Aj. Wagner et al., EXPRESSION, REGULATION, AND CHROMOSOMAL LOCALIZATION OF THE MAX GENE, Proceedings of the National Academy of Sciences of the United Statesof America, 89(7), 1992, pp. 3111-3115
The Max gene encodes a protein that interacts specifically with the My
c protein to form a heterodimer with high affinity for the specific co
gnate DNA binding site of Myc. Here we examine the expression of Max R
NA in comparison to Myc RNA during cell growth and differentiation. Tw
o species of RNA, a major 2.0- and a minor 1.7-kilobase species, hybri
dized specifically to a Max cDNA probe in all human and murine cell li
nes that were tested. Unlike Myc, the steady-state level of Max RNA is
not significantly modulated with respect to proliferation or differen
tiation. Max RNA is expressed in quiescent BALB/c 3T3 cells and is mod
estly increased 3 h after addition of serum to the quiescent cells. In
contrast to Myc RNA, Max RNA does not decline immediately upon induct
ion of differentiation of HL60 cells by dimethyl sulfoxide, and only a
modest decrease of Max RNA was observed 72 h after induction of diffe
rentiation. Unlike Myc RNA, Max RNA is relatively stable with a half-l
ife of > 3 h and, therefore, does not exhibit the characteristic short
half-life of RNAs encoded by most immediate early genes. The human Ma
x gene was localized to chromosome 14, band q23. With respect to the r
ecurring abnormalities in human tumors, this region of chromosome 14 i
s involved in deletions in B-cell chronic lymphocytic leukemia and mal
ignant lymphomas and in the 12;14 translocation in uterine leiomyomas.