The MAX-interacting transcription factor network

被引:117
作者
Hurlin, Peter J.
Huang, Jie
机构
[1] Oregon Hlth & Sci Univ, Shriners Hosp Children, Portland, OR 97201 USA
[2] Oregon Hlth & Sci Univ, Dept Cell & Dev Biol, Portland, OR 97201 USA
基金
美国国家卫生研究院;
关键词
MAX; MYC; MNT; Mad; MXD;
D O I
10.1016/j.semcancer.2006.07.009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The small bHLHZip protein MAX functions at the center of a transcription factor network that governs many aspects of cell behavior, including cell proliferation and tumorigenesis. MAX serves as a cofactor for DNA binding by the various members of this network, which include the MYC family of oncoproteins and a group of putative MYC antagonists that include MNT, MXD1-4 (formerly MAD1, MXI1, MAD3 and MAD4) and MGA. The many heterodimerization partners of MAX raises questions concerning the dynamics of MAX interactions and the functional consequences of the switching of Max partners. Here we review the activities of MAX, its interaction partners, and recent results showing that tissues lacking the MAX-interacting protein MNT are predisposed to tumor formation. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:265 / 274
页数:10
相关论文
共 112 条
[41]   Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants [J].
Hemann, MT ;
Bric, A ;
Teruya-Feldstein, J ;
Herbst, A ;
Nilsson, JA ;
Cordon-Cardo, C ;
Cleveland, JL ;
Tansey, WP ;
Lowe, SW .
NATURE, 2005, 436 (7052) :807-811
[42]  
Hong SL, 2000, GENE DEV, V14, P17
[43]   Of Myc and Mnt [J].
Hooker, CW ;
Hurlin, PJ .
JOURNAL OF CELL SCIENCE, 2006, 119 (02) :208-216
[44]  
HOPEWELL R, 1995, MOL CELL BIOL, V15, P3470
[45]   Whole-genome analysis reveals a strong positional bias of conserved dMyc-dependent E-boxes [J].
Hulf, T ;
Bellosta, P ;
Furrer, M ;
Steiger, D ;
Svensson, D ;
Barbour, A ;
Gallant, P .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (09) :3401-3410
[46]   Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif [J].
Hurlin, PJ ;
Steingrìmsson, E ;
Copeland, NG ;
Jenkins, NA ;
Eisenman, RN .
EMBO JOURNAL, 1999, 18 (24) :7019-7028
[47]   Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis [J].
Hurlin, PJ ;
Zhou, ZQ ;
Toyo-oka, K ;
Ota, S ;
Walker, WL ;
Hirotsune, S ;
Wynshaw-Boris, A .
EMBO JOURNAL, 2003, 22 (18) :4584-4596
[48]   MAD3 AND MAD4 - NOVEL MAX-INTERACTING TRANSCRIPTIONAL REPRESSORS THAT SUPPRESS C-MYC DEPENDENT TRANSFORMATION AND ARE EXPRESSED DURING NEURAL AND EPIDERMAL DIFFERENTIATION [J].
HURLIN, PJ ;
QUEVA, C ;
KOSKINEN, PJ ;
STEINGRIMSSON, E ;
AYER, DE ;
COPELAND, NG ;
JENKINS, NA ;
EISENMAN, RN .
EMBO JOURNAL, 1995, 14 (22) :5646-5659
[49]   Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating, rating cells and mediates repression at Myc binding sites [J].
Hurlin, PJ ;
Queva, C ;
Eisenman, RN .
GENES & DEVELOPMENT, 1997, 11 (01) :44-58
[50]   MAX - FUNCTIONAL DOMAINS AND INTERACTION WITH C-MYC [J].
KATO, GJ ;
LEE, WMF ;
CHEN, LL ;
DANG, CV .
GENES & DEVELOPMENT, 1992, 6 (01) :81-92