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J Biol Chem, Vol. 274, Issue 51, 36344-36350, December 17, 1999
From the Mad:Max heterodimers oppose the growth-promoting
action of Myc:Max heterodimers by recruiting the mSin3-histone
deacetylase (mSin3·HDAC) complex to DNA and functioning as potent
transcriptional repressors. There are four known members of the Mad
family that are indistinguishable in their abilities to interact with
Max, bind DNA, repress transcription, and block Myc + Ras
co-transformation. To investigate functional differences between Mad
family proteins, we have identified additional proteins that interact
with this family. Here we present the identification and
characterization of the novel basic-helix-loop-helix zipper protein Mlx
(Max-like protein x), which is
structurally and functionally related to Max. The similarities between
Mlx and Max include 1) broad expression in many tissues, 2) long
protein half-life, and 3) formation of heterodimers with Mad family
proteins that are capable of specific CACGTG binding. We show that
transcriptional repression by Mad1:Mlx heterodimers is dependent on
dimerization, DNA binding, and recruitment of the mSin3A·HDAC
corepressor complex. In contrast with Max, Mlx interacts only with Mad1
and Mad4. Together, these findings suggest that Mlx may act to
diversify Mad family function by its restricted association with a
subset of the Mad family of transcriptional repressors.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF203978.
Mlx, a Novel Max-like BHLHZip Protein That Interacts with the
Max Network of Transcription Factors*
§¶,§,
**, and
Huntsman Cancer Institute at the University
of Utah, Salt Lake City, Utah 84112-5550 and Fred Hutchinson
Cancer Research Center, Division of Basic Sciences,
Seattle, Washington, 98109
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
A Scholar of the Leukemia Society of America. Supported by
National Institutes of Health Grant GM5568-01. To whom correspondence should be addressed: Huntsman Cancer Institute at the University of
Utah, 2000 East North Campus Dr., Salt Lake City, Utah 84112-5550. Tel.: 801-581-5597; Fax: 801-585-1980; E-mail:
don.ayer@hci.utah.edu.
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