Evidence map›Paper›PMID 23150551›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

A critical role for Mnt in Myc-driven T-cell proliferation and oncogenesis.

Jason M Link, Sara Ota, Zi-Qiang Zhou, Colin J Daniel, Rosalie C Sears, Peter J Hurlin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. MNT: a new target for AML.Blood neoplasia · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Demystifying the Druggability of the MYC Family of Oncogenes.Journal of the American Chemical Society · 2023
    Review
  7. Article
  8. FTO Alleviates CdClInternational journal of molecular sciences · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Detection of Post-translational Modifications on MYC.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Mnt modulates Myc-driven lymphomagenesis.Cell death and differentiation · 2017
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jason M LinkShriners Hospitals for Children-Portland, Portland, OR 97239, USA.
Sara Ota
Zi-Qiang Zhou
Colin J Daniel
Rosalie C Sears
Peter J Hurlin
Shriners Hospitals for Children - Portland · USOregon Health & Science University · US

Funding

Cellular Mechanisms Controlling Myc Protein StabilityR01CA100855 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2003 to 2014
$3.6M
Myc Antagonism and Tumor Suppression by MntR01CA108855 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI HURLIN, PETER JAY · 2004 to 2008
$1.2M
NCI NIH HHS CA108855-06NCI NIH HHS R01 CA100855NCI NIH HHS R01 CA108855
6 · The paper itself

Abstract

Mnt (Max's next tango) is a Max-interacting transcriptional repressor that can antagonize both the proproliferative and proapoptotic functions of Myc in vitro. To ascertain the physiologically relevant functions of Mnt and to help define the relationship between Mnt and Myc in vivo, we generated a series of mouse strains in which Mnt was deleted in T cells in the absence of endogenous c-Myc or in the presence of ectopic c-Myc. We found that apoptosis caused by loss of Mnt did not require Myc but that ectopic Myc expression dramatically decreased the survival of both Mnt-deficient T cells in vivo and Mnt-deficient MEFs in vitro. Consequently, Myc-driven proliferative expansion of T cells in vitro and thymoma formation in vivo were prevented by the absence of Mnt. Consistent with T-cell models, mouse embryo fibroblasts (MEFs) lacking Mnt were refractory to oncogenic transformation by Myc. Tumor suppression caused by loss of Mnt was linked to increased apoptosis mediated by reactive oxygen species (ROS). Thus, although theoretically and experimentally a Myc antagonist, the dominant physiological role of Mnt appears to be suppression of apoptosis. Our results redefine the physiological relationship between Mnt and Myc and requirements for Myc-driven oncogenesis.

Indexed as

Cell ProliferationCell Transformation, NeoplasticAnimalsApoptosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMiceProto-Oncogene Proteins c-mycReactive Oxygen SpeciesRepressor ProteinsT-LymphocytesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMnt protein, mouseProto-Oncogene Proteins c-mycReactive Oxygen SpeciesRepressor Proteins

Identifiers

PMID23150551
PMCPMC3511755
OpenAlexW2019832715

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.