Involvement of human MOF in ATM function

Gupta, Arun, Sharma, Girdhar G., Young, Charles S. H., Agarwal, Manjula, Smith, Edwin R., Paull, Tanya T., Lucchesi, John C., Khanna, Kum Kum, Ludwig, Thomas and Pandita, Tej K. (2005) Involvement of human MOF in ATM function. Molecular and Cellular Biology, 25 12: 5292-5305. doi:10.1128/MCB.25.12.5292-5305.2005

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ192650_OA.pdf Full text (open access) application/pdf 782.59KB 0

Author Gupta, Arun
Sharma, Girdhar G.
Young, Charles S. H.
Agarwal, Manjula
Smith, Edwin R.
Paull, Tanya T.
Lucchesi, John C.
Khanna, Kum Kum
Ludwig, Thomas
Pandita, Tej K.
Title Involvement of human MOF in ATM function
Journal name Molecular and Cellular Biology   Check publisher's open access policy
ISSN 0270-7306
Publication date 2005-06
Sub-type Article (original research)
DOI 10.1128/MCB.25.12.5292-5305.2005
Open Access Status File (Publisher version)
Volume 25
Issue 12
Start page 5292
End page 5305
Total pages 14
Place of publication Washington, DC, United States
Publisher American Society of Microbiology
Language eng
Abstract We have determined that hMOF, the human ortholog of the Drosophila MOF gene (males absent on the first), encoding a protein with histone acetyltransferase activity, interacts with the ATM (ataxia-telangiectasia-mutated) protein. Cellular exposure to ionizing radiation (IR) enhances hMOF-dependent acetylation of its target substrate, lysine 16 (K16) of histone H4 independently of ATM function. Blocking the IR-induced increase in acetylation of histone H4 at K16, either by the expression of a dominant negative mutant {Delta}hMOF or by RNA interference-mediated hMOF knockdown, resulted in decreased ATM autophosphorylation, ATM kinase activity, and the phosphorylation of downstream effectors of ATM and DNA repair while increasing cell killing. In addition, decreased hMOF activity was associated with loss of the cell cycle checkpoint response to DNA double-strand breaks. The overexpression of wild-type hMOF yielded the opposite results, i.e., a modest increase in cell survival and enhanced DNA repair after IR exposure. These results suggest that hMOF influences the function of ATM.
Keyword Atm
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 135 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 140 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Thu, 14 Jan 2010, 14:51:48 EST by Ms May Balasaize on behalf of Faculty Of Health Sciences