The interplay between Mad and Myc in proliferation and differentiation

被引:53
作者
Zhou, ZQ
Hurlin, PJ
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
关键词
D O I
10.1016/S0962-8924(01)82037-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Members of the Myc family of transcription factors are key regulators of cell proliferation, and excessive levels of Myc lead to tumor formation. Mad family proteins are related to Myc, but they antagonize the oncogenic activity of Myc in cell-culture assays. Here, we examine current models of Mad function and the relationship between Mad and Myc in cell proliferation, differentiation and tumorigenesis.
引用
收藏
页码:S10 / S14
页数:5
相关论文
共 31 条
[1]   Function of the c-Myc oncoprotein in chromatin remodeling and transcription [J].
Amati, B ;
Frank, SR ;
Donjerkovic, D ;
Taubert, S .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 2001, 1471 (03) :M135-M145
[2]   The Max network gone mad [J].
Baudino, TA ;
Cleveland, JL .
MOLECULAR AND CELLULAR BIOLOGY, 2001, 21 (03) :691-702
[3]   Mix, a novel max-like BHLHZip protein that interacts with the max network of transcription factors [J].
Billin, AN ;
Eilers, AL ;
Queva, C ;
Ayer, DE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (51) :36344-36350
[4]   MondoA, a novel basic helix-loop-helix-leucine zipper transcriptional activator that constitutes a positive branch of a Max-like network [J].
Billin, AN ;
Eilers, AL ;
Coulter, KL ;
Logan, JS ;
Ayer, DE .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (23) :8845-8854
[5]   c-MYC interacts with INI1/hSNF5 and requires the SWI/SNF complex for transactivation function [J].
Cheng, SWG ;
Davies, KP ;
Yung, E ;
Beltran, RJ ;
Yu, J ;
Kalpana, GV .
NATURE GENETICS, 1999, 22 (01) :102-105
[6]   A role for transcriptional repression of p21CIP1 by c-Myc in overcoming transforming growth factor β-induced cell-cycle arrest [J].
Claassen, GF ;
Hann, SR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (17) :9498-9503
[7]   Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis [J].
Eischen, CM ;
Weber, JD ;
Roussel, MF ;
Sherr, CJ ;
Cleveland, JL .
GENES & DEVELOPMENT, 1999, 13 (20) :2658-2669
[8]   Two MAD tails:: what the recent knockouts of Madl and Mxil tell us about the MYC/MAX/MAD network [J].
Foley, KP ;
Eisenman, RN .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1999, 1423 (03) :M37-M47
[9]   Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation [J].
Foley, KP ;
McArthur, GA ;
Quéva, C ;
Hurlin, PJ ;
Soriano, P ;
Eisenman, RN .
EMBO JOURNAL, 1998, 17 (03) :774-785
[10]   The Myc/Max/Mad network and the transcriptional control of cell behavior [J].
Grandori, C ;
Cowley, SM ;
James, LP ;
Eisenman, RN .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 2000, 16 :653-699