Journal
ONCOGENE
Volume 19, Issue 29, Pages 3266-3277Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1203634
Keywords
bHLHZip; Myc; Max; Rox; cell proliferation
Funding
- Telethon [TGM00S01, TGM06S01] Funding Source: Medline
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The Myc proto-oncogene family members have been identified as the cellular homologs of the transforming oncogene of avian retro viruses. They encode central regulators of mammalian cell proliferation and apoptosis, and they associate with the bHLHZip protein Max to hind specific DNA sequences and regulate the expression of genes important for cell cycle progression. The other family members, Mad1, Mxi1, Mad3, Mad4 and Rox (Mnt) antagonize their activities. The Mads and Ros compete with Myc in heterodimerizing with Max and in binding to the same specific target sequences, These Mads:Max and Rox:Max dimers repress transcription through binding to the mSIN3 corepressor protein and by tethering histone deacetylase-containing complexes to the DNA. In a screen for Rox interactors we isolated Mlx, a bHLHZip protein previously identified in a screen for Mad1 interactors. In the present work we extend the known dimerization partners of Mlx by demonstrating its ability to interact with Rox. Moreover, we show that contrary to previous reports Mlx is able to homodimerize and to bind E-box sequences at low concentration Levels. The possible role of Mlx in an emerging regulatory pathway and acting parallel to the Max driven network is discussed.
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