Abstract:
:The ARF tumour suppressor protein plays a critical role in the activation of p53 in response to oncogenic stress. ARF can activate p53 through nucleolar sequestration of Mdm2. However, several lines of evidence indicate that this is not the only way of action of ARF, and alternative mechanisms must exist. p33ING1 is a putative tumour suppresor, which induces cell-cycle arrest and apoptosis in a p53-dependent manner. Here, we describe that ARF and p33ING1 can interact in vivo. We also show that the subcellular localization of ING1 can be modulated by ARF protein levels, causing a displacement from nuclear to nucleolar localization. Finally, the ability of p33ING1 to cause cell-cycle arrest and induction of p21CIP1, or Mdm2, is impaired in ARF-deficient primary mouse fibroblasts. Based on these observations, we propose that the interaction with p33ING1 represents a novel mechanism for the tumour suppression function of ARF.
journal_name
Oncogenejournal_title
Oncogeneauthors
González L,Freije JM,Cal S,López-Otín C,Serrano M,Palmero Idoi
10.1038/sj.onc.1209526subject
Has Abstractpub_date
2006-08-24 00:00:00pages
5173-9issue
37eissn
0950-9232issn
1476-5594pii
1209526journal_volume
25pub_type
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