Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Mnt loss triggers myc transcription targets, proliferation, apoptosis, and transformation

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Nilsson, J. A.
  • Maclean, K. H.
  • Keller, U. B.
  • Pendeville, H.
  • Baudino, T. A.
  • Cleveland, John

publication date

  • February 2004

journal

  • Molecular and Cellular Biology  Journal

abstract

  • Myc oncoproteins are overexpressed in most cancers and are sufficient to accelerate cell proliferation and provoke transformation. However, in normal cells Myc also triggers apoptosis. All of the effects of Myc require its function as a transcription factor that dimerizes with Max. This complex induces genes containing CACGTG E-boxes, such as Ornithine decarboxylase (Odc), which harbors two of these elements. Here we report that in quiescent cells the Odc E-boxes are occupied by Max and Mnt, a putative Myc antagonist, and that this complex is displaced by Myc-Max complexes in proliferating cells. Knockdown of Mnt expression by stable retroviral RNA interference triggers many targets typical of the "Myc" response and provokes accelerated proliferation and apoptosis. Strikingly, these effects of Mnt knockdown are even manifest in cells lacking c-myc. Moreover, Mnt knockdown is sufficient to transform primary fibroblasts in conjunction with Ras. Therefore, Mnt behaves as a tumor suppressor. These findings support a model where Mnt represses Myc target genes and Myc functions as an oncogene by relieving Mnt-mediated repression.

subject areas

  • Animals
  • Apoptosis
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • Cell Division
  • Cell Transformation, Neoplastic
  • Cells, Cultured
  • Fibroblasts
  • Gene Expression Regulation, Neoplastic
  • Genes, Suppressor
  • Mice
  • Mice, Inbred BALB C
  • Nuclear Proteins
  • Ornithine Decarboxylase
  • Phenotype
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • Repressor Proteins
  • Transcription, Genetic
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/mcb.24.4.1560-1569.2004

PubMed ID

  • 14749372
scroll to property group menus

Additional Document Info

start page

  • 1560

end page

  • 1569

volume

  • 24

issue

  • 4

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support