Regulation of cell growth by the Myc-Max-Mad network: role of Mad proteins and YY1

M Austen, C Cerni, M Henriksson, S Hilfenhaus… - C-Myc in B-Cell …, 1997 - Springer
M Austen, C Cerni, M Henriksson, S Hilfenhaus, JM Lüscher-Firzlaff, A Menkel, C Seelos
C-Myc in B-Cell Neoplasia: 14 th Workshop on Mechanisms in B-Cell Neoplasia, 1997Springer
Since the discovery of the c-Myc dimerization partner Max (Blackwood and Eisenman 1991;
Prendergast et al. 1991) a startling number of proteins capable to interact directly or
indirectly with c-Myc and/or Max have been described (for review see Marcu et al. 1992;
Henriksson and Lüscher 1996). It has become evident that at the center of this network lies
Max which on one hand forms heterodimers with the Myc family of proteins, including c-, N-,
and L-Myc and on the other hand heterodimerizes with proteins of the Mad family, including …
Abstract
Since the discovery of the c-Myc dimerization partner Max (Blackwood and Eisenman 1991; Prendergast et al. 1991) a startling number of proteins capable to interact directly or indirectly with c-Myc and/or Max have been described (for review see Marcu et al. 1992; Henriksson and Lüscher 1996). It has become evident that at the center of this network lies Max which on one hand forms heterodimers with the Myc family of proteins, including c-, N-, and L-Myc and on the other hand heterodimerizes with proteins of the Mad family, including Mad1, Mxi1 (or Mad2), Mad3, and Mad4. In addition Max has also the ability to form homodimers. Thus Max is the true center of this array of proteins which we will refer to as the Myc/Max/Mad network.
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