Abstract:
:The ARF tumor suppressor is a product of the INK4a/ARF locus, which is frequently mutated in human cancer. The expression of ARF is up-regulated in response to certain types of DNA damage, oncogene activation, and interferon stimuli. Through interaction with the p53 negative regulator MDM2, ARF controls a well-described p53/MDM2-dependent checkpoint. However, the mechanism of ARF induction is poorly understood. Using a yeast two-hybrid screen, we identify a novel ARF-interacting protein, N-Myc and STATs interactor (NMI). Previously, NMI was known to be a c-Myc-interacting protein. Here we demonstrate that through competitive binding to the ARF ubiquitin E3 ligase (ubiquitin ligase for ARF [ULF]), NMI protects ARF from ULF-mediated ubiquitin degradation. In response to cellular stresses, NMI is induced, and a fraction of NMI is translocated to the nucleus to stabilize ARF. Thus our work reveals a novel NMI-mediated, transcription-independent ARF induction pathway in response to cellular stresses.
journal_name
Mol Biol Celljournal_title
Molecular biology of the cellauthors
Li Z,Hou J,Sun L,Wen T,Wang L,Zhao X,Xie Q,Zhang SQdoi
10.1091/mbc.E12-04-0304subject
Has Abstractpub_date
2012-12-01 00:00:00pages
4635-46issue
23eissn
1059-1524issn
1939-4586pii
mbc.E12-04-0304journal_volume
23pub_type
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