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p14ARF interacts with E2F factors to form p14ARF–E2F/partner‐DNA complexes repressing E2F‐dependent transcription
Author(s) -
Zhang HaiJun,
Li WenJuan,
Gu YanYan,
Li ShuYan,
An GuoShun,
Ni JuHua,
Jia HongTi
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22446
Subject(s) - p14arf , e2f , transcription factor , e2f1 , microbiology and biotechnology , transcription (linguistics) , biology , cancer research , tumor suppressor gene , gene , chemistry , genetics , carcinogenesis , linguistics , philosophy
Primarily, E2F factors such as E2F1, ‐2, and ‐3 stimulate cell‐cycle progression, while ARF tumor suppressor mediates growth suppression. The ARF gene can be induced by oncogenic signal through activating E2F‐dependent transcription. In turn, ARF may target E2F for its degradation via a p53‐dependent mechanism. However, it remains unclear how the cell keeps the balance between the functional opposites of E2F and ARF. In this study, we demonstrate that p14ARF interacts with E2F1–3 factors to directly repress their transcriptional activities through forming p14ARF–E2F/partner‐DNA super complexes, regardless of E2F protein degradation. The inhibition of E2F transcriptional activities by p14ARF in this manner occurs commonly in a variety of cell types, including p53‐deficient and p53‐wild type cells. Thus, E2F‐mediated activation of the ARF gene and ARF‐mediated functional inhibition of E2F compose a feedback loop, by which the two opposites act in concert to regulate cell proliferation and apoptosis, depending on the cellular context and the environment. J. Cell. Biochem. 109: 693–701, 2010. © 2010 Wiley‐Liss, Inc.