic loci?
J. Cell Sci., March 1, 2005; 118(5): 847 - 854.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
P. Lunghi, A. Costanzo, M. Levrero, and A. Bonati
Treatment with arsenic trioxide (ATO) and MEK1 inhibitor activates the p73-p53AIP1 apoptotic pathway in leukemia cells
Blood, July 15, 2004; 104(2): 519 - 525.
[Abstract] [Full Text] [PDF]


© The Company of Biologists Ltd 2003