![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
RESEARCH COMMUNICATION
1 Dana-Farber Cancer Institute, 2 Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA; 3 UPR9079 CNRS-Ligue Nationale Contre le Cancer, 94800 Villejuif, France; 4 Norris Cotton Cancer Center and Department of Pharmacology and Toxicology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA; 5 Graduate School of Frontier Biosciences, Osaka University, and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Suita, Osaka 565-0871, Japan; 6 Laboratory of Genetic Instability and Cancer, CNRS UPR2169, Institut Gustave Roussy, Villejuif 94805, France
Mutations in the CSA or CSB complementation genes cause the Cockayne syndrome, a severe genetic disorder that results in patients’ death in early adulthood. CSA and CSB act in a transcription-coupled repair (TCR) pathway, but their functional relationship is not understood. We have previously shown that CSA is a subunit of an E3 ubiquitin ligase complex. Here we demonstrate that CSB is a substrate of this ligase: Following UV irradiation, CSB is degraded at a late stage of the repair process in a proteasome- and CSA-dependent manner. Moreover, we demonstrate the importance of CSB degradation for post-TCR recovery of transcription and for the Cockayne syndrome. Our results unravel for the first time the functional relationship between CSA and CSB.
[Keywords: CSB; CSA; ubiquitin–proteasomal degradation]
Received December 30, 2005; revised version accepted March 27, 2006.
E-MAIL groisman{at}vjf.cnrs.fr; FAX 33-1-49583307.
Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.378206
CiteULike 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. M. Kim, Y. Kee, A. Gurtan, and A. D. D'Andrea Cell cycle-dependent chromatin loading of the Fanconi anemia core complex by FANCM/FAAP24 Blood, May 15, 2008; 111(10): 5215 - 5222. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Mirkin, D. Fonseca, S. Mohammed, M. A. Cevher, J. L. Manley, and F. E. Kleiman The 3' processing factor CstF functions in the DNA repair response Nucleic Acids Res., April 1, 2008; 36(6): 1792 - 1804. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. B. Salmon, M. Ljungman, and R. A. Miller Cells From Long-Lived Mutant Mice Exhibit Enhanced Repair of Ultraviolet Lesions J. Gerontol. A Biol. Sci. Med. Sci., March 1, 2008; 63(3): 219 - 231. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. DeHart and V. Planelles Human Immunodeficiency Virus Type 1 Vpr Links Proteasomal Degradation and Checkpoint Activation J. Virol., February 1, 2008; 82(3): 1066 - 1072. [Full Text] [PDF]
|
|
|
|
 |
|
 I. Kuraoka, S. Ito, T. Wada, M. Hayashida, L. Lee, M. Saijo, Y. Nakatsu, M. Matsumoto, T. Matsunaga, H. Handa, et al. Isolation of XAB2 Complex Involved in Pre-mRNA Splicing, Transcription, and Transcription-coupled Repair J. Biol. Chem., January 11, 2008; 283(2): 940 - 950. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Dreher and J. Callis Ubiquitin, Hormones and Biotic Stress in Plants Ann. Bot., May 1, 2007; 99(5): 787 - 822. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Cang, J. Zhang, S. A. Nicholas, A. L. Kim, P. Zhou, and S. P. Goff DDB1 is essential for genomic stability in developing epidermis PNAS, February 20, 2007; 104(8): 2733 - 2737. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Kim and E. T. Kipreos The Caenorhabditis elegans Replication Licensing Factor CDT-1 Is Targeted for Degradation by the CUL-4/DDB-1 Complex Mol. Cell. Biol., February 15, 2007; 27(4): 1394 - 1406. [Abstract] [Full Text] [PDF]
|
|
