An HDAC1-binding domain within FATS bridges p21 turnover to radiation-induced tumorigenesis-Reference-Cited by-同舟云学术

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An HDAC1-binding domain within FATS bridges p21 turnover to radiation-induced tumorigenesis

Published:2010-02-15 Issue:18 Volume:29 Page:2659-2671
ISSN:0950-9232
Container-title:Oncogene
language:en
Short-container-title:Oncogene

Author:

Li Z,Zhang Q,Mao J-H,Weise A,Mrasek K,Fan X,Zhang X,Liehr T,Lu K H,Balmain A,Cai W-W

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Molecular Biology

Link

http://www.nature.com/articles/onc201019.pdf

Reference58 articles.

1. Abbas T, Dutta A . (2009). p21 in cancer: intricate networks and multiple activities. Nat Rev Cancer 9: 400–414.

2. Barboza JA, Liu G, Ju Z, El-Naggar AK, Lozano G . (2006). p21 delays tumor onset by preservation of chromosomal stability. Proc Natl Acad Sci USA 103: 19842–19847.

3. Bendiennat M, Boulaire J, Jascur T, Brickner H, Barbier V, Sarasin A et al. (2003). UV irradiation triggers ubiquitin-dependent degradation of p21(WAF1) to promoter DNA repair. Cell 114: 599–610.

4. Bichara M, Wagner J, Lambert IB . (2006). Mechanisms of tandem repeat instability in bacteria. Mut Res 598: 144–163.

5. Bloom J, Amador V, Bartolini F, DeMartino G, Pagano M . (2003). Proteasome-mediated degradation of p21via N-terminal ubiquitinylation. Cell 115: 71–82.

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